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  • Humans  (1,943)
  • 1985-1989  (1,943)
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-09-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1989 Sep 8;245(4922):1031.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2772652" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4,5-Trichlorophenoxyacetic Acid/*adverse effects ; 2,4-Dichlorophenoxyacetic Acid/*adverse effects ; Dioxins/*adverse effects ; Humans ; Tetrachlorodibenzodioxin/*adverse effects ; United States ; *Veterans ; Vietnam
    Print ISSN: 0036-8075
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1989 May 19;244(4906):823-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543068" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; DNA Probes ; Humans ; Leukemia, Promyelocytic, Acute/enzymology/*genetics ; Nucleic Acid Hybridization ; Peroxidase/*genetics ; Translocation, Genetic
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-20
    Description: Human and murine mononuclear phagocytes express a high-affinity receptor for immunoglobulin G that plays a central role in macrophage antibody-dependent cellular cytotoxicity and clearance of immune complexes. The receptor (FcRI) may also be involved in CD4-independent infection of human macrophages by human immunodeficiency virus. This report describes the isolation of cDNA clones encoding the human FcRI by a ligand-mediated selection technique. Expression of the cDNAs in COS cells gave rise to immunoglobulin G binding of the expected affinity and subtype specificity. RNA blot analysis revealed expression of a 1.7-kilobase transcript in macrophages and in cells of the promonocytic cell line U937 induced with interferon-gamma. The extracellular region of FcRI consists of three immunoglobulin-like domains, two of which share homology with low-affinity receptor domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, J M -- Seed, B -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):378-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911749" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cercopithecus aethiops ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Molecular Weight ; Polymorphism, Genetic ; Receptors, Fc/*genetics ; Transfection
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  • 4
    Publication Date: 1989-04-14
    Description: Previous studies have demonstrated that allelic deletions of the short arm of chromosome 17 occur in over 75% of colorectal carcinomas. Twenty chromosome 17p markers were used to localize the common region of deletion in these tumors to a region contained within bands 17p12 to 17p13.3. This region contains the gene for the transformation-associated protein p53. Southern and Northern blot hybridization experiments provided no evidence for gross alterations of the p53 gene or surrounding sequences. As a more rigorous test of the possibility that p53 was a target of the deletions, the p53 coding regions from two tumors were analyzed; these two tumors, like most colorectal carcinomas, had allelic deletions of chromosome 17p and expressed considerable amounts of p53 messenger RNA from the remaining allele. The remaining p53 allele was mutated in both tumors, with an alanine substituted for valine at codon 143 of one tumor and a histidine substituted for arginine at codon 175 of the second tumor. Both mutations occurred in a highly conserved region of the p53 gene that was previously found to be mutated in murine p53 oncogenes. The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, S J -- Fearon, E R -- Nigro, J M -- Hamilton, S R -- Preisinger, A C -- Jessup, J M -- vanTuinen, P -- Ledbetter, D H -- Barker, D F -- Nakamura, Y -- White, R -- Vogelstein, B -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- HD20619/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):217-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2649981" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Chromosome Deletion ; *Chromosomes, Human, Pair 17/ultrastructure ; Colorectal Neoplasms/*genetics ; Humans ; Mice ; Mice, Nude ; *Mutation ; Neoplasm Proteins/*genetics ; Nucleic Acid Hybridization ; Oncogenes ; Phosphoproteins/*genetics ; Suppression, Genetic ; Tumor Suppressor Protein p53
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):448-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814475" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*therapy ; Female ; Humans ; *Psychotherapy, Group ; Survival Analysis
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1989 Jan 6;243(4887):29-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; *Legislation, Drug ; *Neurotoxins/toxicity ; United States ; United States Food and Drug Administration
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):313-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911743" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; Genetic Linkage ; Humans ; Mental Disorders/*genetics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-04
    Description: This lecture illustrates the early stages in the planning and discovery of propranolol, an adrenaline beta-adrenergic receptor antagonist, and cimetidine, a histamine H2-receptor antagonist--the first examples of clinically useful drugs from each of these classes. The significance of selective agonists, partial agonists, and syntopic antagonists and the importance of the bioassay and the use of molar models in the drug discovery process are discussed. For the future, an outline of potential developments in hormone-receptor concepts is offered leading to the conclusion that progress may depend on improvements in bioassays and related molar modeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black, J -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):486-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Analytical Pharmacology, Rayne Institute, King's College Hospital School of Medicine and Dentistry, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2569237" target="_blank"〉PubMed〈/a〉
    Keywords: *Adrenergic beta-Antagonists/therapeutic use ; Angina Pectoris/drug therapy/physiopathology ; Animals ; Biological Assay ; Duodenal Ulcer/drug therapy ; Epinephrine/analogs & derivatives ; Histamine/analogs & derivatives ; *Histamine H2 Antagonists/therapeutic use ; Humans ; Stomach Ulcer/drug therapy
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  • 9
    Publication Date: 1989-02-10
    Description: Transforming growth factor alpha (TGF-alpha) is produced by and required for the growth of epithelial cells and is angiogenic in vivo. Since epidermal hyperplasia and angiogenesis are hallmarks of psoriasis, TGF-alpha gene expression was analyzed in epidermal biopsies of normal and psoriatic skin. TGF-alpha messenger RNA and protein are much more abundant in lesional psoriatic epidermis than in normal-appearing skin of psoriatic patients or in normal epidermis. In contrast, messenger RNA levels of transforming growth factor beta 1 (TGF-beta 1), which inhibits epithelial cell growth, are not significantly different in normal, uninvolved, and lesional psoriatic epidermis. Thus, psoriatic epidermal hyperplasia may involve increased expression of a keratinocyte mitogen (TGF-alpha) rather than deficient expression of a growth inhibitor (TGF-beta 1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elder, J T -- Fisher, G J -- Lindquist, P B -- Bennett, G L -- Pittelkow, M R -- Coffey, R J Jr -- Ellingsworth, L -- Derynck, R -- Voorhees, J J -- 5-T32-AM07197-10/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Michigan, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2916128" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Northern ; Epidermis/physiopathology ; Gene Expression Regulation/drug effects ; Humans ; Immunoassay ; Psoriasis/*genetics ; Transforming Growth Factors/*genetics/metabolism
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  • 10
    Publication Date: 1989-12-22
    Description: Certain inflammatory stimuli render cultured human vascular endothelial cells hyperadhesive for neutrophils. This state is transient and reversible, in part because activated endothelial cells secrete a leukocyte adhesion inhibitor (LAI). LAI was identified as endothelial interleukin-8 (IL-8), the predominant species of which is an extended amino-terminal IL-8 variant. At nanomolar concentrations, purified endothelial IL-8 and recombinant human IL-8 inhibit neutrophil adhesion to cytokine-activated endothelial monolayers and protect these monolayers from neutrophil-mediated damage. These findings suggest that endothelial-derived IL-8 may function to attenuate inflammatory events at the interface between vessel wall and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gimbrone, M A Jr -- Obin, M S -- Brock, A F -- Luis, E A -- Hass, P E -- Hebert, C A -- Yip, Y K -- Leung, D W -- Lowe, D G -- Kohr, W J -- P01-HL-36028/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1601-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2688092" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Factors/pharmacology ; Cell Adhesion/drug effects ; Cells, Cultured ; Chemotactic Factors/*isolation & purification/pharmacology ; Culture Media/analysis ; Cytokines ; Endothelium, Vascular/cytology/drug effects/*physiology ; Humans ; Interleukin-1/*pharmacology ; Interleukin-8 ; Interleukins/*isolation & purification/pharmacology ; Molecular Sequence Data ; Neutrophils/cytology/drug effects/*physiology ; Recombinant Proteins/pharmacology
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-09-15
    Description: Locomotion and reaching have traditionally been regarded as separate motor activities. In fact, they may be closely connected both from an evolutionary and a neurophysiological viewpoint. Reaching seems to have evolved from the neural systems responsible for the active and precise positioning of the limb during locomotion; moreover, it seems to be organized in the spinal cord. The motor cortex and its corticospinal outflow are preferentially engaged when precise positioning of the limb is needed during locomotion and are also involved during reaching and active positioning of the hand near objects of interest. All of these motor activities require visuomotor coordination, and it is this coordination that could be achieved by the motor cortex and interconnected parietal and cerebellar areas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Georgopoulos, A P -- Grillner, S -- NS17413/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Sep 15;245(4923):1209-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Philip Bard Laboratories for Neurophysiology, Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2675307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Forelimb/*physiology ; Humans ; *Locomotion ; *Psychomotor Performance ; Vertebrates/*physiology
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldberger, A L -- New York, N.Y. -- Science. 1989 Mar 17;243(4897):1419.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2928773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Heart/*physiology ; Heart Conduction System/*physiology ; *Heart Rate ; Humans
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-10
    Description: This article reviews some of the significant contributions of fetal research and fetal tissue research over the past 20 years. The benefits of fetal research include the development of vaccines, advances in prenatal diagnosis, detection of malformations, assessment of safe and effective medications, and the development of in utero surgical therapies. Fetal tissue research benefits vaccine development, assessment of risk factors and toxicity levels in drug production, development of cell lines, and provides a source of fetal cells for ongoing transplantation trials. Together, fetal research and fetal tissue research offer tremendous potential for the treatment of the fetus, neonate, and adult.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, J T -- Sladek, J R Jr -- P01-NS24032/NS/NINDS NIH HHS/ -- P01-NS25778/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Nov 10;246(4931):775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, NY 14642.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2683082" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Congenital Abnormalities/diagnosis ; Female ; *Fetal Diseases ; *Fetal Research ; *Fetus/cytology/surgery ; Genetic Diseases, Inborn ; Humans ; Nontherapeutic Human Experimentation ; Pregnancy ; Prenatal Diagnosis ; *Research ; *Risk Assessment ; Therapeutic Human Experimentation ; Vaccines
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  • 14
    Publication Date: 1989-10-27
    Description: Host cell factors act together with regulatory genes of the human immunodeficiency virus (HIV) to control virus production. Human-Chinese hamster ovary hybrid cell clones were used to probe for human chromosomes involved in regulating HIV gene expression. DNA transfection experiments showed that 4 of 18 clones had high levels of HIV gene expression measured by both extracellular virus production and transactivation of the HIV long terminal repeat in the presence of the trans-activator (tat) gene. Karyotype analyses revealed a 94% concordance (17/18) between human chromosome 12 and HIV gene expression. Other chromosomes had an 11 to 72% concordance with virus production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hart, C E -- Ou, C Y -- Galphin, J C -- Moore, J -- Bacheler, L T -- Wasmuth, J J -- Petteway, S R Jr -- Schochetman, G -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):488-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centers for Disease Control, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2683071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chloramphenicol O-Acetyltransferase/genetics ; *Chromosomes, Human, Pair 12 ; Cricetinae ; Cricetulus ; Gene Expression Regulation, Viral/*genetics ; Genes, tat ; HIV-1/*genetics ; Humans ; Hybrid Cells ; Repetitive Sequences, Nucleic Acid ; Transcriptional Activation
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-12-15
    Description: In the report "X-ray diffraction to 302 giga-pascals: High-pressure crystal structure of cesium iodide" by H. K. Mao et al. (3 Nov., p. 649), reference 10, to a paper by R. Reichlin et al. [Phys. Rev. Lett. 56, 2858 (1986)], was incorrectly numbered (9) in the text (p. 649, column 3, line 1; p. 650, column 1, line 49).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hershfield, M -- Finkelberg, Z -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1375.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595358" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*deficiency/*therapeutic use ; Humans ; Immunologic Deficiency Syndromes/drug therapy/*etiology ; Nucleoside Deaminases/*deficiency/*therapeutic use
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1989 Nov 17;246(4932):878-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814507" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/*prevention & control/rehabilitation ; Humans ; International Cooperation ; Ussr ; United States
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  • 17
    Publication Date: 1989-04-28
    Description: Transcriptional activation of the human interleukin-2 (IL-2) gene, like induction of the IL-2 receptor alpha (IL-2R alpha) gene and the type 1 human immunodeficiency virus (HIV-1), is shown to be modulated by a kappa B-like enhancer element. Mutation of a kappa B core sequence identified in the IL-2 promoter (-206 to -195) partially inhibits both mitogen- and HTLV-I Tax-mediated activation of this transcription unit and blocks the specific binding of two inducible cellular factors. These kappa B-specific proteins (80 to 90 and 50 to 55 kilodaltons) similarly interact with the functional kappa B enhancer present in the IL-2R alpha promoter. These data suggest that these kappa B-specific proteins have a role in the coordinate regulation of this growth factor-growth factor receptor gene system that controls T cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoyos, B -- Ballard, D W -- Bohnlein, E -- Siekevitz, M -- Greene, W C -- A127053-01/PHS HHS/ -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):457-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mount Sinai Medical Center, Department of Microbiology, New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2497518" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cloning, Molecular ; DNA/metabolism ; DNA-Binding Proteins/*metabolism ; *Enhancer Elements, Genetic ; *Gene Expression Regulation ; Genes, Viral ; HIV-1/genetics ; HTLV-I Antigens/pharmacology ; Humans ; Immunoglobulin kappa-Chains/*genetics ; Interleukin-2/*genetics ; Molecular Weight ; Mutation ; Phytohemagglutinins/pharmacology ; Plasmids ; Promoter Regions, Genetic ; RNA, Messenger/biosynthesis ; T-Lymphocytes/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators ; Transcription Factors/pharmacology ; Transcription, Genetic ; Transfection
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-12
    Description: Augmented by public programs such as Social Security and Medicare, incomes of the elderly in the United States have grown more rapidly during the last several decades than have the incomes of other groups, so that on average the elderly are at least as well off as the nonelderly. Not all elderly, however, have done as well: widows, in particular, have high poverty rates. The economic prospects of the elderly during the next few decades are good because of the large work force from the baby-boom cohort. In the distant future a large fraction of the population will be elderly, which will probably lead to a deterioration in their economic status. Today, the main problems center on the distribution of economic resources among the elderly and on uncertainties such as costs of medical care.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurd, M D -- New York, N.Y. -- Science. 1989 May 12;244(4905):659-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Economics, State University of New York, Stony Brook 11794.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2655090" target="_blank"〉PubMed〈/a〉
    Keywords: *Aged ; *Economics ; Humans ; *Income ; Medicaid ; Medicare ; Poverty ; Social Security ; United States
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-28
    Description: The CD4 and CD8 T cell receptor accessory molecules can both be isolated from T lymphocytes in association with p56lck, a membrane-associated, cytoplasmic tyrosine protein kinase that is expressed exclusively in lymphoid cells. The enzymatic activity of p56lck may therefore be regulated by CD4 and CD8 and be important in antigen-induced T cell activation. Exposure of human T cells and some mouse T cells to the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of protein kinase C, caused the dissociation of p56lck and CD4. Activation of protein kinase C may therefore interrupt regulation of p56lck by CD4 and alter the ability of p56lck to interact with polypeptide substrates. In contrast, exposure of cells to TPA did not cause dissociation of p56lck and CD8. Regulation of p56lck by CD4 may therefore differ from regulation by CD8.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurley, T R -- Luo, K -- Sefton, B M -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):407-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Virology Laboratory, Salk Institute, San Diego, CA 92138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2787934" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cell Line ; Enzyme Activation ; Humans ; Leukemia, T-Cell ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Phosphorylation ; Precipitin Tests ; Protein Kinase C/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; T-Lymphocytes/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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  • 20
    Publication Date: 1989-06-16
    Description: Secretory chloride channels can be activated by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase in normal airway epithelial cells but not in cells from individuals with cystic fibrosis (CF). In excised, inside-out patches of apical membrane of normal human airway cells and airway cells from three patients with CF, the chloride channels exhibited a characteristic outwardly rectifying current-voltage relation and depolarization-induced activation. Channels from normal tissues were activated by both cAMP-dependent protein kinase and protein kinase C. However, chloride channels from CF patients could not be activated by either kinase. Thus, gating of normal epithelial chloride channels is regulated by both cAMP-dependent protein kinase and protein kinase C, and regulation by both kinases is defective in CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, T C -- Lu, L -- Zeitlin, P L -- Gruenert, D C -- Huganir, R -- Guggino, W B -- 1-K08-HL02188/HL/NHLBI NIH HHS/ -- R01-DK 39619/DK/NIDDK NIH HHS/ -- R01-HL 40178/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1351-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Johns Hopkins University, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2472005" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Chloride Channels ; Chlorides/*physiology ; Cystic Fibrosis/*physiopathology ; Electrophysiology ; Fetus ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Protein Kinase C/*physiology ; Protein Kinases/*physiology ; Respiratory System/cytology/physiopathology
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  • 21
    Publication Date: 1989-06-23
    Description: An airway epithelial cell line (CF/T43) was developed by infecting cultured airway epithelial cells from patients with cystic fibrosis (CF) with the pZIPneoSV(X)1/SV40T retrovirus and selecting for G418 resistance and ion transport properties. The distinctive chloride secretory phenotypes of the CF cell line CF/T43 and a normal cell line (NL/T4) were not perturbed by SV40T-induced cell transformation. Epithelial cell lines generated from CF cells with the SV40T gene can be used to test candidate CF genes and to evaluate the molecular mechanisms responsible for the CF phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jetten, A M -- Yankaskas, J R -- Stutts, M J -- Willumsen, N J -- Boucher, R C -- HL41983/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 23;244(4911):1472-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2472008" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Antigens, Polyomavirus Transforming/*genetics ; Calcimycin/pharmacology ; Cell Line ; Cell Membrane/physiology ; Chloride Channels ; Chlorides/*physiology ; Colforsin/pharmacology ; Cystic Fibrosis/pathology/*physiopathology ; Electric Conductivity ; Epithelium/drug effects/pathology/physiology ; Ethers/pharmacology ; Freeze Fracturing ; Humans ; Intercellular Junctions ; Ion Channels/physiology ; Ionomycin ; Membrane Proteins/*physiology ; Microscopy, Electron ; Nasal Polyps ; Simian virus 40/*immunology ; *Transformation, Genetic
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jukes, T H -- New York, N.Y. -- Science. 1989 May 5;244(4904):515.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2717938" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dimethylhydrazines/adverse effects ; *Fruit ; Herbicides ; Humans ; Neoplasms/*chemically induced ; Plant Growth Regulators ; Succinates/*adverse effects
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahn, C R -- Goldstein, B J -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2662406" target="_blank"〉PubMed〈/a〉
    Keywords: Diabetes Mellitus/*physiopathology ; Humans ; Insulin/*physiology ; Insulin Resistance
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  • 24
    Publication Date: 1989-01-13
    Description: The chemical synthesis of biologically active peptides and polypeptides can be achieved by using a convergent strategy of condensing protected peptide segments to form the desired molecule. An oxime support increases the ease with which intermediate protected peptides can be synthesized and makes this approach useful for the synthesis of peptides in which secondary structural elements have been redesigned. The extension of these methods to large peptides and proteins, for which folding of secondary structures into functional tertiary structures is critical, is discussed. Models of apolipoproteins, the homeo domain from the developmental protein encoded by the Antennapedia gene of Drosophila, a part of the Cro repressor, and the enzyme ribonuclease T1 and a structural analog have been synthesized with this method.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, E T -- Mihara, H -- Laforet, G A -- Kelly, J W -- Walters, L -- Findeis, M A -- Sasaki, T -- DK07825/DK/NIDDK NIH HHS/ -- GM12054/GM/NIGMS NIH HHS/ -- HL-186577/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):187-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Bioorganic Chemistry and Biochemistry, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492114" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apolipoprotein A-I ; Apolipoproteins A/chemical synthesis ; Humans ; Indicators and Reagents ; Lipoproteins, HDL/chemical synthesis ; Peptides/*chemical synthesis ; Protein Conformation ; Proteins/*chemical synthesis
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  • 25
    Publication Date: 1989-12-22
    Description: A human acute lymphoblastic leukemia (ALL) cell line that was transplanted into immune-deficient SCID mice proliferated in the hematopoietic tissues, invaded various organs, and led to the death of the mice. The distribution of leukemic cells in SCID mice was similar to the course of the disease in children. A-1 cells marked with a retrovirus vector showed clonal evolution after the transplant. SCID mice that were injected with bone marrow from three patients with non-T ALL had leukemic cells in their bone marrow and spleen. This in vivo model of human leukemia is an approach to understanding leukemic growth and progression and is a novel system for testing new treatment strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamel-Reid, S -- Letarte, M -- Sirard, C -- Doedens, M -- Grunberger, T -- Fulop, G -- Freedman, M H -- Phillips, R A -- Dick, J E -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1597-600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595371" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/pathology ; Cell Line ; Clone Cells ; DNA, Neoplasm/isolation & purification ; Humans ; Immunologic Deficiency Syndromes/*pathology ; Kidney/pathology ; Liver/pathology ; Mice ; Mice, Mutant Strains ; Neoplasm Transplantation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*pathology ; Transplantation, Heterologous
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  • 26
    Publication Date: 1989-05-19
    Description: The staphylococcal toxins are responsible for a number of diseases in man and other animals. Many of them have also long been known to be powerful T cell stimulants. They do not, however, stimulate all T cells. On the contrary, each toxin reacts with human T cells bearing particular V beta sequences as part of their receptors for major histocompatibility complex protein-associated antigen. The specificity of these toxins for V beta s puts them in the recently described class of superantigens and may account for the differential sensitivity of different individuals to the toxic effects of these proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kappler, J -- Kotzin, B -- Herron, L -- Gelfand, E W -- Bigler, R D -- Boylston, A -- Carrel, S -- Posnett, D N -- Choi, Y -- Marrack, P -- AI-17134/AI/NIAID NIH HHS/ -- AI-18785/AI/NIAID NIH HHS/ -- AI-22295/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 May 19;244(4906):811-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2524876" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies ; Antigens, CD3 ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; Bacterial Toxins/immunology/*pharmacology ; HLA Antigens/analysis ; Humans ; Immunoassay ; Lymphocyte Activation ; Receptors, Antigen, T-Cell/analysis/*immunology ; *Staphylococcus ; T-Lymphocytes/*immunology
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  • 27
    Publication Date: 1989-12-08
    Description: Vascular permeability factor (VPF) is a 40-kilodalton disulfide-linked dimeric glycoprotein that is active in increasing blood vessel permeability, endothelial cell growth, and angiogenesis. These properties suggest that the expression of VPF by tumor cells could contribute to the increased neovascularization and vessel permeability that are associated with tumor vasculature. The cDNA sequence of VPF from human U937 cells was shown to code for a 189-amino acid polypeptide that is similar in structure to the B chain of platelet-derived growth factor (PDGF-B) and other PDGF-B-related proteins. The overall identity with PDGF-B is 18%. However, all eight of the cysteines in PDGF-B were found to be conserved in human VPF, an indication that the folding of the two proteins is probably similar. Clusters of basic amino acids in the COOH-terminal halves of human VPF and PDGF-B are also prevalent. Thus, VPF appears to be related to the PDGF/v-sis family of proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keck, P J -- Hauser, S D -- Krivi, G -- Sanzo, K -- Warren, T -- Feder, J -- Connolly, D T -- New York, N.Y. -- Science. 1989 Dec 8;246(4935):1309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Culture and Biochemistry, Monsanto Company, St. Louis, MO 63167.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2479987" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Capillary Permeability/physiology ; Cell Division/physiology ; Cloning, Molecular ; Endothelium, Vascular/*cytology ; *Growth Substances ; Guinea Pigs ; Humans ; Lymphokines/*physiology ; Molecular Sequence Data ; Neovascularization, Pathologic/physiopathology ; Oncogene Proteins v-sis ; Platelet-Derived Growth Factor/physiology ; Retroviridae Proteins, Oncogenic/physiology ; Sequence Homology, Nucleic Acid ; Transforming Growth Factors ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 28
    Publication Date: 1989-09-08
    Description: Approximately 70 percent of the mutations in cystic fibrosis patients correspond to a specific deletion of three base pairs, which results in the loss of a phenylalanine residue at amino acid position 508 of the putative product of the cystic fibrosis gene. Extended haplotype data based on DNA markers closely linked to the putative disease gene locus suggest that the remainder of the cystic fibrosis mutant gene pool consists of multiple, different mutations. A small set of these latter mutant alleles (about 8 percent) may confer residual pancreatic exocrine function in a subgroup of patients who are pancreatic sufficient. The ability to detect mutations in the cystic fibrosis gene at the DNA level has important implications for genetic diagnosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerem, B -- Rommens, J M -- Buchanan, J A -- Markiewicz, D -- Cox, T K -- Chakravarti, A -- Buchwald, M -- Tsui, L C -- DK34944/DK/NIDDK NIH HHS/ -- GM33771/GM/NIGMS NIH HHS/ -- HD00774/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Sep 8;245(4922):1073-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2570460" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Chromosome Deletion ; Cystic Fibrosis/diagnosis/enzymology/*genetics ; DNA Mutational Analysis ; *Genes, Recessive ; Genetic Linkage ; Genetic Markers ; Haplotypes ; Humans ; Pancreas/enzymology ; Polymorphism, Restriction Fragment Length
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  • 29
    Publication Date: 1989-03-10
    Description: Antisense RNA-mediated inhibition of gene expression was used to investigate the biological function of the c-raf-1 gene in a radiation-resistant human squamous carcinoma cell line, SQ-20B. S1 nuclease protection assays revealed that transfection of full-length raf complementary DNA in the antisense orientation (AS) leads to a specific reduction (greater than tenfold) of steady-state levels of the endogenous c-raf-1 sense (S) transcript in SQ-20B cells. In nude mice, the malignant potential of SQ-20B cells transfected with raf (S) was significantly increased relative to that of SQ-20B cells transfected with raf (AS). SQ-20B cells containing transfected raf (S) maintained a radiation-resistant phenotype as compared to those cells harboring the AS version, which appeared to have enhanced radiation sensitivity. These data indicate that the reduced expression of endogenous c-raf-1 is sufficient to modulate the tumorigenicity and the radiation-resistant phenotype of SQ-20B cells, thus implicating c-raf-1 in a pathway important to the genesis of this type of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, U -- Pfeifer, A -- Brennan, T -- Beckett, M -- Weichselbaum, R R -- Dritschilo, A -- Mark, G E -- New York, N.Y. -- Science. 1989 Mar 10;243(4896):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Medicine, Vincent T. Lombardi Comprehensive Cancer Research Center, Georgetown University Medical Center, Washington 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2466340" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Southern ; Carcinoma, Squamous Cell/*genetics ; Cell Line ; Cell Survival/*radiation effects ; Clone Cells ; Dose-Response Relationship, Radiation ; *Gene Expression Regulation ; Humans ; Kinetics ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Nucleic Acid Hybridization ; *Proto-Oncogenes ; RNA/*genetics ; RNA, Antisense ; RNA, Messenger/*antagonists & inhibitors ; Transcription, Genetic ; Transfection ; Transplantation, Heterologous ; Tumor Cells, Cultured/*radiation effects
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerr, R A -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):170.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2521400" target="_blank"〉PubMed〈/a〉
    Keywords: Armenia ; *Disasters ; *Facility Design and Construction ; Humans ; *Mortality ; Urban Population
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirk, D -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):464-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2756429" target="_blank"〉PubMed〈/a〉
    Keywords: *Embryo, Mammalian ; Germany, West ; Humans ; *Legislation, Medical ; *Research
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-27
    Description: Two human cell lines (termed rho 0), which had been completely depleted of mitochondrial DNA (mtDNA) by long-term exposure to ethidium bromide, were found to be dependent on uridine and pyruvate for growth because of the absence of a functional respiratory chain. Loss of either of these two metabolic requirements was used as a selectable marker for the repopulation of rho 0 cells with exogenous mitochondria by complementation. Transformants obtained with various mitochondrial donors exhibited a respiratory phenotype that was in most cases distinct from that of the rho 0 parent or the donor, indicating that the genotypes of the mitochondrial and nuclear genomes as well as their specific interactions play a role in the respiratory competence of a cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, M P -- Attardi, G -- GM11726/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):500-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814477" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Fusion ; Cell Line ; *DNA, Mitochondrial ; Humans ; Mitochondria/*physiology ; Oxygen Consumption/physiology ; *Transformation, Genetic
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kluender, K R -- Greenberg, S -- New York, N.Y. -- Science. 1989 Jun 30;244(4912):1530.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2740894" target="_blank"〉PubMed〈/a〉
    Keywords: Cognition/physiology ; Hearing/physiology ; Humans ; Phonetics ; Speech Perception/*physiology
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koppenol, W H -- Bounds, P L -- New York, N.Y. -- Science. 1989 Oct 20;246(4928):311.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biodynamics Institute and Departments of Chemistry and Biochemistry, Louisiana State University, Baton Rouge, LA 70803, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Dose-Response Relationship, Radiation ; Humans ; *Radiation, Ionizing
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1989 Nov 24;246(4933):981.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2587989" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Legal ; Female ; Humans ; National Institutes of Health (U.S.)/*organization & administration ; Politics ; Pregnancy ; United States ; United States Dept. of Health and Human Services
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, Daniel E -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644373" target="_blank"〉PubMed〈/a〉
    Keywords: Chimera ; *DNA, Recombinant ; *Genetic Engineering ; Genetic Therapy ; Humans ; Risk ; Risk Assessment
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1989 May 5;244(4904):513.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2717937" target="_blank"〉PubMed〈/a〉
    Keywords: Accidents, Traffic/*legislation & jurisprudence/prevention & control ; *Alcoholic Intoxication ; *Ethics ; Humans ; Statistics as Topic ; Vaccines/adverse effects
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1989 Oct 13;246(4927):189.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799380" target="_blank"〉PubMed〈/a〉
    Keywords: *Human Genome Project ; Humans ; Resource Allocation ; *Risk Assessment
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, Daniel E -- New York, N.Y. -- Science. 1989 Aug 11;245(4918):573.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644383" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Confidentiality ; *Editorial Policies ; *Fraud ; Humans ; Peer Review ; *Publishing ; *Research ; Research Personnel ; *Science ; *Scientific Misconduct
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-02-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1989 Feb 3;243(4891):585.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2916112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens ; Food Additives ; *Hazardous Substances ; Humans ; *Legislation, Drug
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  • 41
    Publication Date: 1989-04-21
    Description: A specific assay has been developed for a blood-borne non-A, non-B hepatitis (NANBH) virus in which a polypeptide synthesized in recombinant yeast clones of the hepatitis C virus (HCV) is used to capture circulating viral antibodies. HCV antibodies were detected in six of seven human sera that were shown previously to transmit NANBH to chimpanzees. Assays of ten blood transfusions in the United States that resulted in chronic NANBH revealed that there was at least one positive blood donor in nine of these cases and that all ten recipients seroconverted during their illnesses. About 80 percent of chronic, post-transfusion NANBH (PT-NANBH) patients from Italy and Japan had circulating HCV antibody; a much lower frequency (15 percent) was observed in acute, resolving infections. In addition, 58 percent of NANBH patients from the United States with no identifiable source of parenteral exposure to the virus were also positive for HCV antibody. These data indicate that HCV is a major cause of NANBH throughout the world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, G -- Choo, Q L -- Alter, H J -- Gitnick, G L -- Redeker, A G -- Purcell, R H -- Miyamura, T -- Dienstag, J L -- Alter, M J -- Stevens, C E -- New York, N.Y. -- Science. 1989 Apr 21;244(4902):362-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2496467" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/*analysis ; Blood Donors ; Blood Transfusion ; Hepatitis C/*immunology/transmission ; Hepatitis Viruses/*immunology ; Hepatitis, Viral, Human/*immunology ; Humans ; Italy ; Japan ; United States
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  • 42
    Publication Date: 1989-08-18
    Description: CD4 is a cell surface glycoprotein that is thought to interact with nonpolymorphic determinants of class II major histocompatibility (MHC) molecules. CD4 is also the receptor for the human immunodeficiency virus (HIV), binding with high affinity to the HIV-1 envelope glycoprotein, gp120. Homolog-scanning mutagenesis was used to identify CD4 regions that are important in class II MHC binding and to determine whether the gp120 and class II MHC binding sites of CD4 are related. Class II MHC binding was abolished by mutations in each of the first three immunoglobulin-like domains of CD4. The gp120 binding could be abolished without affecting class II MHC binding and vice versa, although at least one mutation examined reduced both functions significantly. These findings indicate that, while there may be overlap between the gp120 and class II MHC binding sites of CD4, these sites are distinct and can be separated. Thus it should be possible to design CD4 analogs that can block HIV infectivity but intrinsically lack the ability to affect the normal immune response by binding to class II MHC molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamarre, D -- Ashkenazi, A -- Fleury, S -- Smith, D H -- Sekaly, R P -- Capon, D J -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):743-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie, Institut de Recherches Cliniques de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Surface ; Binding Sites ; DNA, Recombinant ; HIV/*metabolism ; HIV Envelope Protein gp120 ; HLA-DP Antigens/immunology ; Histocompatibility Antigens Class II/*immunology ; Humans ; Hybridomas ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, HIV ; Receptors, Virus/genetics/immunology/*metabolism ; Retroviridae Proteins/immunology/*metabolism ; Rosette Formation ; Structure-Activity Relationship ; T-Lymphocytes/immunology/metabolism ; Transfection
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  • 43
    Publication Date: 1989-12-22
    Description: CD16 is a low-affinity immunoglobulin G (IgG) Fc receptor that is expressed on natural killer (NK) cells, granulocytes, activated macrophages, and some T lymphocytes. Two similar genes, CD16-I and CD16-II, encode membrane glycoproteins that are anchored by phosphatidylinositol (PI)-glycan and transmembrane polypeptides, respectively. The primary structural requirements for PI-linkage were examined by constructing a series of hybrid cDNA molecules. Although both cDNA's have an identical COOH-terminal hydrophobic segment, CD16-I has Ser203 whereas CD16-II has Phe203. Conversion of Phe to Ser in CD16-II permits expression of a PI-glycan-anchored glycoprotein, whereas conversion of Ser to Phe in CD16-I prevents PI-glycan linkage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanier, L L -- Cwirla, S -- Yu, G -- Testi, R -- Phillips, J H -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1611-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Becton Dickinson Monoclonal Center, Inc., Mountain View, CA 94043.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2531919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*genetics ; Antigens, Differentiation/*genetics/metabolism ; Base Sequence ; Cell Line ; Cell Membrane/immunology ; Codon/genetics ; *Genes, Immunoglobulin ; Granulocytes/immunology ; Humans ; Membrane Glycoproteins/*genetics ; Molecular Sequence Data ; *Phenylalanine ; Receptors, Fc/*genetics/metabolism ; Receptors, IgG ; *Serine ; Transfection
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-31
    Description: The drug sensitivities of human immunodeficiency virus (HIV) isolates from a group of patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) who were receiving zidovudine (3'-azido-3'-deoythymidine, AZT) therapy were tested by means of a newly developed plaque assay in CD4+ HeLa cells. Fifty percent inhibitory dose (ID50) values of 18 isolates from untreated individuals ranged between 0.01 microM and 0.05 microM. In contrast, most isolates from patients who had received zidovudine for 6 months or more exhibited decreased sensitivity characterized by changes in ID50 or ID95 values (or both), with isolates from several patients (5/15) showing 100-fold increases in ID50. The latter isolates were also insensitive to 3'-azido-2',3'-dideoxyuridine; however, the isolates were still sensitive to 2',3'-dideoxycytidine, 2',3'-dideoxy-2',3'-didehydrothymidine, or phosphonoformate. It cannot be determined from this small sample of patients whether development of a less sensitive virus phenotype results in clinical resistance. Appearance of such variants was not associated with a consistent increase in viral p24 concentrations in patient plasma and did not herald any sudden deterioration in clinical status. More extensive studies are required to determine the clinical significance. Thus, it would be premature to alter any treatment protocols for HIV-infected individuals at present.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larder, B A -- Darby, G -- Richman, D D -- AI-52578/AI/NIAID NIH HHS/ -- AI-62548/AI/NIAID NIH HHS/ -- HB-67019/HB/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Sciences, Wellcome Research Laboratories, Beckenham, Kent BR3 3BS, United Kingdon.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2467383" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Complex/drug therapy/microbiology ; Acquired Immunodeficiency Syndrome/drug therapy/*microbiology ; Dideoxynucleosides/pharmacology ; Drug Resistance ; Foscarnet ; HIV/*drug effects/immunology/isolation & purification ; HIV Core Protein p24 ; HeLa Cells ; Humans ; Microbial Sensitivity Tests ; Phosphonoacetic Acid/analogs & derivatives/pharmacology ; Retroviridae Proteins/analysis ; Reverse Transcriptase Inhibitors ; Viral Plaque Assay ; Virus Replication/drug effects ; Zalcitabine ; Zidovudine/*pharmacology/therapeutic use
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  • 45
    Publication Date: 1989-12-01
    Description: Human immunodeficiency virus (HIV) isolates with reduced sensitivity to zidovudine (3'-azido-3'-deoxythymidine, AZT) from individuals with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex were studied to determine the genetic basis of their resistance. Most were sequential isolates obtained at the initiation of and during therapy. Comparative nucleotide sequence analysis of the reverse transcriptase (RT) coding region from five pairs of sensitive and resistant isolates identified three predicted amino acid substitutions common to all the resistant strains (Asp67----Asn, Lys70----Arg, Thr215----Phe or Tyr) plus a fourth in three isolates (Lys219----Gln). Partially resistant isolates had combinations of these four changes. An infectious molecular clone constructed with these four mutations in RT yielded highly resistant HIV after transfection of T cells. The reproducible nature of these mutations should make it possible to develop rapid assays to predict zidovudine resistance by performing polymerase chain reaction amplification of nucleic acid from peripheral blood lymphocytes, thereby circumventing current lengthy HIV isolation and sensitivity testing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larder, B A -- Kemp, S D -- New York, N.Y. -- Science. 1989 Dec 1;246(4934):1155-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Sciences Department, Wellcome Research Laboratories, Beckenham, Kent, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2479983" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Complex/drug therapy/microbiology ; Acquired Immunodeficiency Syndrome/drug therapy/*microbiology ; Amino Acid Sequence ; Cloning, Molecular ; Drug Resistance/genetics ; Genes, Viral ; HIV-1/drug effects/*enzymology/genetics ; Humans ; Molecular Sequence Data ; *Mutation ; RNA-Directed DNA Polymerase/*genetics ; Zidovudine/pharmacology/*therapeutic use
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  • 46
    Publication Date: 1989-06-09
    Description: Respondents in the 1988 General Social Survey (GSS) were asked to scan their acquaintance networks to identify all those who had been a victim of a homicide or had acquired immunodeficiency syndrome (AIDS). Estimates of the sex, race, age, and regional breakdowns for homicides in the last year and for people with AIDS were compared with official statistics. The GSS estimates for the distribution of homicide victims replicate the official statistics quite well. The GSS estimates for AIDS cases suggest that the data provided to the Centers for Disease Control may underestimate by a substantial margin the prevalence of AIDS in the white population of higher socioeconomic status, overstate the relative prevalence of the disease in the minority populations, underestimate the prevalence of the disease in the Midwest, and overstate it for the East.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laumann, E O -- Gagnon, J H -- Michaels, S -- Michael, R T -- Coleman, J S -- N0I-HD-8-2907/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1186-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sociology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543079" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*epidemiology ; Centers for Disease Control and Prevention (U.S.) ; Demography ; Female ; Humans ; Male ; Population Surveillance ; United States
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  • 47
    Publication Date: 1989-05-26
    Description: Spondyloepiphyseal dysplasias (SED) are a heterogeneous group of inherited disorders characterized by disproportionate short stature and pleiotropic involvement of the skeletal and ocular systems. Evidence has suggested that SED may result from structural defects in type II collagen. To confirm the validity of this hypothesis, the structure of the "candidate" type II collagen gene (COL2A1) has been directly examined in a relatively large SED family. Coarse scanning of the gene by Southern blot hybridization identified an abnormal restriction pattern in one of the affected members of the kindred. Analysis of selected genomic fragments, amplified by the polymerase chain reaction, precisely localized the molecular defect and demonstrated that all affected family members carried the same heterozygous single-exon deletion. As a consequence of the mutation, nearly 90 percent of the assembled type II collagen homotrimers are expected to contain one or more procollagen subunits harboring an interstitial deletion of 36 amino acids in the triple helical domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, B -- Vissing, H -- Ramirez, F -- Rogers, D -- Rimoin, D -- AR-38648/AR/NIAMS NIH HHS/ -- HD-22657/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 May 26;244(4907):978-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, State University of New York Health Science Center, Brooklyn 11203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543071" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Child, Preschool ; Chromosome Deletion ; Collagen/*genetics ; DNA Restriction Enzymes ; DNA-Directed DNA Polymerase ; Exons ; Female ; Gene Amplification ; Humans ; Macromolecular Substances ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Osteochondrodysplasias/*genetics ; Pedigree ; Procollagen/genetics
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  • 48
    Publication Date: 1989-04-28
    Description: Confirmed infection with HTLV-II (human T cell leukemia virus type II) has been described only in rare cases. The major limitation to serological diagnosis of HTLV-II has been the difficulty of distinguishing HTLV-II from HTLV-I (human T cell leukemia virus type I) infection, because of substantial cross-reactivity between the viruses. A sensitive modification of the polymerase chain reaction method was used to provide unambiguous molecular evidence that a significant proportion of intravenous drug abusers are infected with HTLV, and the majority of these individuals are infected with HTLV-II rather than HTLV-I. Of 23 individuals confirmed by polymerase chain reaction analysis to be infected with HTLV, 21 were identified to be infected with HTLV-II, and 2 were infected with HTLV-I. Molecular identification of an HTLV-II--infected population provides an opportunity to investigate the pathogenicity of HTLV-II in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, H -- Swanson, P -- Shorty, V S -- Zack, J A -- Rosenblatt, J D -- Chen, I S -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):471-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diagnostics Division, Abbott Laboratories, North Chicago, IL 60064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2655084" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Viral/analysis ; DNA-Directed DNA Polymerase ; Genes, Viral ; HTLV-I Antibodies/analysis ; HTLV-I Infections/diagnosis/epidemiology/etiology ; HTLV-II Antibodies/*analysis ; HTLV-II Infections/diagnosis/*epidemiology/etiology ; Human T-lymphotropic virus 1/genetics/immunology ; Human T-lymphotropic virus 2/genetics/immunology ; Humans ; Immunoblotting ; Immunoenzyme Techniques ; Louisiana ; Molecular Sequence Data ; Sequence Homology, Nucleic Acid ; Substance-Related Disorders/*complications
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):355.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2756424" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*analysis ; *Forensic Medicine ; Humans
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Jun 30;244(4912):1543.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2740900" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Sequence ; Budgets/economics ; *Chromosome Mapping ; *Chromosomes, Human ; Humans ; International Cooperation ; National Institutes of Health (U.S.)/*organization & administration ; Research Support as Topic ; United States
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727701" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chile ; *Hominidae ; Humans ; *Paleontology
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chile ; *Hominidae ; Humans ; North America ; *Paleontology
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  • 53
    Publication Date: 1989-12-08
    Description: Vascular endothelial growth factor (VEGF) was purified from media conditioned by bovine pituitary folliculostellate cells (FC). VEGF is a heparin-binding growth factor specific for vascular endothelial cells that is able to induce angiogenesis in vivo. Complementary DNA clones for bovine and human VEGF were isolated from cDNA libraries prepared from FC and HL60 leukemia cells, respectively. These cDNAs encode hydrophilic proteins with sequences related to those of the A and B chains of platelet-derived growth factor. DNA sequencing suggests the existence of several molecular species of VEGF. VEGFs are secreted proteins, in contrast to other endothelial cell mitogens such as acidic or basic fibroblast growth factors and platelet-derived endothelial cell growth factor. Human 293 cells transfected with an expression vector containing a bovine or human VEGF cDNA insert secrete an endothelial cell mitogen that behaves like native VEGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, D W -- Cachianes, G -- Kuang, W J -- Goeddel, D V -- Ferrara, N -- New York, N.Y. -- Science. 1989 Dec 8;246(4935):1306-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genetech, South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2479986" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Cattle ; Cell Division ; Cloning, Molecular ; Endothelium, Vascular/*cytology ; Gene Library ; Humans ; Lymphokines/genetics/*physiology/secretion ; Molecular Sequence Data ; Neovascularization, Pathologic/*physiopathology ; Sequence Homology, Nucleic Acid ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):467-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2502841" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Clinical Trials as Topic ; Designer Drugs ; Humans ; Levodopa/therapeutic use ; Monoamine Oxidase Inhibitors/*therapeutic use ; Neurons/physiology ; Parkinson Disease/*drug therapy ; Parkinson Disease, Secondary/chemically induced ; Phenethylamines/*therapeutic use ; Pyridines/adverse effects/metabolism ; Selegiline/*therapeutic use ; Substantia Nigra/pathology/physiopathology
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levitan, I B -- New York, N.Y. -- Science. 1989 Jun 23;244(4911):1423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2544028" target="_blank"〉PubMed〈/a〉
    Keywords: Chloride Channels ; Chlorides/physiology ; Cystic Fibrosis/genetics/*physiopathology ; Epithelium/physiopathology ; Humans ; Membrane Proteins/physiology ; Protein Kinases/physiology
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1033-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727690" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*analysis ; Expert Testimony ; Forensic Medicine/*legislation & jurisprudence ; Humans
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1666-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2928802" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Biological Evolution ; Europe ; *Fossils ; Hominidae/*anatomy & histology ; Humans ; *Paleontology
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-02-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1989 Feb 17;243(4893):892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2919284" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/*transplantation ; Follow-Up Studies ; Humans ; Parkinson Disease/*surgery
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  • 59
    Publication Date: 1989-06-16
    Description: Apical membrane chloride channels control chloride secretion by airway epithelial cells. Defective regulation of these channels is a prominent characteristic of cystic fibrosis. In normal intact cells, activation of protein kinase C (PKC) by phorbol ester either stimulated or inhibited chloride secretion, depending on the physiological status of the cell. In cell-free membrane patches, PKC also had a dual effect: at a high calcium concentration, PKC inactivated chloride channels; at a low calcium concentration, PKC activated chloride channels. In cystic fibrosis cells, PKC-dependent channel inactivation was normal, but activation was defective. Thus it appears that PKC phosphorylates and regulates two different sites on the channel or on an associated membrane protein, one of which is defective in cystic fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, M -- McCann, J D -- Anderson, M P -- Clancy, J P -- Liedtke, C M -- Nairn, A C -- Greengard, P -- Welsch, M J -- DK27651/DK/NIDDK NIH HHS/ -- HL29851/HL/NHLBI NIH HHS/ -- HL42385/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Membrane Transport, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2472006" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/physiology ; Chloride Channels ; Chlorides/*physiology ; Cystic Fibrosis/*physiopathology ; Enzyme Activation ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Protein Kinase C/*physiology ; Respiratory Physiological Phenomena ; Respiratory System/cytology/*physiopathology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-27
    Description: The processes that underlie perception of consonants and vowels are specifically phonetic, distinct from those that localize sources and assign auditory qualities to the sound from each source. This specialization, or module, increases the rate of information flow, establishes the parity between sender and receiver that every communication system must have, and provides for the natural development of phonetic structures in the species and in the individual. The phonetic module has certain properties in common with modules that are "closed" (for example, sound localization or echo ranging in bats) and, like other members of this class, is so placed in the architecture of the auditory system as to preempt information that is relevant to its special function. Accordingly, this information is not available to such "open" modules as those for pitch, loudness, and timbre.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liberman, A M -- Mattingly, I G -- H-01994/PHS HHS/ -- New York, N.Y. -- Science. 1989 Jan 27;243(4890):489-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Haskins Laboratories, New Haven, CT 06511.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2643163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Auditory Perception/physiology ; Communication ; Humans ; *Phonetics ; Speech ; Speech Perception/*physiology
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  • 61
    Publication Date: 1989-05-05
    Description: An approach based on the polymerase chain reaction has been devised to clone new members of the family of genes encoding guanosine triphosphate-binding protein (G protein)-coupled receptors. Degenerate primers corresponding to consensus sequences of the third and sixth transmembrane segments of available receptors were used to selectively amplify and clone members of this gene family from thyroid complementary DNA. Clones encoding three known receptors and four new putative receptors were obtained. Sequence comparisons established that the new genes belong to the G protein-coupled receptor family. Close structural similarity was observed between one of the putative receptors and the 5HT1a receptor. Two other molecules displayed common sequence characteristics, suggesting that they are members of a new subfamily of receptors with a very short nonglycosylated (extracellular) amino-terminal extension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Libert, F -- Parmentier, M -- Lefort, A -- Dinsart, C -- Van Sande, J -- Maenhaut, C -- Simons, M J -- Dumont, J E -- Vassart, G -- New York, N.Y. -- Science. 1989 May 5;244(4904):569-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Recherche Interdisciplinaire, Faculte de Medecine, Universite Libre de Bruxelles, Campus Erasme, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2541503" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Cloning, Molecular ; DNA/genetics ; DNA-Directed DNA Polymerase ; GTP-Binding Proteins/*metabolism ; *Gene Amplification ; Humans ; Molecular Sequence Data ; Receptors, Adrenergic, alpha/genetics ; Receptors, Adrenergic, beta/genetics ; Receptors, Muscarinic/genetics ; Receptors, Neurokinin-2 ; Receptors, Neurotransmitter/*genetics ; Receptors, Serotonin/genetics ; Sequence Homology, Nucleic Acid ; Thyroid Gland/analysis ; Transcription, Genetic
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-10
    Description: A method was developed for selectively isolating genes from localized regions of the human genome that are contained in interspecific hybrid cells. Complementary human DNA was prepared from a human-rodent somatic cell hybrid that contained less than 1% human DNA, by using consensus 5' intron splice sequences as primers. These primers would select immature, unspliced messenger RNA (still retaining species-specific repeat sequences) as templates. Screening a derived complementary DNA library for human repeat sequences resulted in the isolation of human clones at the anticipated frequency with characteristics expected of exons of transcribed human genes--single copy sequences that hybridized to discrete bands on Northern (RNA) blots.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, P -- Legerski, R -- Siciliano, M J -- GM19436/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1989 Nov 10;246(4931):813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2479099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Blotting, Southern ; Chromosome Mapping ; Chromosomes, Human, Pair 19 ; Cloning, Molecular ; Cricetinae ; DNA/biosynthesis/genetics/*isolation & purification ; Humans ; *Hybrid Cells ; Introns ; Nucleic Acid Hybridization ; RNA/genetics ; Repetitive Sequences, Nucleic Acid ; Restriction Mapping ; Templates, Genetic
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  • 63
    Publication Date: 1989-01-13
    Description: In the polymerase chain reaction (PCR), two specific oligonucleotide primers are used to amplify the sequences between them. However, this technique is not suitable for amplifying genes that encode molecules where the 5' portion of the sequences of interest is not known, such as the T cell receptor (TCR) or immunoglobulins. Because of this limitation, a novel technique, anchored polymerase chain reaction (A-PCR), was devised that requires sequence specificity only on the 3' end of the target fragment. It was used to analyze TCR delta chain mRNA's from human peripheral blood gamma delta T cells. Most of these cells had a V delta gene segment not previously described (V delta 3), and the delta chain junctional sequences formed a discrete subpopulation compared with those previously reported.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loh, E Y -- Elliott, J F -- Cwirla, S -- Lanier, L L -- Davis, M M -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Microbiology and Immunology, Stanford University School of Medicine, CA 94305-5402.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2463672" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Gene Amplification ; *Genes ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Oligonucleotide Probes ; RNA, Messenger/genetics ; RNA-Directed DNA Polymerase ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/immunology
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  • 64
    Publication Date: 1989-07-28
    Description: A 47-kilodalton neutrophil cytosol factor (NCF-47k), required for activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase superoxide (O2-.) production, is absent in most patients with autosomal recessive chronic granulomatous disease (AR-CGD). NCF-47k cDNAs were cloned from an expression library. The largest clone predicted a 41.9-kD protein that contained an arginine and serine-rich COOH-terminal domain with potential protein kinase C phosphorylation sites. A 33-amino acid segment of NCF-47k shared 49% identity with ras p21 guanosine triphosphatase activating protein. Recombinant NCF-47k restored O2-. -producing activity to AR-CGD neutrophil cytosol in a cell-free assay. Production of active recombinant NCF-47k will enable functional regions of this molecule to be mapped.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lomax, K J -- Leto, T L -- Nunoi, H -- Gallin, J I -- Malech, H L -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):409-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bacterial Diseases Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2547247" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Blotting, Northern ; Cloning, Molecular ; DNA/*genetics ; Granulomatous Disease, Chronic/enzymology/*genetics ; Humans ; Immunoblotting ; Molecular Sequence Data ; NADH, NADPH Oxidoreductases/*metabolism ; NADPH Oxidase ; Neutrophils/*metabolism ; Phosphoproteins/*genetics/metabolism ; Phosphorylation ; Recombinant Proteins/genetics/metabolism ; Superoxides/metabolism
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-07
    Description: In the report "Honeyguides and honey gatherers: Interspecific communication in a symbiotic relationship" by H. A. Isack and H.-U. Reyer (10 Mar., p. 1343), the third and fourth sentences of the first full paragraph of column 2 on page 1344 should have read "This whistle, known in Boran language as "Fuulido," is produced by blowing air into clasped fists, modified snail shells, or hollowed-out doum palm nuts(Hyphaene coriacea Gaertn.) Shouting and knocking on dry wood are also used to draw the birds' attention."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luehrmann, A -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2662407" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Child ; *Computer-Assisted Instruction ; *Computers ; Curriculum ; *Education ; Humans
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-31
    Description: The ion current induced by the glutamate receptor agonist N-methyl-D-aspartate (NMDA) in voltage-clamped hippocampal neurons was inhibited by ethanol (EtOH). Inhibition increased in a concentration-dependent manner over the range 5 to 50 mM, a range that also produces intoxication. The amplitude of the NMDA-activated current was reduced 61 percent by 50 mM EtOH; in contrast, this concentration of EtOH reduced the amplitude of current activated by the glutamate receptor agonists kainate and quisqualate by only 18 and 15 percent, respectively. The potency for inhibition of the NMDA-activated current by several alcohols is linearly related to their intoxicating potency, suggesting that alcohol-induced inhibition of responses to NMDA receptor activation may contribute to the neural and cognitive impairments associated with intoxication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lovinger, D M -- White, G -- Weight, F F -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1721-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2467382" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Butanol ; Aspartic Acid/*analogs & derivatives/pharmacology ; Butanols/pharmacology ; Calcium Channels/drug effects/physiology ; Chloride Channels ; Chlorides/physiology ; Electric Conductivity ; Ethanol/adverse effects/*pharmacology ; Hippocampus/cytology/*physiology ; Humans ; Ion Channels/drug effects/*physiology ; Kainic Acid/pharmacology ; Membrane Proteins/physiology ; Methanol/pharmacology ; N-Methylaspartate ; Neurons/*physiology ; Oxadiazoles/pharmacology ; Pentanols/pharmacology ; Quisqualic Acid ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/physiology ; Sodium Channels/drug effects/physiology ; gamma-Aminobutyric Acid/pharmacology
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-03
    Description: An important control point in gene expression is at the level of messenger RNA (mRNA) stability. The mRNAs of certain regulatory cellular proteins such as oncogenes, cytokines, lymphokines, and transcriptional activators are extremely labile. These messages share a common AUUUA pentamer in their 3' untranslated region, which confers cytoplasmic instability. A cytosolic protein was identified that binds specifically to RNA molecules containing four reiterations of the AUUUA structural element. This protein consists of three subunits and binds rapidly to AUUUA-containing RNA. Such protein-RNA complexes are resistant to the actions of denaturing and reducing agents, demonstrating very stable binding. The time course, stability, and specificity of the protein-AUUUA interaction suggests the possibility that the formation of this complex may target susceptible mRNA for rapid cytoplasmic degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malter, J S -- CA01427-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Nov 3;246(4930):664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Tulane University School of Medicine, New Orleans, LA 70112.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814487" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding, Competitive ; Carrier Proteins/isolation & purification/*metabolism ; Cell Line ; Humans ; Kinetics ; Macromolecular Substances ; Molecular Weight ; *Nucleocytoplasmic Transport Proteins ; RNA, Messenger/*metabolism ; *RNA-Binding Proteins ; Ribonuclease, Pancreatic
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  • 68
    Publication Date: 1989-08-18
    Description: Keratinocyte growth factor (KGF) is a human mitogen that is specific for epithelial cells. The complementary DNA sequence of KGF demonstrates that it is a member of the fibroblast growth factor family. The KGF transcript was present in stromal cells derived from epithelial tissues. By comparison with the expression of other epithelial cell mitogens, only KGF, among known human growth factors, has the properties of a stromal mediator of epithelial cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finch, P W -- Rubin, J S -- Miki, T -- Ron, D -- Aaronson, S A -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):752-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2475908" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division ; Codon ; DNA/genetics/isolation & purification ; Epithelial Cells ; Epithelium/analysis/metabolism ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors/genetics ; Fibroblasts/metabolism ; Gene Expression Regulation ; Growth Substances/*genetics/physiology ; Humans ; Mesoderm/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; RNA/analysis ; Sequence Homology, Nucleic Acid ; Skin/analysis ; Tissue Distribution ; Transcription, Genetic
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Grady, R T -- Goddard, I -- Bateman, R M -- DiMichele, W A -- Funk, V A -- Kress, W J -- Mooi, R -- Cannell, P F -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1651.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2928798" target="_blank"〉PubMed〈/a〉
    Keywords: *Genetics ; Humans ; *Linguistics ; Phylogeny
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  • 70
    Publication Date: 1989-07-07
    Description: Insulin receptor complementary DNA has been cloned from an insulin-resistant individual whose receptors have impaired tyrosine protein kinase activity. One of this individual's alleles has a mutation in which valine is substituted for Gly996, the third glycine in the conserved Gly-X-Gly-X-X-Gly motif in the putative binding site fo adenosine triphosphate. Expression of the mutant receptor by transfection into Chinese hamster ovary cells confirmed that the mutation impairs tyrosine kinase activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Odawara, M -- Kadowaki, T -- Yamamoto, R -- Shibasaki, Y -- Tobe, K -- Accili, D -- Bevins, C -- Mikami, Y -- Matsuura, N -- Akanuma, Y -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):66-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2544998" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Diabetes Mellitus, Type 2/*genetics ; *Genes ; Humans ; Insulin Resistance ; Molecular Sequence Data ; *Mutation ; Protein-Tyrosine Kinases/*genetics ; Receptor, Insulin/*genetics
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groth, E 3rd -- New York, N.Y. -- Science. 1989 May 19;244(4906):755.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727678" target="_blank"〉PubMed〈/a〉
    Keywords: *Food Contamination ; *Fruit ; Herbicides ; Humans ; Neoplasms/*chemically induced ; Plant Growth Regulators ; Risk Factors ; Succinates/*adverse effects
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1989 Mar 10;243(4896):1287.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2646714" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies/*history ; History, 20th Century ; Humans ; *Street Drugs ; Substance-Related Disorders/*prevention & control ; United States
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1386-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595361" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics ; Chromosome Deletion ; Colonic Neoplasms/genetics ; Humans ; Lung Neoplasms/genetics ; *Mutation ; Neoplasms/*genetics ; *Oncogenes ; Suppression, Genetic/*genetics
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-12-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1561.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/genetics ; B-Lymphocytes/immunology ; DNA Nucleotidyltransferases/genetics/metabolism ; Genes ; *Genes, Immunoglobulin ; Humans ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/immunology ; VDJ Recombinases
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):161-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; *Estradiol/adverse effects ; Europe ; *European Union ; Humans ; *Meat ; United States
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1387.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2556793" target="_blank"〉PubMed〈/a〉
    Keywords: Child, Preschool ; *Chromosomes, Human, Pair 11 ; *Cloning, Molecular ; Humans ; Kidney/embryology ; Kidney Neoplasms/*genetics ; Suppression, Genetic/*genetics ; Wilms Tumor/*genetics
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1376-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595359" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/transmission ; *Behavior ; Brain/drug effects/physiopathology ; *Cocaine/pharmacology ; Disease Outbreaks ; Dopamine/physiology ; Drug and Narcotic Control ; Humans ; Legislation, Drug ; Reward ; *Substance-Related Disorders/drug therapy/epidemiology/physiopathology/prevention ; & control ; United States
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  • 78
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-09-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Sep 1;245(4921):924.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2772645" target="_blank"〉PubMed〈/a〉
    Keywords: Cystic Fibrosis/*genetics ; *Genes ; Humans ; *Mass Media ; United States
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2740912" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*transmission ; HIV/isolation & purification/pathogenicity/ultrastructure ; Humans ; Male ; Spermatozoa/*microbiology/ultrastructure
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1254, 1256.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734608" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; HIV Antibodies/*biosynthesis ; HIV-1/*immunology ; Humans ; Mutation ; Pan troglodytes ; Vaccines, Inactivated/immunology ; Viral Vaccines/*immunology
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 26;244(4907):917.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727686" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy ; *Clinical Trials as Topic ; Hospitals, Community ; Humans
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 26;244(4907):916-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2727685" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy ; Antiviral Agents/therapeutic use ; Budgets ; *Clinical Trials as Topic/economics ; Humans ; Opportunistic Infections/drug therapy
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 19;244(4906):768.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658052" target="_blank"〉PubMed〈/a〉
    Keywords: Accidents ; *Bone Marrow Transplantation ; History, 20th Century ; Humans ; Nuclear Reactors ; Radiation Injuries/etiology/*therapy ; Ukraine
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 12;244(4905):654-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2566202" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics/pathology ; Female ; *Gene Amplification ; Gene Expression Regulation ; Humans ; Lymph Nodes/pathology ; *Neoplasm Recurrence, Local ; Ovarian Neoplasms/*genetics ; Prognosis ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; Receptor, ErbB-2
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1664-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2494699" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/genetics/pathology ; *Amyloid/genetics/physiology ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Gene Expression Regulation ; Humans ; Interleukin-1/physiology ; Nerve Growth Factors/physiology ; Neurons/pathology ; Protease Inhibitors ; *Protein Precursors/genetics/physiology
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-04-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):147-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2704994" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; *Neoplasm Metastasis
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  • 87
    Publication Date: 1989-12-08
    Description: The fragile X syndrome is the most common cause of familial mental retardation. Genetic counseling and gene isolation are hampered by a lack of DNA markers close to the disease locus. Two somatic cell hybrids that each contain a human X chromosome with a breakpoint close to the fragile X locus have been characterized. A new DNA marker (DXS296) lies between the chromosome breakpoints and is the closest marker to the fragile X locus yet reported. The Hunter syndrome gene, which causes iduronate sulfatase deficiency, is located at the X chromosome breakpoint that is distal to this new marker, thus localizing the Hunter gene distal to the fragile X locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suthers, G K -- Callen, D F -- Hyland, V J -- Kozman, H M -- Baker, E -- Eyre, H -- Harper, P S -- Roberts, S H -- Hors-Cayla, M C -- Davies, K E -- New York, N.Y. -- Science. 1989 Dec 8;246(4935):1298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Histopathology, Adelaide Children's Hospital, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2573953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Female ; Fragile X Syndrome/*genetics ; Genetic Counseling ; *Genetic Linkage ; *Genetic Markers ; Genomic Library ; Humans ; Hybrid Cells ; Likelihood Functions ; Mice ; Mucopolysaccharidosis II/genetics ; Mutation ; Nucleic Acid Hybridization ; Polymorphism, Restriction Fragment Length ; Sex Chromosome Aberrations/*genetics ; Translocation, Genetic
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szymusiak, R -- McGinty, D -- Sterman, M B -- New York, N.Y. -- Science. 1989 Sep 15;245(4923):1165.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2781274" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Humans ; Sleep/*physiology
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  • 89
    Publication Date: 1989-10-27
    Description: Allele loss is a hallmark of chromosome regions harboring recessive oncogenes. Lung cancer frequently demonstrates loss of heterozygosity on 17p. Recent evidence suggests that the p53 gene located on 17p13 has many features of such an antioncogene. The p53 gene was frequently mutated or inactivated in all types of human lung cancer. The genetic abnormalities of p53 include gross changes such as homozygous deletions and abnormally sized messenger RNAs along with a variety of point or small mutations, which map to the p53 open reading frame and change amino acid sequence in a region highly conserved between mouse and man. In addition, very low or absent expression of p53 messenger RNA in lung cancer cell lines compared to normal lung was seen. These findings, coupled with the previous demonstration of 17p allele loss in lung cancer, strongly implicate p53 as an anti-oncogene whose disruption is involved in the pathogenesis of human lung cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, T -- Nau, M M -- Chiba, I -- Birrer, M J -- Rosenberg, R K -- Vinocour, M -- Levitt, M -- Pass, H -- Gazdar, A F -- Minna, J D -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute-Navy Medical Oncology Branch, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2554494" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carcinoid Tumor/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Small Cell/genetics ; Chromosomes, Human, Pair 17 ; DNA, Neoplasm/genetics ; Gene Amplification ; Humans ; Lung Neoplasms/*genetics ; Mutation ; Oncogene Proteins/*genetics ; Phosphoproteins/*genetics ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Ribonucleases ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53
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  • 90
    Publication Date: 1989-01-06
    Description: The temperature dependences of the reduction potentials (E degrees') of wild-type human myoglobin (Mb) and three site-directed mutants have been measured by the use of thin-layer spectroelectrochemistry. Residue Val68, which is in van der Waals contact with the heme in Mb, has been replaced by Glu, Asp, and Asn. The changes in E degrees' and the standard entropy (delta S degrees') and enthalpy (delta H degrees') of reduction in the mutant proteins were determined relative to values for wild type; the change in E degrees' at 25 degrees C was about -200 millivolts for the Glu and Asp mutants, and about -80 millivolts for the Asn mutant. At pH 7.0, reduction of Fe(III) to Fe(II) in the Glu and Asp mutants is accompanied by uptake of a proton by the protein. These studies demonstrate that Mb can tolerate substitution of a buried hydrophobic group by potentially charged and polar residues and that such amino acid replacements can lead to substantial changes in the redox thermodynamics of the protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varadarajan, R -- Zewert, T E -- Gray, H B -- Boxer, S G -- DK 19038/DK/NIDDK NIH HHS/ -- GM 27738/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 6;243(4887):69-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2563171" target="_blank"〉PubMed〈/a〉
    Keywords: Asparagine ; Aspartic Acid ; Glutamates ; Glutamic Acid ; Heme/metabolism ; Humans ; Mutation ; Myoglobin/*metabolism ; Oxidation-Reduction ; Protein Conformation ; Recombinant Proteins/*metabolism ; Thermodynamics ; Valine
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-21
    Description: In the Table of Contents of the 24 March 1989 issue, the title of the report "Histamine is an intracellular messenger mediating platelet aggregation" by S. P. Saxena et al. appearing on page 1596 was incorrectly printed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tong, L -- Milburn, M V -- de Vos, A M -- Kim, S H -- New York, N.Y. -- Science. 1989 Jul 21;245(4915):244.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2665078" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Molecular Structure ; Protein Conformation ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins p21(ras)
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-11-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldrop, M M -- New York, N.Y. -- Science. 1989 Nov 3;246(4930):572-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814483" target="_blank"〉PubMed〈/a〉
    Keywords: *Computers ; *Game Theory ; *Games, Experimental ; Humans ; *Thinking
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  • 93
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, S -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):431-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814471" target="_blank"〉PubMed〈/a〉
    Keywords: Coronary Disease/etiology ; Humans ; Lung Neoplasms/*etiology ; Smoking/adverse effects ; Stress, Psychological/*complications
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  • 94
    Publication Date: 1989-02-03
    Description: The biological effects of ras oncogene activation in B cells were studied by using amphotropic retroviral vectors to introduce H- or N-ras oncogenes into human B lymphoblasts immortalized by Epstein-Barr virus. Expression of both H- and N-ras oncogenes led to malignant transformation of these cells, as shown by clonogenicity in semisolid media and tumorigenicity in immunodeficient mice. In addition, terminal differentiation into plasma cells was detectable as specific changes in morphology, immunoglobulin secretion, and cell surface antigen expression. This combined effect, promoting growth and differentiation in human lymphoblasts, represents a novel biological action of ras oncogenes and has implications for the pathogenesis of terminally differentiated B-lymphoid malignancies such as multiple myeloma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seremetis, S -- Inghirami, G -- Ferrero, D -- Newcomb, E W -- Knowles, D M -- Dotto, G P -- Dalla-Favera, R -- CA-37165/CA/NCI NIH HHS/ -- CA49236/CA/NCI NIH HHS/ -- EY 06337/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 3;243(4891):660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism/*pathology ; Cell Differentiation ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; DNA Replication ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression Regulation ; *Genes, ras ; *Herpesvirus 4, Human ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/etiology ; Phenotype ; Plasma Cells/*pathology
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-10-13
    Description: Lectins on cell surfaces mediate cell-cell interactions by combining with complementary carbohydrates on apposing cells. They play a key role in the control of various normal and pathological processes in living organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharon, N -- Lis, H -- New York, N.Y. -- Science. 1989 Oct 13;246(4927):227-34.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2552581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Physiological Phenomena ; Cell Communication/*physiology ; Cell Differentiation ; Entamoeba histolytica/physiology ; Fabaceae/physiology ; Humans ; Lectins/*physiology ; Myxomycetes/physiology ; Orthomyxoviridae/physiology ; Plant Lectins ; Plants, Medicinal
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-04-21
    Description: The incremental threshold of the isolated rod visual system is believed, under certain conditions, to obey Weber's law (that is, to increase in direct proportion to the intensity of the background). This relation was tested at several background wavelengths, over an intensity range for which the target was seen only by the rods. Although the slope on long-wavelength background approximates unity (that is, Weber's law on log-log coordinates), it averages less than 0.8 on short- and middle-wavelength backgrounds. This is the same value as that found for the thresholds of a typical, complete achromat--who lacks cone vision--regardless of background wavelength. These results force the conclusion that Weber's law for incremental threshold detection is achieved not by the rods alone but only by the rods acting together with the cones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharpe, L T -- Fach, C -- Nordby, K -- Stockman, A -- New York, N.Y. -- Science. 1989 Apr 21;244(4902):354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurologische Universitatsklinik, Freiburg im Breisgau, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2711186" target="_blank"〉PubMed〈/a〉
    Keywords: Dark Adaptation ; Humans ; Light ; Photoreceptor Cells/*physiology ; Vision, Ocular/*physiology
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-04
    Description: The effects of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a neurotoxin that produces the symptoms of Parkinson's disease, can be fully prevented in experimental animals by inhibiting monoamine oxidase B. On the basis of this observation, a double-blind, placebo-controlled study in patients with early Parkinson's disease was initiated to determine whether deprenyl (a selective monoamine oxidase B inhibitor) would delay the need for L-dopa therapy by slowing the progression of the disease. Fifty-four patients were randomly assigned to deprenyl (10 mg/day) or placebo treatment groups and followed until L-dopa therapy was indicated or until the patient had been in the study for 3 years. Analysis of Kaplan-Meier survival curves for each group showed that deprenyl delayed the need for L-dopa therapy; the average time until L-dopa was needed was 312.1 days for patients in the placebo group and 548.9 days for patients in the deprenyl group. Disease progression, as monitored by five different assessment scales, was slowed (by 40 to 83% per year) in the deprenyl group compared to placebo. Therefore, early deprenyl therapy delays the requirement for antiparkinsonian medication, possibly by slowing progression of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tetrud, J W -- Langston, J W -- New York, N.Y. -- Science. 1989 Aug 4;245(4917):519-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Parkinson's Foundation, San Jose 95128.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2502843" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Aged ; Clinical Trials as Topic ; Double-Blind Method ; Female ; Humans ; Levodopa/therapeutic use ; Male ; Middle Aged ; Monoamine Oxidase Inhibitors/*therapeutic use ; Parkinson Disease/*drug therapy/physiopathology ; Parkinson Disease, Secondary/chemically induced ; Phenethylamines/*therapeutic use ; Pyridines/adverse effects/antagonists & inhibitors ; Random Allocation ; Selegiline/adverse effects/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 1989-04-14
    Description: To examine the extent and variation of allelic loss in a common adult tumor, polymorphic DNA markers were studied from every nonacrocentric autosomal arm in 56 paired colorectal carcinoma and adjacent normal colonic mucosa specimens. This analysis was termed an allelotype, in analogy with a karyotype. Three major conclusions were drawn from this analysis: (i) Allelic deletions were remarkably common; one of the alleles of each polymorphic marker tested was lost in at least some tumors, and some tumors lost more than half of their parental alleles. (ii) In addition to allelic deletions, new DNA fragments not present in normal tissue were identified in five carcinomas; these new fragments contained repeated sequences of the variable number of tandem repeat type. (iii) Patients with more than the median percentage of allelic deletions had a considerably worse prognosis than did the other patients, although the size and stage of the primary tumors were very similar in the two groups. In addition to its implications concerning the genetic events underlying tumorigenesis, tumor allelotype may provide a molecular tool for improved estimation of prognosis in patients with colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogelstein, B -- Fearon, E R -- Kern, S E -- Hamilton, S R -- Preisinger, A C -- Nakamura, Y -- White, R -- CA41183/CA/NCI NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):207-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2565047" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Chromosome Aberrations/genetics ; Chromosome Disorders ; Colorectal Neoplasms/*genetics ; DNA, Neoplasm/genetics ; Humans ; *Karyotyping ; Polymorphism, Restriction Fragment Length
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, C -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):699.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2772633" target="_blank"〉PubMed〈/a〉
    Keywords: *Dna ; *Forensic Medicine ; Humans ; *Nucleotide Mapping
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, C -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1133.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2524878" target="_blank"〉PubMed〈/a〉
    Keywords: *Death ; Georgia (Republic) ; Humans ; Physicians ; *Riots ; Social Control, Formal ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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