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  • Humans  (188)
  • Cell Line  (35)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • SPACE RADIATION
  • American Association for the Advancement of Science (AAAS)  (201)
  • 1985-1989  (201)
  • 1988  (115)
  • 1986  (86)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (201)
  • Wiley-Blackwell  (253)
Years
  • 1985-1989  (201)
Year
  • 1
    Publication Date: 1988-11-11
    Description: Increasing mortality in intravenous (IV) drug users not reported to surveillance as acquired immunodeficiency syndrome (AIDS) has occurred in New York City coincident with the AIDS epidemic. From 1981 to 1986, narcotics-related deaths increased on average 32% per year from 492 in 1981 to 1996 in 1986. This increase included deaths from AIDS increasing from 0 to 905 and deaths from other causes, many of which were infectious diseases, increasing from 492 to 1091. Investigations of these deaths suggest a causal association with human immunodeficiency virus (HIV) infection. These deaths may represent a spectrum of HIV-related disease that has not been identified through AIDS surveillance and has resulted in a large underestimation of the impact of AIDS on IV drug users and blacks and Hispanics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoneburner, R L -- Des Jarlais, D C -- Benezra, D -- Gorelkin, L -- Sotheran, J L -- Friedman, S R -- Schultz, S -- Marmor, M -- Mildvan, D -- Maslansky, R -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AIDS Research Unit, New York City Department of Health, NY 10013.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187532" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications/*epidemiology/microbiology ; Cause of Death ; Endocarditis/complications ; Hiv ; HIV Seropositivity ; Homosexuality ; Humans ; Male ; New York City ; Pneumonia/complications ; Substance-Related Disorders/*complications/epidemiology/mortality ; Tuberculosis/complications
    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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  • 2
    Publication Date: 1988-07-15
    Description: In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by thermally degraded polychlorinated biphenyls. Because these chemicals persist in human tissue, children born to female patients after the outbreak were exposed in utero. In 1985, 117 children born to affected women and 108 unexposed controls were examined and evaluated. The exposed children were shorter and lighter than controls; they had abnormalities of gingiva, skin, nails, teeth, and lungs more frequently than did controls. The exposed children showed delay of developmental milestones, deficits on formal developmental testing, and abnormalities on behavioral assessment. These findings are most consistent with a generalized disorder of ectodermal tissue. This syndrome is one of very few documented to result from transplacental exposure to pollutant chemicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogan, W J -- Gladen, B C -- Hung, K L -- Koong, S L -- Shih, L Y -- Taylor, J S -- Wu, Y C -- Yang, D -- Ragan, N B -- Hsu, C C -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):334-6.〈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/3133768" target="_blank"〉PubMed〈/a〉
    Keywords: Conjunctivitis/chemically induced/congenital ; Female ; Growth Disorders/chemically induced ; Humans ; Lactation ; Maternal-Fetal Exchange ; Nails, Malformed ; Oils/*adverse effects ; Pigmentation Disorders/chemically induced/congenital ; Polychlorinated Biphenyls/*poisoning ; Pregnancy ; Taiwan
    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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  • 3
    Publication Date: 1986-08-22
    Description: A new family of protein kinase C-related genes has been identified in bovine, human, and rat genomes. The alpha-, beta-, and gamma-type protein kinase sequences are highly homologous, include a kinase domain, and potential calcium-binding sites, and they contain interspersed variable regions. The corresponding genes are located on distinct human chromosomes; the possibility of even greater genetic complexity of this gene family is suggested by Northern and Southern hybridization analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coussens, L -- Parker, P J -- Rhee, L -- Yang-Feng, T L -- Chen, E -- Waterfield, M D -- Francke, U -- Ullrich, A -- New York, N.Y. -- Science. 1986 Aug 22;233(4766):859-66.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3755548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Chromosome Mapping ; Chromosomes, Human, 16-18 ; Dna ; Genes ; Humans ; Nucleic Acid Hybridization ; Protein Kinase C/*genetics ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1988-08-26
    Description: In situ hybridization was used to assess total amyloid protein precursor (APP) messenger RNA and the subset of APP mRNA containing the Kunitz protease inhibitor (KPI) insert in 11 Alzheimer's disease (AD) and 7 control brains. In AD, a significant twofold increase was observed in total APP mRNA in nucleus basalis and locus ceruleus neurons but not in hippocampal subicular neurons, neurons of the basis pontis, or occipital cortical neurons. The increase in total APP mRNA in locus ceruleus and nucleus basalis neurons was due exclusively to an increase in APP mRNA lacking the KPI domain. These findings suggest that increased production of APP lacking the KPI domain in nucleus basalis and locus ceruleus neurons may play an important role in the deposition of cerebral amyloid that occurs in AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palmert, M R -- Golde, T E -- Cohen, M L -- Kovacs, D M -- Tanzi, R E -- Gusella, J F -- Usiak, M F -- Younkin, L H -- Younkin, S G -- 5T32GM07250/GM/NIGMS NIH HHS/ -- AG06656/AG/NIA NIH HHS/ -- MH43444/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1080-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropathology, Case Western Reserve University, School of Medicine, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457949" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid/*genetics ; Bacteriophage lambda/genetics ; Brain/metabolism ; Cerebral Cortex/metabolism ; *Gene Expression Regulation ; Humans ; Locus Coeruleus/metabolism ; Neurons/metabolism ; Nucleic Acid Hybridization ; Operator Regions, Genetic ; Plasmids ; Protein Precursors/*genetics ; RNA/genetics ; RNA, Complementary ; RNA, Messenger/*genetics/metabolism ; Repressor Proteins/metabolism ; Transcription, Genetic ; Trypsin Inhibitors/genetics
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  • 5
    Publication Date: 1988-02-12
    Description: Mesoderm induction in the amphibian embryo can be studied by exposing animal region explants (destined to become ectoderm) to appropriate stimuli and assaying the appearance of mesodermal products like alpha-actin messenger RNA. Transforming growth factor beta 2 (TGF-beta 2), but not TGF-beta 1, was active in alpha-actin induction, while addition of fibroblast growth factor had a small synergistic effect. Medium conditioned by Xenopus XTC cells (XTC-CM), known to have powerful mesoderm-inducing activity, was shown to contain TGF-beta-like activity as measured by a radioreceptor binding assay, colony formation in NRK cells, and growth inhibition in CCL64 cells. The activity of XTC-CM in mesoderm induction and in growth inhibition of CCL64 cells was inhibited partially by antibodies to TGF-beta 2 but not by antibodies to TGF-beta 1. Thus, a TGF-beta 2-like molecule may be involved in mesoderm induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosa, F -- Roberts, A B -- Danielpour, D -- Dart, L L -- Sporn, M B -- Dawid, I B -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):783-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3422517" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Amphibians/*embryology ; Animals ; Cell Division/drug effects ; Cell Line ; Embryo, Nonmammalian/physiology ; Growth Substances/*physiology ; Mesoderm/*physiology ; Peptides/pharmacology/*physiology ; RNA, Messenger/genetics ; Transforming Growth Factors ; Xenopus
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  • 6
    Publication Date: 1988-05-20
    Description: Class II major histocompatibility (MHC) molecules have an immunoregulatory role. These cell-surface glycoproteins present fragments of protein antigens (or peptides) to thymus-derived lymphocytes (T cells). Nucleotide sequence polymorphism in the genes that encode the class II MHC products determines the specificity of the immune response and is correlated with the development of autoimmune diseases. This study identifies certain class II polymorphic amino acid residues that are strongly associated with susceptibility to insulin-dependent diabetes mellitus, rheumatoid arthritis, and pemphigus vulgaris. These findings implicate particular class II MHC isotypes in susceptibility to each disease and suggest new prophylactic and therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Todd, J A -- Acha-Orbea, H -- Bell, J I -- Chao, N -- Fronek, Z -- Jacob, C O -- McDermott, M -- Sinha, A A -- Timmerman, L -- Steinman, L -- New York, N.Y. -- Science. 1988 May 20;240(4855):1003-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3368786" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arthritis, Rheumatoid/immunology ; Autoantibodies/*genetics ; Autoimmune Diseases/*genetics ; Diabetes Mellitus, Type 1/immunology ; HLA-D Antigens/*genetics ; Humans ; Major Histocompatibility Complex ; Molecular Sequence Data ; Pemphigus/immunology
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  • 7
    Publication Date: 1988-05-06
    Description: Acute promyelocytic leukemia (subtype M3) is characterized by malignant promyelocytes exhibiting an abundance of abnormally large or aberrant primary granules. Myeloperoxidase (MPO) activity of these azurophilic granules, as assessed by cytochemical staining, is unusually intense. In addition, M3 is universally associated with a chromosomal translocation, t(15;17)(q22;q11.2). In this report, the MPO gene was localized to human chromosome 17 (q12-q21), the region of the breakpoint on chromosome 17 in the t(15;17), by somatic cell hybrid analysis and in situ chromosomal hybridization. By means of MPO complementary DNA clones for in situ hybridization and Southern blot analysis, the effect of this specific translocation on the MPO gene was examined. In all cases of M3 examined, MPO is translocated to chromosome 15. Genomic blot analyses indicate rearrangement of MPO in leukemia cells of two of four cases examined. These findings suggest that MPO may be pivotal in the pathogenesis of acute promyelocytic leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weil, S C -- Rosner, G L -- Reid, M S -- Chisholm, R L -- Lemons, R S -- Swanson, M S -- Carrino, J J -- Diaz, M O -- Le Beau, M M -- 1R01 CA44475/CA/NCI NIH HHS/ -- CA09273/CA/NCI NIH HHS/ -- CA16910/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):790-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Northwestern University Medical Center, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896388" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 15 ; Chromosomes, Human, Pair 17 ; DNA/genetics ; DNA Restriction Enzymes ; DNA, Recombinant ; Humans ; Leukemia, Myeloid, Acute/*enzymology/genetics ; Nucleic Acid Hybridization ; Peroxidase/*genetics ; Plasmids ; Polymorphism, Restriction Fragment Length ; *Translocation, Genetic
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  • 8
    Publication Date: 1988-09-23
    Description: The study of human hematopoietic cells and the human immune system is hampered by the lack of a suitable experimental model. Experimental data are presented showing that human fetal liver hematopoietic cells, human fetal thymus, and human fetal lymph node support the differentiation of mature human T cells and B cells after engraftment into mice with genetically determined severe combined immunodeficiency. The resultant SCID-hu mice are found to have a transient wave of human CD4+ and CD8+ T cells and human IgG (immunoglobulin G) in the peripheral circulation. The functional status of the human immune system within this mouse model is not yet known.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCune, J M -- Namikawa, R -- Kaneshima, H -- Shultz, L D -- Lieberman, M -- Weissman, I L -- AI09072/AI/NIAID NIH HHS/ -- CA03352/CA/NCI NIH HHS/ -- CA20408/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1632-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2971269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/physiology ; Cell Differentiation ; *Chimera ; Hematopoietic Stem Cells/*physiology ; Humans ; Liver/cytology ; Liver Transplantation ; Lymph Nodes/transplantation ; Mice ; Mice, Mutant Strains/*immunology ; *Models, Biological ; T-Lymphocytes/physiology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/anatomy & histology/physiology/transplantation ; Transplantation, Heterologous
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  • 9
    Publication Date: 1986-12-12
    Description: A direct measurement of the avidity of the junction between a cytotoxic T lymphocyte and its target cell was achieved by using a biophysical approach. A micromanipulation technique was used to determine the force required to separate a cytotoxic T cell (human clone F1, with specificity for HLA-DRw6) from its specific target cell (JY: HLA-A2, -B7, -DR4, w6) prior to delivery of the lethal hit. The force required to separate the F1-JY pair is 1.5 X 10(4) dynes per square centimeter. This junction avidity for F1-JY pairs is 6 to 13 times greater than that for F1-F1 and JY-JY pairs; the F1-JY conjugate requires a stronger separating force and is more easily rejoined than the homologous cell pairs. This study provides an estimate of the avidity of cytotoxic T cells for their target cells and insights into the biophysical correlates of the molecular complexes formed in the interaction of cytotoxic T cells and their targets during the cytotoxic process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sung, K L -- Sung, L A -- Crimmins, M -- Burakoff, S J -- Chien, S -- CA-13429/CA/NCI NIH HHS/ -- P01 HL 16851/HL/NHLBI NIH HHS/ -- R23 CA-37955/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1405-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3491426" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Communication ; Cytotoxicity, Immunologic ; HLA-DR Antigens/immunology ; HLA-DR6 Antigen ; Humans ; Mathematics ; T-Lymphocytes, Cytotoxic/*cytology/immunology ; Time Factors
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  • 10
    Publication Date: 1988-06-03
    Description: The human immunodeficiency virus type 1 (HIV-1) uses the CD4 protein as a receptor for infection of susceptible cells. A candidate structure for the HIV-1 binding site on the CD4 protein was identified by epitope mapping with a family of eight functionally distinct CD4-specific monoclonal antibodies in conjunction with a panel of large CD4-derived synthetic peptides. All of the seven epitopes that were located reside within two immunoglobulin-like disulfide loops situated between residues 1 and 168 of the CD4 protein. The CD4-specific monoclonal antibody OKT4A, a potent inhibitor of HIV-1 binding, recognized a site between residues 32 and 47 on the CD4 protein. By analogy to other members of the immunoglobulin superfamily of proteins, this particular region has been predicted to exist as a protruding loop. A synthetic analog of this loop (residues 25 to 58) showed a concentration-dependent inhibition of HIV-1-induced cell fusion. It is proposed that a loop extending from residues 37 to 53 of the CD4 protein is a binding site for the AIDS virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jameson, B A -- Rao, P E -- Kong, L I -- Hahn, B H -- Shaw, G M -- Hood, L E -- Kent, S B -- AI25784/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1335-9.〈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/2453925" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Binding, Competitive ; Cell Fusion ; Disulfides/metabolism ; Epitopes/immunology ; Fluorescent Antibody Technique ; HIV/immunology/*metabolism ; HIV Envelope Protein gp120 ; Humans ; Immunoglobulins ; Peptide Fragments/chemical synthesis/immunology ; Protein Conformation ; Radioimmunoassay ; Receptors, HIV ; Receptors, Virus/*immunology ; Retroviridae Proteins/immunology ; T-Lymphocytes, Helper-Inducer/immunology/*microbiology
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