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  • Adult  (228)
  • Rabbits
  • American Association for the Advancement of Science (AAAS)  (364)
  • Blackwell Publishing Ltd
  • 1990-1994  (125)
  • 1980-1984  (239)
  • 1925-1929
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  • American Association for the Advancement of Science (AAAS)  (364)
  • Blackwell Publishing Ltd
  • Springer  (9)
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Year
  • 1
    Publication Date: 1990-06-22
    Description: The vast repertoire of immunoglobulins and T cell receptors is generated, in part, by V(D)J recombination, a series of genomic rearrangements that occur specifically in developing lymphocytes. The recombination activating gene, RAG-1, which is a gene expressed exclusively in maturing lymphoid cells, was previously isolated. RAG-1 inefficiently induced V(D)J recombinase activity when transfected into fibroblasts, but cotransfection with an adjacent gene, RAG-2, has resulted in at least a 1000-fold increase in the frequency of recombination. The 2.1-kilobase RAG-2 complementary DNA encodes a putative protein of 527 amino acids whose sequence is unrelated to that of RAG-1. Like RAG-1, RAG-2 is conserved between species that carry out V(D)J recombination, and its expression pattern correlates precisely with that of V(D)J recombinase activity. In addition to being located just 8 kilobases apart, these convergently transcribed genes are unusual in that most, if not all, of their coding and 3' untranslated sequences are contained in single exons. RAG-1 and RAG-2 might activate the expression of the V(D)J recombinase but, more likely, they directly participate in the recombination reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oettinger, M A -- Schatz, D G -- Gorka, C -- Baltimore, D -- GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1517-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360047" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Evolution ; Cattle ; Cell Line ; Chickens ; Cricetinae ; DNA/*genetics ; DNA Nucleotidyltransferases/*genetics ; *DNA-Binding Proteins ; Dogs ; Female ; *Gene Rearrangement, B-Lymphocyte ; *Gene Rearrangement, T-Lymphocyte ; *Homeodomain Proteins ; Humans ; Male ; Mice ; Molecular Sequence Data ; *Multigene Family ; Nuclear Proteins ; Nucleic Acid Hybridization ; Opossums ; Proteins/*genetics ; Rabbits ; Recombination, Genetic/*genetics ; Restriction Mapping ; Transfection ; Turtles ; VDJ Recombinases
    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: 1990-09-28
    Description: Methodology has been developed that enables virtually complete purification and abundant recovery of early hematopoietic progenitors from normal human adult peripheral blood. A fraction of the pure progenitors is multipotent (generates mixed colonies) and exhibits self-renewal capacity (gives rise to blast cell colonies). This methodology provides a fundamental tool for basic and clinical studies on hematopoiesis. Optimal in vitro cloning of virtually pure progenitors requires not only the stimulatory effect of interleukin-3, granulocyte-macrophage colony-stimulating factor, and erythropoietin, but also the permissive action of basic fibroblast growth factor. These findings suggest a regulatory role for this growth factor in early hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabbianelli, M -- Sargiacomo, M -- Pelosi, E -- Testa, U -- Isacchi, G -- Peschle, C -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1561-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology and Oncology, Istituto Superiore di Sanita, Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218497" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Monoclonal/immunology ; Cell Separation ; Cells, Cultured ; Clone Cells ; Erythropoietin/pharmacology ; Fibroblast Growth Factor 2/*pharmacology ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects ; Humans ; Interleukin-3/pharmacology ; Monocytes/*cytology/drug effects ; Recombinant Proteins/pharmacology
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  • 3
    Publication Date: 1990-11-30
    Description: The gene designated gamma 134.5 maps in the inverted repeats flanking the long unique sequence of herpes simplex virus-1 (HSV-1) DNA, and therefore it is present in two copies per genome. This gene is not essential for viral growth in cell culture. Four recombinant viruses were genetically engineered to test the function of this gene. These were (i) a virus from which both copies of the gene were deleted, (ii) a virus containing a stop codon in both copies of the gene, (iii) a virus containing after the first codon an insert encoding a 16-amino acid epitope known to react with a specific monoclonal antibody, and (iv) a virus in which the deleted sequences were restored. The viruses from which the gene was deleted or which carried stop codons were avirulent on intracerebral inoculation of mice. The virus with the gene tagged by the sequence encoding the epitope was moderately virulent, whereas the restored virus reacquired the phenotype of the parent virus. Significant amounts of virus were recovered only from brains of animals inoculated with virulent viruses. Inasmuch as the product of the gamma 134.5 gene extended the host range of the virus by enabling it to replicate and destroy brain cells, it is a viral neurovirulence factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, J -- Kern, E R -- Whitley, R J -- Roizman, B -- AI 1588-11/AI/NIAID NIH HHS/ -- AI 24009/AI/NIAID NIH HHS/ -- CA 47451/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1262-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173860" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, Viral/genetics/immunology ; Base Sequence ; Chromosome Deletion ; *Chromosome Mapping ; Codon ; DNA, Viral/genetics ; Encephalitis/*microbiology ; *Genes, Viral ; Herpes Simplex/*microbiology ; Humans ; *Immediate-Early Proteins ; Molecular Sequence Data ; Rabbits ; Repetitive Sequences, Nucleic Acid ; Simplexvirus/*genetics/growth & development/pathogenicity ; Thymidine Kinase/genetics ; Transfection ; Viral Proteins/*genetics ; Viral Regulatory and Accessory Proteins/genetics/immunology
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  • 4
    Publication Date: 1990-02-09
    Description: Gene mutation in vivo in human T lymphocytes appears to occur preferentially in dividing cells. Individuals with multiple sclerosis (MS) are assumed to have one or more populations of diving T cells that are being stimulated by autoantigens. Mutant T cell clones from MS patients were isolated and tested for reactivity to myelin basic protein, an antigen that is thought to participate in the induction of the disease. The hypoxanthine guanine phosphoribosyltransferase (hprt) clonal assay was used to determine mutant frequency values in MS patients with chronic progressive disease. Eleven of 258 thioguanine-resistant (hprt-) T cell clones from five of the six MS patients who were tested proliferated in response to human myelin basic protein without prior in vitro exposure to this antigen. No wild-type clones from these patients, nor any hprt- or wild-type clones from three healthy individuals responded to myelin basic protein. Thus, T cell clones that react with myelin basic protein can be isolated from the peripheral blood of MS patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allegretta, M -- Nicklas, J A -- Sriram, S -- Albertini, R J -- CA30688-07/CA/NCI NIH HHS/ -- NS00849/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Laboratory, University of Vermont, Burlington 05401.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1689076" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autoantigens/immunology ; Cell Division ; Clone Cells/immunology ; Female ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Middle Aged ; Multiple Sclerosis/genetics/*immunology ; Mutation ; Myelin Basic Protein/*immunology ; T-Lymphocytes/drug effects/*immunology ; Thioguanine/pharmacology ; X Chromosome
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1990 Nov 16;250(4983):900-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237436" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Neoplasms/*mortality ; United States
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  • 6
    Publication Date: 1990-12-14
    Description: The principal neutralizing determinant (PND) of human immunodeficiency virus (HIV)-1 resides within the V3 loop of the envelope protein. Antibodies elicited by peptides of this region were able to neutralize diverse isolates. Serum from one of three animals immunized with the human T cell lymphoma virus (HTLV)-IIIMN PND peptide, RP142, neutralized MN and the sequence-divergent HTLV-IIIB isolate. Serum from one of three animals immunized with a 13-amino acid IIIB PND peptide (RP337) also neutralized both of these isolates. Characterization of these sera revealed that the cross-neutralizing antibodies bound the amino acid sequence GlyProGlyArgAlaPhe (GPGRAF) that is present in both isolates. This sequence is frequently found in the PNDs analyzed in randomly selected HIV-1 isolates. Sera from two rabbits immunized with a peptide containing only the GPGRAF residues neutralized divergent isolates, including IIIB and MN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Javaherian, K -- Langlois, A J -- LaRosa, G J -- Profy, A T -- Bolognesi, D P -- Herlihy, W C -- Putney, S D -- Matthews, T J -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical School, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1703322" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Amino Acid Sequence ; Animals ; Enzyme-Linked Immunosorbent Assay ; Epitopes/*immunology ; Guinea Pigs ; HIV Antibodies/*immunology ; HIV Antigens/*immunology ; HIV-1/*immunology ; Humans ; Immune Sera/immunology ; Immunization ; Molecular Sequence Data ; Neutralization Tests ; Rabbits ; Viral Envelope Proteins/immunology
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  • 7
    Publication Date: 1990-04-27
    Description: Affinity-purified, polyclonal antibodies to the gamma subunit of the dihydropyridine (DHP)-sensitive, voltage-dependent calcium channel have been used to isolate complementary DNAs to the rabbit skeletal muscle protein from an expression library. The deduced primary structure indicates that the gamma subunit is a 25,058-dalton protein that contains four transmembrane domains and two N-linked glycosylation sites, consistent with biochemical analyses showing that the gamma subunit is a glycosylated hydrophobic protein. Nucleic acid hybridization studies indicate that there is a 1200-nucleotide transcript in skeletal muscle but not in brain or heart. The gamma subunit may play a role in assembly, modulation, or the structure of the skeletal muscle calcium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jay, S D -- Ellis, S B -- McCue, A F -- Williams, M E -- Vedvick, T S -- Harpold, M M -- Campbell, K P -- HL-14388/HL/NHLBI NIH HHS/ -- HL-37187/HL/NHLBI NIH HHS/ -- HL-39265/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):490-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/2158672" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Calcium Channels/drug effects/physiology ; DNA/isolation & purification ; Dihydropyridines/*pharmacology ; Disulfides ; Electrophoresis, Polyacrylamide Gel ; Immunoassay ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Muscles/*analysis ; Nucleic Acid Hybridization ; Protein Conformation ; RNA, Messenger/analysis ; Rabbits ; Sequence Homology, Nucleic Acid
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  • 8
    Publication Date: 1990-11-02
    Description: The TFP1 gene of the yeast Saccharomyces cerevisiae encodes two proteins: the 69-kilodalton (kD) catalytic subunit of the vacuolar proton-translocating adenosine triphosphatase (H(+)-ATPase) and a 50-kD protein. The 69-kD subunit is encoded by the 5' and 3' thirds of the TFP1 coding region, whereas the 50-kD protein is encoded by the central third. Evidence is presented that both the 69-kD and 50-kD proteins are obtained from a single translation product that is cleaved to release the 50-kD protein and spliced to form the 69-kD subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kane, P M -- Yamashiro, C T -- Wolczyk, D F -- Neff, N -- Goebl, M -- Stevens, T H -- GM38006/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):651-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2146742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Genes, Fungal ; Protein Biosynthesis ; *Protein Processing, Post-Translational ; Proton-Translocating ATPases/*biosynthesis/genetics ; RNA, Messenger/analysis ; Rabbits ; Saccharomyces cerevisiae/*enzymology ; Vacuoles/*enzymology
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  • 9
    Publication Date: 1991-06-14
    Description: In the interleukin-2 (IL-2) system, intracellular signal transduction is triggered by the beta chain of the IL-2 receptor (IL-2R beta); however, the responsible signaling mechanism remains unidentified. Evidence for the formation of a stable complex of IL-2R beta and the lymphocyte-specific protein tyrosine kinase p56lck is presented. Specific association sites were identified in the tyrosine kinase catalytic domain of p56lck and in the cytoplasmic domain of IL-2R beta. As a result of interaction, IL-2R beta became phosphorylated in vitro by p56lck. Treatment of T lymphocytes with IL-2 promotes p56lck kinase activity. These data suggest the participation of p56lck as a critical signaling molecule downstream of IL-2R via a novel interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatakeyama, M -- Kono, T -- Kobayashi, N -- Kawahara, A -- Levin, S D -- Perlmutter, R M -- Taniguchi, T -- New York, N.Y. -- Science. 1991 Jun 14;252(5012):1523-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2047859" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Antigens, CD/immunology ; Base Sequence ; Binding Sites ; Cell Division/drug effects ; Cell Line ; Humans ; Interleukin-2/pharmacology ; Killer Cells, Natural/cytology/drug effects/immunology ; Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Lymphocytes/drug effects/*immunology ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Oligonucleotide Probes ; Protein-Tyrosine Kinases/genetics/isolation & purification/*metabolism ; Receptors, Interleukin-2/genetics/isolation & purification/*physiology ; *Signal Transduction ; Transfection
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  • 10
    Publication Date: 1991-12-30
    Description: Familial hypercholesterolemia (FH) is an inherited disorder in humans that is caused by a deficiency of low density lipoprotein receptors (LDLRs). An animal model for FH, the Watanabe Heritable Hyperlipidemic rabbit, was used to develop an approach for liver-directed gene therapy based on transplantation of autologous hepatocytes that were genetically corrected ex vivo with recombinant retroviruses. Animals transplanted with LDLR-transduced autologous hepatocytes demonstrated a 30 to 50 percent decrease in total serum cholesterol that persisted for the duration of the experiment (122 days). Recombinant-derived LDLR RNA was harvested from tissues with no diminution for up to 6.5 months after transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chowdhury, J R -- Grossman, M -- Gupta, S -- Chowdhury, N R -- Baker, J R Jr -- Wilson, J M -- P01-DK-42718/DK/NIDDK NIH HHS/ -- R01-DK-34357/DK/NIDDK NIH HHS/ -- R01-DK42193-01/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1722351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression ; *Genetic Therapy ; Hypercholesterolemia/*genetics/*therapy ; Liver/physiology ; Liver Transplantation/physiology ; RNA/genetics/isolation & purification ; Rabbits ; Receptors, LDL/analysis/*genetics ; Recombinant Proteins/analysis ; Serum Albumin/analysis/genetics ; *Transfection ; beta-Galactosidase/analysis/genetics
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  • 11
    Publication Date: 1991-03-22
    Description: Defensins (molecular weight 3500 to 4000) act in the mammalian immune response by permeabilizing the plasma membranes of a broad spectrum of target organisms, including bacteria, fungi, and enveloped viruses. The high-resolution crystal structure of defensin HNP-3 (1.9 angstrom resolution, R factor 0.19) reveals a dimeric beta sheet that has an architecture very different from other lytic peptides. The dimeric assembly suggests mechanisms by which defensins might bind to and permeabilize the lipid bilayer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, C P -- Yee, J -- Selsted, M E -- Eisenberg, D -- New York, N.Y. -- Science. 1991 Mar 22;251(5000):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eisenberg, Molecular Biology Institute, Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006422" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blood Proteins/chemistry/*ultrastructure ; Cell Membrane Permeability ; Crystallography ; Defensins ; Guinea Pigs ; Humans ; Macromolecular Substances ; Membrane Proteins/chemistry/ultrastructure ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Protein Conformation ; Rabbits ; Rats ; Structure-Activity Relationship ; X-Ray Diffraction ; *alpha-Defensins
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  • 12
    Publication Date: 1991-03-15
    Description: The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talbot, J D -- Marrett, S -- Evans, A C -- Meyer, E -- Bushnell, M C -- Duncan, G H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de neurophysiologie comportementale, Faculte de medecine dentaire, Universite de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003220" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Anxiety/physiopathology ; Brain Mapping ; Cerebral Cortex/*physiology ; Functional Laterality ; Hot Temperature ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; Tomography, Emission-Computed
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moffat, A S -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1483.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1896855" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; Adolescent ; Adult ; Female ; *Health Surveys ; Humans ; Male ; National Institutes of Health (U.S.) ; *Sexual Behavior ; Sexually Transmitted Diseases/prevention & control ; United States
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-11-29
    Description: The N-end rule relates the in vivo half-life of a protein to the identity of its amino-terminal residue. Distinct versions of the N-end rule operate in all eukaryotes examined. It is shown that the bacterium Escherichia coli also has the N-end rule pathway. Amino-terminal arginine, lysine, leucine, phenylalanine, tyrosine, and tryptophan confer 2-minute half-lives on a test protein; the other amino-terminal residues confer greater than 10-hour half-lives on the same protein. Amino-terminal arginine and lysine are secondary destabilizing residues in E. coli because their activity depends on their conjugation to the primary destabilizing residues leucine or phenylalanine by leucine, phenylalanine-transfer RNA-protein transferase. The adenosine triphosphate-dependent protease Clp (Ti) is required for the degradation of N-end rule substrates in E. coli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tobias, J W -- Shrader, T E -- Rocap, G -- Varshavsky, A -- DK39520/DK/NIDDK NIH HHS/ -- GM31530/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 29;254(5036):1374-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1962196" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteria/*metabolism ; Bacterial Proteins/*metabolism ; Escherichia coli/enzymology/metabolism ; Half-Life ; Kinetics ; Molecular Sequence Data ; Rabbits ; Reticulocytes/metabolism ; Saccharomyces cerevisiae/enzymology/metabolism ; Structure-Activity Relationship ; beta-Galactosidase/*metabolism
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 May 24;252(5009):1070.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2031180" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Chromosome Mapping ; Female ; Fragile X Syndrome/*genetics ; Humans ; Male ; *Mutation ; X Chromosome
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-07-05
    Description: Bone-conducted ultrasonic hearing has been found capable of supporting frequency discrimination and speech detection in normal, older hearing-impaired, and profoundly deaf human subjects. When speech signals were modulated into the ultrasonic range, listening to words resulted in the clear perception of the speech stimuli and not a sense of high-frequency vibration. These data suggest that ultrasonic bone conduction hearing has potential as an alternative communication channel in the rehabilitation of hearing disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lenhardt, M L -- Skellett, R -- Wang, P -- Clarke, A M -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):82-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Otolaryngology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063208" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Bone Conduction ; Hearing Loss, Sensorineural ; Humans ; Middle Aged ; Sound Spectrography ; *Speech Perception ; *Ultrasonics
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-09-13
    Description: Interleukin-8 (IL-8) is an inflammatory cytokine that activates neutrophil chemotaxis, degranulation, and the respiratory burst. Neutrophils express receptors for IL-8 that are coupled to guanine nucleotide-binding proteins (G proteins); binding of IL-8 to its receptor induces the mobilization of intracellular calcium stores. A cDNA clone from HL-60 neutrophils, designated p2, has now been isolated that encodes a human IL-8 receptor. When p2 is expressed in oocytes from Xenopus laevis, the oocytes bind 125I-labeled IL-8 specifically and respond to IL-8 by mobilizing calcium stores with an EC50 of 20 nM. This IL-8 receptor has 77% amino acid identity with a second human neutrophil receptor isotype that binds IL-8 with higher affinity. It also exhibits 69% amino acid identity with a protein reported to be an N-formyl peptide receptor from rabbit neutrophils, but less than 30% identity with all other known G protein-coupled receptors, including the human N-formyl peptide receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, P M -- Tiffany, H L -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1280-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1891716" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Cloning, Molecular/methods ; DNA/genetics ; Gene Library ; Humans ; Interleukin-8/*metabolism/pharmacology ; Kinetics ; Molecular Sequence Data ; Neutrophils/immunology ; Oocytes/drug effects/physiology ; Protein Biosynthesis ; Rabbits ; Receptors, Immunologic/drug effects/*genetics/physiology ; Receptors, Interleukin-8A ; Recombinant Proteins/metabolism ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Transcription, Genetic ; Xenopus
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  • 18
    Publication Date: 1992-04-03
    Description: Colorectal (CR) tumors are usually curable if detected before metastasis. Because genetic alterations are associated with the development of these tumors, mutant genes may be found in the stool of individuals with CR neoplasms. The stools of nine patients whose tumors contained mutations of K-ras were analyzed. In eight of the nine cases, the ras mutations were detectable in DNA purified from the stool. These patients included those with benign and malignant neoplasms from proximal and distal colonic epithelium. Thus, colorectal tumors can be detected by a noninvasive method based on the molecular pathogenesis of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sidransky, D -- Tokino, T -- Hamilton, S R -- Kinzler, K W -- Levin, B -- Frost, P -- Vogelstein, B -- CA06973/CA/NCI NIH HHS/ -- CA35494/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):102-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Johns Hopkins University, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566048" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amino Acid Sequence ; Base Sequence ; Blotting, Southern ; Carcinoma/diagnosis/*genetics/pathology ; Colonic Neoplasms/diagnosis/*genetics/pathology ; DNA, Neoplasm/genetics/*isolation & purification ; Feces/chemistry ; Female ; *Genes, ras ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction ; Prognosis ; Rectal Neoplasms/diagnosis/*genetics/pathology
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):24.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566053" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Female ; *Health Promotion ; Humans ; Infant ; Infant Mortality ; Male ; Middle Aged ; *Minority Groups ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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  • 20
    Publication Date: 1992-05-01
    Description: Induction of ferritin synthesis in cultured cells by heme or iron is accompanied by degradation of the ferritin repressor protein (FRP). Intermediates in the degradative pathway apparently include FRP covalently linked in larger aggregates. The effect of iron on FRP degradation is enhanced by porphyrin precursors but is decreased by inhibitors of porphyrin synthesis, which implies that heme is an active agent. These results suggest that translational induction in this system may be caused by enhanced repressor degradation. While unique among translational regulatory systems, this process is common to a variety of other biosynthetic control mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goessling, L S -- Daniels-McQueen, S -- Bhattacharyya-Pakrasi, M -- Lin, J J -- Thach, R E -- AI 20484/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 May 1;256(5057):670-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Washington University, St. Louis, MO 63130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1316633" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Aminolevulinate Synthetase/genetics ; Aminolevulinic Acid/pharmacology ; Animals ; Cell Line ; Cell Line, Transformed ; Ferritins/biosynthesis/*genetics ; Fibroblasts/metabolism ; Iron/pharmacology ; Iron Regulatory Protein 1 ; Iron-Regulatory Proteins ; Mice ; Papillomaviridae ; Porphobilinogen/pharmacology ; *Protein Biosynthesis ; RNA, Messenger/*genetics ; RNA-Binding Proteins/*metabolism ; Rabbits
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wertman, K F -- Drubin, D G -- GM42759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):759-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439782" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*chemistry/genetics/metabolism ; Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Models, Molecular ; Molecular Structure ; Mutation ; Rabbits ; Tetrahymena/chemistry
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-04-24
    Description: Blood pressure and tissue perfusion are controlled in part by the level of intrinsic (myogenic) vascular tone. However, many of the molecular determinants of this response are unknown. Evidence is now presented that the degree of myogenic tone is regulated in part by the activation of large-conductance calcium-activated potassium channels in arterial smooth muscle. Tetraethylammonium ion (TEA+) and charybdotoxin (CTX), at concentrations that block calcium-activated potassium channels in smooth muscle cells isolated from cerebral arteries, depolarized and constricted pressurized cerebral arteries with myogenic tone. Both TEA+ and CTX had little effect on arteries when intracellular calcium was reduced by lowering intravascular pressure or by blocking calcium channels. Elevation of intravascular pressure through membrane depolarization and an increase in intracellular calcium may activate calcium-activated potassium channels. Thus, these channels may serve as a negative feedback pathway to control the degree of membrane depolarization and vasoconstriction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brayden, J E -- Nelson, M T -- HL 35911/HL/NHLBI NIH HHS/ -- HL 44455/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 24;256(5056):532-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Vermont, Colchester 05446.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arteries/*physiology ; Calcium/*pharmacology ; Cerebral Arteries/physiology ; Charybdotoxin ; Dihydropyridines/pharmacology ; Electric Conductivity ; Membrane Potentials/physiology ; Muscle, Smooth, Vascular/*physiology ; Nimodipine/pharmacology ; Peptides/pharmacology ; Potassium Channels/drug effects/*physiology ; Rabbits ; Scorpion Venoms/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Vasoconstriction/drug effects
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  • 23
    Publication Date: 1992-12-18
    Description: The proto-oncogene products c-Fos and c-Jun heterodimerize through their leucine zippers to form the AP-1 transcription factor. The transcriptional activity of the heterodimer is regulated by signal-dependent phosphorylation and dephosphorylation events. The stability of c-Fos was found to also be controlled by intracellular signal transduction. In transient expression and in vitro degradation experiments, the stability of c-Fos was decreased when the protein was dimerized with phosphorylated c-Jun. c-Jun protein isolated from phorbol ester-induced cells did not target c-Fos for degradation, which suggests that c-Fos is transiently stabilized after stimulation of cell growth. v-Fos protein, the retroviral counterpart of c-Fos, was not susceptible to degradation targeted by c-Jun.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papavassiliou, A G -- Treier, M -- Chavrier, C -- Bohmann, D -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Differentiation Program, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1470918" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Codon/genetics ; HeLa Cells ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Oncogene Proteins v-fos/genetics/*metabolism ; Phosphorylation ; Protein Biosynthesis ; Proto-Oncogene Proteins c-fos/genetics/*metabolism ; Proto-Oncogene Proteins c-jun/genetics/*metabolism ; Rabbits ; Recombinant Proteins/metabolism ; Reticulocytes/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Transfection
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  • 24
    Publication Date: 1992-12-11
    Description: Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, A E -- Polverini, P J -- Kunkel, S L -- Harlow, L A -- DiPietro, L A -- Elner, V M -- Elner, S G -- Strieter, R M -- AR30692/AR/NIAMS NIH HHS/ -- AR41492/AR/NIAMS NIH HHS/ -- HL39926/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1281554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/physiopathology ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Chemotaxis/*drug effects ; Cornea/*drug effects/physiology ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects/*physiology ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Interleukin-8/genetics/*pharmacology ; Macrophages/*physiology ; Mice ; Molecular Sequence Data ; Monocytes/physiology ; *Neovascularization, Pathologic ; Oligonucleotides, Antisense/*pharmacology ; Rabbits ; Rats ; Recombinant Proteins/pharmacology ; Synovial Fluid/physiology ; Tumor Necrosis Factor-alpha/genetics ; Umbilical Veins
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  • 25
    Publication Date: 1992-12-18
    Description: During generalized immune complex-induced inflammation of the peritoneal cavity, two peaks of tumor necrosis factor (TNF) were observed in the peritoneal exudate of normal mice. In mast cell-deficient mice, the first peak was undetected, and the second peak of TNF and neutrophil influx were significantly reduced. Antibody to TNF significantly inhibited neutrophil infiltration in normal but not in mast cell-deficient mice. Mast cell repletion of the latter normalized TNF, neutrophil mobilization, and the effect of the antibody to TNF. Thus, in vivo, mast cells produce the TNF that augments neutrophil emigration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Y -- Ramos, B F -- Jakschik, B A -- HL31922/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1470922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/*immunology ; Chickens ; Immunoglobulin G/immunology ; Inflammation ; Interleukin-1/pharmacology ; Leukotrienes/pharmacology ; Mast Cells/*physiology ; Mice ; Mice, Mutant Strains ; Neutrophils/drug effects/*physiology ; Ovalbumin/immunology ; Peritonitis/immunology/*physiopathology ; Rabbits ; Tumor Necrosis Factor-alpha/metabolism/pharmacology/*physiology
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  • 26
    Publication Date: 1992-11-27
    Description: Peptide nucleic acids (PNAs) are polyamide oligomers that can strand invade duplex DNA, causing displacement of one DNA strand and formation of a D-loop. Binding of either a T10 PNA or a mixed sequence 15-mer PNA to the transcribed strand of a G-free transcription cassette caused 90 to 100 percent site-specific termination of pol II transcription elongation. When a T10 PNA was bound on the nontranscribed strand, site-specific inhibition never exceeded 50 percent. Binding of PNAs to RNA resulted in site-specific termination of both reverse transcription and in vitro translation, precisely at the position of the PNA.RNA heteroduplex. Nuclear microinjection of cells constitutively expressing SV40 large T antigen (T Ag) with either a 15-mer or 20-mer PNA targeted to the T Ag messenger RNA suppressed T Ag expression. This effect was specific in that there was no reduction in beta-galactosidase expression from a coinjected expression vector and no inhibition of T Ag expression after microinjection of a 10-mer PNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanvey, J C -- Peffer, N J -- Bisi, J E -- Thomson, S A -- Cadilla, R -- Josey, J A -- Ricca, D J -- Hassman, C F -- Bonham, M A -- Au, K G -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Glaxo Inc. Research Institute, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics ; Base Sequence ; DNA/*metabolism ; Deoxyribonuclease HindIII/antagonists & inhibitors ; Gene Expression/drug effects ; HeLa Cells ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*metabolism/pharmacology ; Oligonucleotides, Antisense/*metabolism/pharmacology ; *Peptide Nucleic Acids ; Plasmids ; Protein Biosynthesis/drug effects ; RNA/metabolism ; Rabbits ; Rats ; Transcription, Genetic/drug effects
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  • 27
    Publication Date: 1990-12-21
    Description: Previous studies have emphasized that genetic susceptibility to breast cancer is rare and is expressed primarily as premenopausal breast cancer, bilateral breast cancer, or both. Proliferative breast disease (PBD) is a significant risk factor for the development of breast cancer and appears to be a precursor lesion. PBD and breast cancer were studied in 103 women from 20 kindreds that were selected for the presence of two first degree relatives with breast cancer and in 31 control women. Physical examination, screening mammography, and four-quadrant fine-needle breast aspirates were performed. Cytologic analysis of breast aspirates revealed PBD in 35% of clinically normal female first degree relatives of breast cancer cases and in 13% of controls. Genetic analysis suggests that genetic susceptibility causes both PBD and breast cancer in these kindreds. This study supports the hypothesis that this susceptibility is responsible for a considerable portion of breast cancer, including unilateral and postmenopausal breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skolnick, M H -- Cannon-Albright, L A -- Goldgar, D E -- Ward, J H -- Marshall, C J -- Schumann, G B -- Hogle, H -- McWhorter, W P -- Wright, E C -- Tran, T D -- CA-28854/CA/NCI NIH HHS/ -- CA-42014/CA/NCI NIH HHS/ -- CA-48711/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1715-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Utah Regional Cancer Center, University of Utah Medical Center, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270486" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Diseases/*genetics/pathology ; Breast Neoplasms/*genetics/pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Menopause ; Middle Aged ; Pedigree
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, C -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):803.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305252" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Educational Measurement ; Humans ; Research Support as Topic ; *Science ; United States ; Universities
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  • 29
    Publication Date: 1991-12-20
    Description: Dimerization among transcription factors has become a recurrent theme in the regulation of eukaryotic gene expression. Hepatocyte nuclear factor-1 alpha (HNF-1 alpha) is a homeodomain-containing protein that functions as a dimer. A dimerization cofactor of HNF-1 alpha (DCoH) was identified that displayed a restricted tissue distribution and did not bind to DNA, but, rather, selectively stabilized HNF-1 alpha dimers. The formation of a stable tetrameric DCoH-HNF-1 alpha complex, which required the dimerization domain of HNF-1 alpha, did not change the DNA binding characteristics of HNF-1 alpha, but enhanced its transcriptional activity. However, DCoH did not confer transcriptional activation to the GAL4 DNA binding domain. These results indicate that DCoH regulates formation of transcriptionally active tetrameric complexes and may contribute to the developmental specificity of the complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendel, D B -- Khavari, P A -- Conley, P B -- Graves, M K -- Hansen, L P -- Admon, A -- Crabtree, G R -- CA 09302/CA/NCI NIH HHS/ -- HD 07201/HD/NICHD NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1762-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763325" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/physiology ; Chromosome Deletion ; DNA-Binding Proteins/*metabolism ; Gene Library ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Humans ; *Hydro-Lyases ; Liver/physiology ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Protein Biosynthesis ; RNA, Messenger/genetics ; Rabbits ; Rats ; Reticulocytes/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-12-06
    Description: Heterotrimeric guanine nucleotide-binding regulatory proteins (G proteins) dissociate into guanosine triphosphate (GTP)-bound alpha subunits and a complex of beta and gamma subunits after interaction with receptors. The GTP-alpha subunit complex activates appropriate effectors, such as adenylyl cyclase, retinal phosphodiesterase, phospholipase C, and ion channels. G protein beta gamma subunits have been found to have regulatory effects on certain types of adenylyl cyclase. In the presence of Gs alpha, the alpha subunit of the G protein that activates adenylyl cyclase, one form of adenylyl cyclase was inhibited by beta gamma, some forms were activated by beta gamma, and some forms were not affected by beta gamma. These interactions suggest mechanisms for communication between distinct signal-transducing pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, W J -- Gilman, A G -- GM34497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1500-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmacology, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1962211" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/classification/genetics/*metabolism ; Animals ; Base Sequence ; Cattle ; Cloning, Molecular ; Enzyme Activation ; GTP-Binding Proteins/*physiology ; Guanosine Triphosphate/physiology ; Molecular Sequence Data ; Oligodeoxyribonucleotides/chemistry ; Rabbits ; Recombinant Proteins
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  • 31
    Publication Date: 1991-11-22
    Description: Acidic and basic fibroblast growth factors (FGFs) are members of a family of proteins that are broad-spectrum mitogens, have diverse hormone-like activities, and function in tumorigenesis. FGF's ability to raise the concentration of intracellular calcium ion suggests that FGF could induce the synthesis of endothelium-derived relaxing factor (EDRF) and consequently vasodilation. Systemic administration of FGF decreased arterial blood pressure. This effect was mediated by EDRF and by adenosine triphosphate-sensitive potassium ion channels. The hypotensive effect of FGF was segregated from its mitogenic activity by protein engineering. These results extend the range of FGF autocrine activities and potential therapeutic applications, emphasize the role of endothelium as an arterial blood pressure--regulating organ, and provide insight on the structural basis of FGF functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuevas, P -- Carceller, F -- Ortega, S -- Zazo, M -- Nieto, I -- Gimenez-Gallego, G -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1208-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital Universitario Ramon y Cajal, Carretera de Colmenar, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/*drug effects ; Dose-Response Relationship, Drug ; Fibroblast Growth Factors/chemistry/*pharmacology ; Glyburide/pharmacology ; Nitric Oxide/physiology ; Potassium Channels/drug effects ; Rabbits ; Rats ; Structure-Activity Relationship ; Time Factors
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  • 32
    Publication Date: 1991-02-25
    Description: An inducible rabbit endothelial adhesion molecule that is selective for mononuclear leukocytes has been identified. This adhesion protein was expressed on the surface of activated cultured endothelium in two forms, 118 and 98 kilodaltons, the amino-terminal sequence of each being highly homologous to human VCAM-1. In dietary hypercholesterolemic and Watanabe heritable hyperlipidemic rabbit models of atherosclerosis, this adhesion molecule was found to be expressed in a localized fashion by aortic endothelium that overlies early foam cell lesions. This lesion-localized expression suggests a potential endothelium-dependent mechanism for mononuclear leukocyte recruitment during atherogenesis and may provide a molecular marker for early atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cybulsky, M I -- Gimbrone, M A Jr -- P01-HL-36028/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):788-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990440" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Arteriosclerosis/etiology/*metabolism ; Cell Adhesion Molecules/*biosynthesis ; Cells, Cultured ; Diet, Atherogenic ; Endothelium, Vascular/*metabolism ; Leukocytes, Mononuclear/*physiology ; Lipopolysaccharides ; Molecular Sequence Data ; Rabbits
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-03-08
    Description: Glucose uptake into pancreatic beta cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal beta-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of beta cells to hyperglycemia may improve the management and prevention of diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Unger, R H -- 1-PO1-DK42582-01/DK/NIDDK NIH HHS/ -- 5-R37-DK02700-31/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1200-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Diabetes Research, Gifford Laboratories, Dallas, TX.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006409" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Child ; Diabetes Mellitus/*metabolism ; Diabetes Mellitus, Type 1/genetics/metabolism ; Diabetes Mellitus, Type 2/genetics/metabolism ; Glucose/*metabolism ; Humans ; Hyperglycemia/etiology/*metabolism ; Islets of Langerhans/*metabolism ; Middle Aged ; Models, Biological ; Monosaccharide Transport Proteins/genetics/*metabolism
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  • 34
    Publication Date: 1992-10-30
    Description: Fatal familial insomnia (FFI) and a subtype of familial Creutzfeldt-Jakob disease (CJD), two clinically and pathologically distinct diseases, are linked to the same mutation at codon 178 (Asn178) of the prion protein gene. The possibility that a second genetic component modified the phenotypic expression of the Asn178 mutation was investigated. FFI and the familial CJD subtype segregated with different genotypes determined by the Asn178 mutation and the methionine-valine polymorphism at codon 129. The Met129, Asn178 allele segregated with FFI in all 15 affected members of five kindreds whereas the Val129, Asn178 allele segregated with the familial CJD subtype in all 15 affected members of six kindreds. Thus, two distinct disease phenotypes linked to a single pathogenic mutation can be determined by a common polymorphism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldfarb, L G -- Petersen, R B -- Tabaton, M -- Brown, P -- LeBlanc, A C -- Montagna, P -- Cortelli, P -- Julien, J -- Vital, C -- Pendelbury, W W -- 1 R01 AGNS08155-02/AG/NIA NIH HHS/ -- AG-08012-02/AG/NIA NIH HHS/ -- NS 14509-13/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):806-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Central Nervous System Studies, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439789" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Asparagine/genetics ; Chromosomes, Human, Pair 20 ; Codon ; Creutzfeldt-Jakob Syndrome/*genetics ; DNA/*genetics ; Genotype ; Humans ; Middle Aged ; *Mutation ; *Phenotype ; *Polymorphism, Genetic ; Prion Diseases/*genetics ; Prions/genetics ; Valine/genetics
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  • 35
    Publication Date: 1992-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Epstein, H F -- Fischman, D A -- Bader, D -- Changeux, J P -- Buckhold, K -- Ordahl, C P -- Hoffman, E -- Kedes, L H -- Konieczny, S -- Leinwand, L A -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):738.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1496388" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Humans ; Male ; Muscles/*transplantation ; Muscular Dystrophies/*surgery ; Transplantation/adverse effects
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonenstein, F L -- New York, N.Y. -- Science. 1992 Aug 14;257(5072):861.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1502545" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; Adolescent ; Adult ; *Contraceptive Devices, Male ; Female ; Humans ; Male ; Sex Education ; *Sexual Behavior ; United States
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):25.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1320289" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; Adult ; Aged ; Centers for Disease Control and Prevention (U.S.) ; Data Collection ; Female ; France ; HIV Infections/prevention & control ; *Homosexuality ; Humans ; Male ; Middle Aged ; *Sexual Behavior ; United States
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  • 38
    Publication Date: 1992-12-18
    Description: Optical methods were used to locate the cell bodies of directionally selective ganglion cells in isolated rabbit retinas. These neurons detect the direction in which images move across the retinal surface and transmit that information to the brain. The receptive field of each identified cell was determined, after which the cell was injected with Lucifer yellow. An image of the receptive field border was then projected onto the fluorescent image of the dendrites, allowing precise comparison between them. The size of the receptive field matched closely the size of the dendritic arbor of that cell. This result restricts the types of convergence that can be postulated in modeling the mechanism of retinal directional selectivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, G -- Masland, R H -- R37-EY01075/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1949-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neuroscience, Harvard Medical School, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1470920" target="_blank"〉PubMed〈/a〉
    Keywords: Amidines ; Animals ; Dendrites/physiology/*ultrastructure ; *Eye Movements ; Fluorescent Dyes ; Optic Nerve/physiology ; Rabbits ; Retinal Ganglion Cells/*cytology/physiology ; Video Recording
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  • 39
    Publication Date: 1992-11-13
    Description: Linkage analysis of ten Utah kindreds and one Texas kindred with multiple cases of cutaneous malignant melanoma (CMM) provided evidence that a locus for familial melanoma susceptibility is in the chromosomal region 9p13-p22. The genetic markers analyzed reside in a candidate region on chromosome 9p21, previously implicated by the presence of homozygous deletions in melanoma tumors and by the presence of a germline deletion in an individual with eight independent melanomas. Multipoint linkage analysis was performed between the familial melanoma susceptibility locus (MLM) and two short tandem repeat markers, D9S126 and the interferon-alpha (IFNA) gene, which reside in the region of somatic loss in melanoma tumors. An analysis incorporating a partially penetrant dominant melanoma susceptibility locus places MLM near IFNA and D9S126 with a maximum location score of 12.71. Therefore, the region frequently deleted in melanoma tumors on 9p21 presumably contains a locus that plays a critical role in predisposition to familial melanoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon-Albright, L A -- Goldgar, D E -- Meyer, L J -- Lewis, C M -- Anderson, D E -- Fountain, J W -- Hegi, M E -- Wiseman, R W -- Petty, E M -- Bale, A E -- CA 42014/CA/NCI NIH HHS/ -- CA 48711/CA/NCI NIH HHS/ -- RR 00064/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1148-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439824" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; Base Sequence ; Child ; Chromosome Aberrations ; *Chromosomes, Human, Pair 9 ; Dysplastic Nevus Syndrome/genetics ; Female ; Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Lod Score ; Male ; Melanoma/*genetics ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Skin Neoplasms/*genetics ; Texas ; Utah
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  • 40
    Publication Date: 1990-08-24
    Description: A general measure of the rate of senescence is the acceleration of mortality rate, represented here by the time required for the mortality rate to double (MRD). Rhesus monkeys have an MRD close to that of humans, about 8 years; their shorter life-span results mainly from higher mortality at all ages. In contrast, some groups with short life-spans (rodents and galliform birds) have shorter MRDs and faster senescence. On the basis of the Gompertz mortality rate model, one may estimate the MRD from the maximum life-span (tmax) and the overall population mortality rate. Such calculations show that certain birds have MRDs that are as long as that of humans. These results show that high overall mortality rates or small body sizes do not preclude slow rates of senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finch, C E -- Pike, M C -- Witten, M -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):902-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California, University Park 90089.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392680" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; *Aging ; *Animal Population Groups ; Animals ; Birds ; *Hominidae ; Humans ; Mammals ; Mathematics ; Models, Statistical ; *Mortality
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  • 41
    Publication Date: 1990-06-01
    Description: Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those afflicted in their fifth or sixth decade. Immunohistochemical and biochemical studies have indicated that the amyloid subunit in HCHWA-D is antigenically related to and homologous in sequence with the amyloid beta protein isolated from brains of patients with Alzheimer's disease and Down syndrome. The amyloid beta protein is encoded by the amyloid beta protein precursor (APP) gene located on chromosome 21. Restriction fragment length polymorphisms detected by the APP gene were used to examine whether this gene is a candidate for the genetic defect in HCHWA-D. The data indicate that the APP gene is tightly linked to HCHWA-D and therefore, in contrast to familial Alzheimer's disease, cannot be excluded as the site of mutation in HCHWA-D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Broeckhoven, C -- Haan, J -- Bakker, E -- Hardy, J A -- Van Hul, W -- Wehnert, A -- Vegter-Van der Vlis, M -- Roos, R A -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1120-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Born Bunge Foundation, Department of Biochemistry, University of Antwerp, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1971458" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid/*genetics ; Amyloid beta-Protein Precursor ; Amyloidosis/complications/*genetics ; Cerebral Hemorrhage/etiology/*genetics ; Cerebrovascular Disorders/complications/*genetics ; Female ; Genes, Dominant ; Genetic Linkage ; Humans ; Lod Score ; Male ; Middle Aged ; Netherlands ; Pedigree ; Polymorphism, Restriction Fragment Length ; Protein Precursors/*genetics
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  • 42
    Publication Date: 1990-07-13
    Description: Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder characterized by abnormalities in multiple tissues derived from the neural crest. No reliable cellular phenotypic marker has been identified, which has hampered direct efforts to identify the gene. The chromosome location of the NF1 gene has been previously mapped genetically to 17q11.2, and data from two NF1 patients with balanced translocations in this region have further narrowed the candidate interval. The use of chromosome jumping and yeast artificial chromosome technology has now led to the identification of a large (approximately 13 kilobases) ubiquitously expressed transcript (denoted NF1LT) from this region that is definitely interrupted by one and most likely by both translocations. Previously identified candidate genes, which failed to show abnormalities in NF1 patients, are apparently located within introns of NF1LT, on the antisense strand. A new mutation patient with NF1 has been identified with a de novo 0.5-kilobase insertion in the NF1LT gene. These observations, together with the high spontaneous mutation rate of NF1 (which is consistent with a large locus), suggest that NF1LT represents the elusive NF1 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, M R -- Marchuk, D A -- Andersen, L B -- Letcher, R -- Odeh, H M -- Saulino, A M -- Fountain, J W -- Brereton, A -- Nicholson, J -- Mitchell, A L -- NS23410/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2134734" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Hybrid Cells ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Neurofibromatosis 1/*genetics ; Protein Biosynthesis ; RNA, Neoplasm/*genetics ; Transcription, Genetic ; *Translocation, Genetic ; Tumor Cells, Cultured
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  • 43
    Publication Date: 1990-08-31
    Description: Visual presentation of words activates extrastriate regions of the occipital lobes of the brain. When analyzed by positron emission tomography (PET), certain areas in the left, medial extrastriate visual cortex were activated by visually presented pseudowords that obey English spelling rules, as well as by actual words. These areas were not activated by nonsense strings of letters or letter-like forms. Thus visual word form computations are based on learned distinctions between words and nonwords. In addition, during passive presentation of words, but not pseudowords, activation occurred in a left frontal area that is related to semantic processing. These findings support distinctions made in cognitive psychology and computational modeling between high-level visual and semantic computations on single words and describe the anatomy that may underlie these distinctions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, S E -- Fox, P T -- Snyder, A Z -- Raichle, M E -- HL 13851/HL/NHLBI NIH HHS/ -- NS 06833/NS/NINDS NIH HHS/ -- NS 25233/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1041-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2396097" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cerebral Cortex/*physiology/radionuclide imaging ; Cerebrovascular Circulation ; Female ; Humans ; *Language ; Male ; Middle Aged ; Oxygen Radioisotopes ; Tomography, Emission-Computed ; *Vision, Ocular ; Visual Cortex/*physiology/radionuclide imaging
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovascular Diseases/*therapy ; *Genetic Therapy ; Humans ; Hypercholesterolemia/*therapy ; Rabbits ; Receptors, LDL/genetics
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phinney, S D -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1595.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2363041" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Dietary Fats ; Fatty Acids, Omega-3 ; Humans ; Japan ; Leukemia, Radiation-Induced/*epidemiology ; Male ; Neoplasms, Radiation-Induced/*epidemiology/prevention & control
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-06-28
    Description: The arterial pressure of the adult human rarely deviates from normal by more than 10 to 15 percent during each day. To achieve such constancy, the body has a network of pressure control systems. Several are based on neural receptors that respond within seconds to help correct any abnormal pressure. The activities of these systems are followed within minutes by activation of hormonal controllers. Within hours or days, a kidney pressure control system is induced that increases body fluid volume when the pressure falls (or decreases the volume when the pressure rises). This kidney-fluid system is the dominant method of establishing long-term pressure control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guyton, A C -- HL 11678-23/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 28;252(5014):1813-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Mississippi School of Medicine, Jackson 39216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063193" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Blood Pressure/*physiology ; Body Fluids/*physiology ; Chemoreceptor Cells/physiology ; Homeostasis ; Humans ; Kidney/*physiology ; Nervous System Physiological Phenomena ; Pressoreceptors/physiology
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):372-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2017676" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*epidemiology/prevention & ; control/transmission ; Adolescent ; Adult ; Africa ; Asia ; Disease Outbreaks ; Female ; Humans ; Latin America ; Male ; Middle Aged ; North America ; World Health Organization
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  • 48
    Publication Date: 1991-02-15
    Description: In the medullary segment of the thick ascending limb of the loop of Henle (mTALH), arachidonic acid (AA) is metabolized by a cytochrome P450-dependent monooxygenase to products that affect ion transport. The linkage between changes in ion transport and AA metabolism in isolated cells of the mTALH was examined. AA produced a concentration-dependent inhibition of 86Rb uptake--an effect that was prevented by selective blockade of cytochrome P450 monooxygenases. Inhibition by cytochrome P450 blockade of the effect of AA on 86Rb uptake could be circumvented by addition of the principal products of AA metabolism in the mTALH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escalante, B -- Erlij, D -- Falck, J R -- McGiff, J C -- HL34300/HL/NHLBI NIH HHS/ -- R01 DK33612/DK/NIDDK NIH HHS/ -- R01 HL25394/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):799-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, New York Medical College, Valhalla 10595.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846705" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acid ; Arachidonic Acids/*metabolism/physiology ; Biological Transport/physiology ; Carrier Proteins/metabolism ; Cytochrome P-450 Enzyme System/*metabolism ; Furosemide/pharmacology ; In Vitro Techniques ; Loop of Henle/drug effects/*metabolism ; Ouabain/pharmacology ; Potassium/*metabolism ; Rabbits ; Rubidium Radioisotopes ; Sodium/*metabolism ; Sodium-Potassium-Chloride Symporters ; Sodium-Potassium-Exchanging ATPase/metabolism
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  • 49
    Publication Date: 1991-10-25
    Description: The rate of net hepatic glycogenolysis was assessed in humans by serially measuring hepatic glycogen concentration at 3- to 12-hour intervals during a 68-hour fast with 13C nuclear magnetic resonance spectroscopy. The net rate of gluconeogenesis was calculated by subtracting the rate of net hepatic glycogenolysis from the rate of glucose production in the whole body measured with tritiated glucose. Gluconeogenesis accounted for 64 +/- 5% (mean +/- standard error of the mean) of total glucose production during the first 22 hours of fasting. In the subsequent 14-hour and 18-hour periods of the fast, gluconeogenesis accounted for 82 +/- 5% and 96 +/- 1% of total glucose production, respectively. These data show that gluconeogenesis accounts for a substantial fraction of total glucose production even during the first 22 hours of a fast in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothman, D L -- Magnusson, I -- Katz, L D -- Shulman, R G -- Shulman, G I -- DK-34576/DK/NIDDK NIH HHS/ -- DK-40936/DK/NIDDK NIH HHS/ -- MO1-RR-00125-26/RR/NCRR NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948033" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Blood Glucose/metabolism ; Carbon Isotopes ; Fasting ; Female ; Glucagon/blood ; *Gluconeogenesis ; Humans ; Hydrocortisone/blood ; Insulin/blood ; Kinetics ; Liver/*metabolism ; Liver Glycogen/*metabolism ; Magnetic Resonance Spectroscopy/methods ; Male ; Nitrogen/*urine
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-03-29
    Description: The mechanisms by which peripheral nerve injuries sometimes lead to causalgia, aberrant burning pain peripheral to the site of nerve damage, are uncertain, although the sympathetic nervous system is known to be involved. Whether such syndromes could be the result of the development of responsiveness by some cutaneous pain receptors (C-fiber nociceptors) to sympathetic efferent activity as a consequence of the nerve injury was tested in an animal model. After nerve damage but not in its absence, sympathetic stimulation and norepinephrine were excitatory for a subset of skin C-fiber nociceptors and enhanced the responsiveness of these nociceptors to tissue-damaging stimulation. These effects were demonstratable within days after nerve lesions, occurred at the cutaneous receptive terminal region, were manifest in sensory fibers that had not degenerated after the injury, and were mediated by alpha 2-adrenergic-like receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, J -- Perl, E R -- NS10321/NS/NINDS NIH HHS/ -- NS14899/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 29;251(5001):1608-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of North Carolina, Department of Physiology, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2011742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Hot Temperature ; Neurons, Afferent/drug effects/*physiology ; Nociceptors/drug effects/*physiology ; Norepinephrine/*pharmacology ; *Peripheral Nerve Injuries ; Peripheral Nerves/drug effects/physiology ; Physical Stimulation ; Rabbits ; Reference Values ; Skin/innervation ; Sympathetic Nervous System/physiology
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  • 51
    Publication Date: 1992-10-23
    Description: Advanced glycosylation end products (AGEs) form spontaneously from glucose-derived Amadori products and accumulate on long-lived tissue proteins. AGEs have been implicated in the pathogenesis of several of the complications of aging and diabetes, including atherosclerosis and renal disease. With the use of recently developed AGE-specific antibodies, an AGE-modified form of human hemoglobin has been identified. Termed hemoglobin-AGE (Hb-AGE), this modified species accounts for 0.42 percent of circulating hemoglobin in normal individuals but increases to 0.75 percent in patients with diabetes-induced hyperglycemia. In a group of diabetic patients treated with the advanced glycosylation inhibitor aminoguanidine, Hb-AGE levels decreased significantly over a 1-month period. Hemoglobin-AGE measurements may provide an index of long-term tissue modification by AGEs and prove useful in assessing the contribution of advanced glycosylation to a variety of diabetic and age-related complications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makita, Z -- Vlassara, H -- Rayfield, E -- Cartwright, K -- Friedman, E -- Rodby, R -- Cerami, A -- Bucala, R -- DK19655-15/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):651-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Medical Research, Manhasset, NY 11030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411574" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aging/*blood ; Biomarkers/blood ; Diabetes Mellitus, Type 1/*blood/drug therapy ; Diabetes Mellitus, Type 2/*blood/drug therapy ; Enzyme-Linked Immunosorbent Assay ; Glycosylation ; Guanidines/*therapeutic use ; Hemoglobins/*analysis ; Humans ; Middle Aged
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkelstein, R A -- New York, N.Y. -- Science. 1992 Aug 14;257(5072):862.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1502547" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Bangladesh/epidemiology ; Child ; Cholera/epidemiology/*prevention & control ; *Cholera Vaccines ; Humans
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 53
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Risch, N -- HG00348/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 14;255(5046):803-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1536004" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alzheimer Disease/genetics ; Breast Neoplasms/genetics ; Data Interpretation, Statistical ; Diabetes Mellitus/genetics ; *Disease Susceptibility ; Genetic Linkage ; Humans ; *Lod Score ; Middle Aged
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  • 54
    Publication Date: 1990-08-17
    Description: In 1988 to 1989, 698 adult cadavers in Abidjan's two largest morgues were studied, representing 38 to 43% of all adult deaths in the city over the study period, and 6 to 7% of annual deaths. Forty-one percent of male and 32% of female cadavers were infected with human immunodeficiency virus (HIV). Fifteen percent of adult male and 13% of adult female annual deaths are due to acquired immunodeficiency syndrome (AIDS). In Abidjan, AIDS is the leading cause of death and years of potential life lost in adult men, followed by unintentional injuries and tuberculosis. In women, AIDS is the second leading cause of death and premature mortality, after deaths related to pregnancy and abortion. AIDS-specific and AIDS-proportional mortality rates may be higher in other African cities where AIDS has been found for a longer time than in Abidjan.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Cock, K M -- Barrere, B -- Diaby, L -- Lafontaine, M F -- Gnaore, E -- Porter, A -- Pantobe, D -- Lafontant, G C -- Dago-Akribi, A -- Ette, M -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):793-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Infectious Diseases, Centers for Disease Control, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2167515" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology/*mortality ; Adolescent ; Adult ; Africa ; Cause of Death ; Cote d'Ivoire ; Female ; HIV Seropositivity ; HIV-1/immunology ; HIV-2/immunology ; Humans ; Male
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  • 55
    Publication Date: 1990-09-07
    Description: Heart rate is determined by pacemaker currents, of which the most important is the hyperpolarization-activated current I(f). Heart rate and I(f) are increased by beta-adrenergic agonists and decreased by muscarinic agonists released from cardiac sympathetic and vagal nerves, respectively. The hypothesis that the receptors for each agonist are directly coupled to I(f) channels by G proteins was tested. Under substrate-free conditions, preactivated G protein Gs stimulated and preactivated G protein G(o) inhibited I(f) channels of sinoatrial node pacemaker cells. These effects were mimicked by the corresponding preactivated alpha subunits of the G proteins. Unexpectedly, the two G proteins acted simultaneously, with G(o) being the more potent. This result may explain in molecular terms the classical observation in cardiac physiology, that vagal inhibition of heart rate is much greater on a background of sympathetic stimulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yatani, A -- Okabe, K -- Codina, J -- Birnbaumer, L -- Brown, A M -- DK19318/DK/NIDDK NIH HHS/ -- HL36930/HL/NHLBI NIH HHS/ -- HL39262/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Sep 7;249(4973):1163-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1697697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/physiology ; Cell-Free System ; Electric Conductivity ; GTP-Binding Proteins/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; *Heart Rate ; In Vitro Techniques ; Ion Channels/*physiology ; Rabbits ; Receptors, Adrenergic/physiology ; Receptors, Muscarinic/physiology ; Sinoatrial Node/*physiology ; Thionucleotides/pharmacology
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  • 56
    Publication Date: 1990-10-12
    Description: Since 1979, a continuing study of monozygotic and dizygotic twins, separated in infancy and reared apart, has subjected more than 100 sets of reared-apart twins or triplets to a week of intensive psychological and physiological assessment. Like the prior, smaller studies of monozygotic twins reared apart, about 70% of the variance in IQ was found to be associated with genetic variation. On multiple measures of personality and temperament, occupational and leisure-time interests, and social attitudes, monozygotic twins reared apart are about as similar as are monozygotic twins reared together. These findings extend and support those from numerous other twin, family, and adoption studies. It is a plausible hypothesis that genetic differences affect psychological differences largely indirectly, by influencing the effective environment of the developing child. This evidence for the strong heritability of most psychological traits, sensibly construed, does not detract from the value or importance of parenting, education, and other propaedeutic interventions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouchard, T J Jr -- Lykken, D T -- McGue, M -- Segal, N L -- Tellegen, A -- AG06886/AG/NIA NIH HHS/ -- MH37860/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):223-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Minnesota, Minneapolis 55455.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218526" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Analysis of Variance ; Anthropometry ; Child ; *Child Rearing ; Humans ; *Intelligence ; Minnesota ; Personality ; Phenotype ; Twins/*psychology ; Twins, Dizygotic/psychology ; Twins, Monozygotic/psychology
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  • 57
    Publication Date: 1990-11-16
    Description: Hyperkalemic periodic paralysis (HYPP) is an autosomal dominant disorder characterized by episodes of muscle weakness due to depolarization of the muscle cell membrane associated with elevated serum potassium. Electrophysiological studies have implicated the adult muscle sodium channel. Here, portions of the adult muscle sodium channel alpha-subunit gene were cloned and mapped near the human growth hormone locus (GH1) on chromosome 17. In a large pedigree displaying HYPP with myotonia, these two loci showed tight linkage to the genetic defect with no recombinants detected. Thus, it is likely that the sodium channel alpha-subunit gene contains the HYPP mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontaine, B -- Khurana, T S -- Hoffman, E P -- Bruns, G A -- Haines, J L -- Trofatter, J A -- Hanson, M P -- Rich, J -- McFarlane, H -- Yasek, D M -- NS-22224/NS/NINDS NIH HHS/ -- NS-24279/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 16;250(4983):1000-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurogenetics Laboratory, Massachusetts General Hospital, Charlestown, MA 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173143" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 17 ; Genes/genetics ; Growth Hormone/genetics ; Humans ; Hyperkalemia/*genetics ; Muscles/*physiology ; Paralyses, Familial Periodic/*genetics ; Pedigree ; Rats ; Sodium Channels/*genetics
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  • 58
    Publication Date: 1990-06-22
    Description: Positron emission tomography (PET) was used to measure changes in regional cerebral blood flow of normal subjects, while they were discriminating different attributes (shape, color, and velocity) of the same set of visual stimuli. Psychophysical evidence indicated that the sensitivity for discriminating subtle stimulus changes was higher when subjects focused attention on one attribute than when they divided attention among several attributes. Correspondingly, attention enhanced the activity of different regions of extrastriate visual cortex that appear to be specialized for processing information related to the selected attribute.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corbetta, M -- Miezin, F M -- Dobmeyer, S -- Shulman, G L -- Petersen, S E -- HL 13851/HL/NHLBI NIH HHS/ -- NS 06833/NS/NINDS NIH HHS/ -- NS 25233/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1556-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360050" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Arousal ; Attention/*physiology ; Cerebrovascular Circulation/physiology ; Color ; Discrimination (Psychology)/*physiology ; Humans ; Tomography, Emission-Computed ; Visual Cortex/*physiology
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  • 59
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1240-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2399461" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; DNA, Viral/blood ; Fatigue Syndrome, Chronic/*microbiology ; Human T-lymphotropic virus 2/*isolation & purification ; Humans ; Polymerase Chain Reaction
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  • 60
    Publication Date: 1990-09-21
    Description: The primary structure of lipopolysaccharide binding protein (LBP), a trace plasma protein that binds to the lipid A moiety of bacterial lipopolysaccharides (LPSs), was deduced by sequencing cloned complementary DNA. LBP shares sequence identity with another LPS binding protein found in granulocytes, bactericidal/permeability-increasing protein, and with cholesterol ester transport protein of the plasma. LBP may control the response to LPS under physiologic conditions by forming high-affinity complexes with LPS that bind to monocytes and macrophages, which then secrete tumor necrosis factor. The identification of this pathway for LPS-induced monocyte stimulation may aid in the development of treatments for diseases in which Gram-negative sepsis or endotoxemia are involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumann, R R -- Leong, S R -- Flaggs, G W -- Gray, P W -- Wright, S D -- Mathison, J C -- Tobias, P S -- Ulevitch, R J -- AI 15136/AI/NIAID NIH HHS/ -- AI 25563/AI/NIAID NIH HHS/ -- GM 28485/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1429-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402637" target="_blank"〉PubMed〈/a〉
    Keywords: *Acute-Phase Proteins ; Amino Acid Sequence ; Animals ; Base Sequence ; Blood Proteins/*genetics ; Carrier Proteins/*genetics/metabolism ; Gene Library ; Humans ; Kinetics ; Lipid A/metabolism ; Lipopolysaccharides/*metabolism/pharmacology ; Male ; *Membrane Glycoproteins ; Molecular Sequence Data ; Oligonucleotide Probes ; Rabbits ; Sequence Homology, Nucleic Acid ; Sheep ; Staphylococcus aureus ; Tumor Necrosis Factor-alpha/biosynthesis
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  • 61
    Publication Date: 1990-08-03
    Description: Human immunodeficiency virus (HIV) frequently causes neurological dysfunction and is abundantly expressed in the central nervous system (CNS) of acquired immunodeficiency syndrome (AIDS) patients with HIV encephalitis or myelopathy. The virus is found mostly in cells of the monocyte-macrophage lineage within the CNS, but the possibility of infection of other glial cells has been raised. Therefore, the effects of different HIV-1 and HIV-2 strains were studied in primary cultures of adult human brain containing microglial cells, the resident CNS macrophages, and astrocytes. These cultures could be productively infected with macrophage-adapted HIV-1 isolates but not with T lymphocyte-adapted HIV-1 isolates or two HIV-2 isolates. As determined with a triple-label procedure, primary astrocytes did not express HIV gag antigens and remained normal throughout the 3-week course of infection. In contrast, virus replicated in neighboring microglial cells, often leading to their cell fusion and death. The death of microglial cells, which normally serve immune functions in the CNS, may be a key factor in the pathogenesis of AIDS encephalitis or myelopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watkins, B A -- Dorn, H H -- Kelly, W B -- Armstrong, R C -- Potts, B J -- Michaels, F -- Kufta, C V -- Dubois-Dalcq, M -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):549-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2200125" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain/*microbiology ; Cells, Cultured ; Fluorescent Antibody Technique ; HIV-1/pathogenicity/*physiology ; HIV-2/pathogenicity/physiology ; Humans ; Kinetics ; Neuroglia/*microbiology ; Species Specificity ; Virus Replication
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 Dec 20;254(5039):1712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763317" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Ascorbic Acid/*therapeutic use ; Diet ; Humans ; Nutritional Physiological Phenomena
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  • 63
    Publication Date: 1991-01-25
    Description: CP-96,345 [(2S, 3S)-cis-2-(diphenylmethyl)-N-[(2-methoxyphenyl)- methyl]-1-azabicyclo[2.2.2]octan-3-amine] is a potent nonpeptide antagonist of the substance P (NK1) receptor. CP-96,345 inhibited 3H-labeled substance P binding and was a classical competitive antagonist in the NK1 monoreceptor dog carotid artery preparation. CP-96,345 inhibited substance P-induced salivation in the rat, a classical in vivo bioassay, but did not inhibit NK2, NK3, or numerous other receptors; it is thus a selective NK1 antagonist. This compound may prove to be a powerful tool for investigation of the physiological properties of substance P and exploration of its role in diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snider, R M -- Constantine, J W -- Lowe, J A 3rd -- Longo, K P -- Lebel, W S -- Woody, H A -- Drozda, S E -- Desai, M C -- Vinick, F J -- Spencer, R W -- New York, N.Y. -- Science. 1991 Jan 25;251(4992):435-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Exploratory Medicinal Chemistry, Central Research Division, Pfizer Inc., Groton, CT 06340.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1703323" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Biphenyl Compounds/chemistry/*pharmacology ; Carotid Arteries/drug effects ; Cattle ; Dogs ; Molecular Structure ; Muscle Contraction/drug effects ; Muscle Relaxation/drug effects ; Rabbits ; Rats ; Receptors, Neurokinin-1 ; Receptors, Neurotransmitter/*antagonists & inhibitors ; Salivation/drug effects ; Stereoisomerism ; Substance P/metabolism/pharmacology
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  • 64
    Publication Date: 1991-10-18
    Description: Modern life-sustaining therapy often succeeds in postponing death but may be ineffective at restoring health. Decisions that influence the time and circumstances of an individual's death are now common and require an accurate and comprehensive characterization of likely outcome. Evaluation of alternative outcomes requires acknowledgement that most patients find some outcomes to be worse than death. Improved understanding of major predictors of patient outcome, combined with rapidly expanding technical abilities to collect and manipulate large amounts of detailed clinical data, have created a new intellectual and technical basis for estimating outcomes from intensive medical care. Such objective probability estimates, such as the system described here, can reduce uncertainty about difficult clinical decisions and can be used by physicians, patients, and society to reorient health care toward more scientifically and ethically defensible approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knaus, W A -- Wagner, D P -- Lynn, J -- HS05787/HS/AHRQ HHS/ -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):389-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, George Washington University Medical Center, Washington, DC 20037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925596" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Critical Illness/*mortality ; Decision Support Techniques ; *Ethics, Medical ; Hospitalization ; Humans ; *Probability ; *Resource Allocation ; Social Values ; Time Factors
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-01-11
    Description: The function of the c-Myc oncoprotein and its role in cell growth control is unclear. A basic region of c-Myc is structurally related to the basic motifs of helix-loop-helix (HLH) and leucine zipper proteins, which provide sequence-specific DNA binding function. The c-Myc basic region was tested for its ability to bind DNA by attaching it to the HLH dimerization interface of the E12 enhancer binding factor. Dimers of the chimeric protein, termed E6, specifically bound an E box element (GGCCACGTGACC) recognized by other HLH proteins in a manner dependent on the integrity of the c-Myc basic motif. Methylation of the core CpG in the E box recognition site specifically inhibited binding by E6, but not by two other HLH proteins. Expression of E6 (but not an E6 DNA binding mutant) suppressed the ability of c-myc to cooperate with H-ras in a rat embryo fibroblast transformation assay, suggesting that the DNA recognition specificity of E6 is related to that of c-Myc in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prendergast, G C -- Ziff, E B -- New York, N.Y. -- Science. 1991 Jan 11;251(4990):186-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987636" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Transformation, Neoplastic ; Cloning, Molecular ; DNA/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Genes, ras ; Leucine Zippers ; Macromolecular Substances ; Methylation ; Molecular Sequence Data ; Mutagenesis ; Oligonucleotide Probes ; Protein Conformation ; Proto-Oncogene Proteins c-myc/genetics/*metabolism ; Rabbits ; Rats ; Recombinant Fusion Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-05-29
    Description: During replication, hepatitis delta virus (HDV) switches from production of small to large delta antigen. Both antigen isoforms have an HDV genome binding domain and are packaged into hepatitis B virus (HBV)-derived envelopes but differ at their carboxy termini. The large antigen was shown to contain a terminal CXXX box and undergo prenylation. The large, but not the small, antigen formed secreted particles when expressed singly with HBV surface antigen. Mutation of Cys211 in the CXXX box of the large antigen abolished both prenylation and particle formation, suggesting that this site is important for virion morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glenn, J S -- Watson, J A -- Havel, C M -- White, J M -- New York, N.Y. -- Science. 1992 May 29;256(5061):1331-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1598578" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, Viral/genetics/isolation & purification/*metabolism ; Cell Line ; Cysteine ; Hepatitis Delta Virus/genetics/metabolism/*physiology ; Hepatitis delta Antigens ; Mevalonic Acid/*metabolism ; Mice ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Proline/metabolism ; Protein Biosynthesis ; RNA, Messenger/metabolism ; Rabbits ; Reticulocytes/metabolism ; Serine ; Transfection ; Virus Replication
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  • 67
    Publication Date: 1992-08-28
    Description: Extracellular signals that promote cell growth activate cascades of protein kinases. The kinases are dephosphorylated and deactivated by a single type-2A protein phosphatase. The catalytic subunit of type-2A protein phosphatase was phosphorylated by tyrosine-specific protein kinases. Phosphorylation was enhanced in the presence of the phosphatase inhibitor okadaic acid, consistent with an autodephosphorylation reaction. More than 90% of the activity of phosphatase 2A was lost when thioadenosine triphosphate was used to produce a thiophosphorylated protein resistant to autodephosphorylation. Phosphorylation in vitro occurred exclusively on Tyr307. Phosphorylation was catalyzed by p60v-src, p56lck, epidermal growth factor receptors, and insulin receptors. Transient deactivation of phosphatase 2A might enhance transmission of cellular signals through kinase cascades within cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- Martin, B L -- Brautigan, D L -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1261-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology and Medicine, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1325671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ethers, Cyclic/pharmacology ; Gene Expression Regulation/drug effects/*physiology ; Humans ; In Vitro Techniques ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Okadaic Acid ; Oncogene Protein pp60(v-src)/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation/drug effects ; Protein Phosphatase 2 ; Protein-Tyrosine Kinases/physiology ; Rabbits ; Receptor, Epidermal Growth Factor/physiology ; Receptor, Insulin/physiology ; Thionucleotides/pharmacology ; Tyrosine/*metabolism
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  • 68
    Publication Date: 1992-11-13
    Description: A national probability survey of human immunodeficiency virus (HIV)-related risk factors among the general heterosexual population, the National AIDS (acquired immunodeficiency syndrome) Behavioral Surveys, has obtained data from 10,630 respondents. Data are presented on the prevalence of HIV-related risks in the general heterosexual population, on the distribution of the three largest risk groups across social strata, and on the prevalence and distribution of condom use among heterosexuals reporting a risk factor. Between 15 and 31 percent of heterosexuals nationally and 20 and 41 percent in cities with a high prevalence of AIDS reported an HIV risk factor. Condom use was relatively low. Only 17 percent of those with multiple sexual partners, 12.6 percent of those with risky sexual partners, and 10.8 percent of untested transfusion recipients used condoms all the time. Overall, the results suggest that current HIV prevention programs have, to a very limited extent, reached those heterosexuals with multiple sexual partners but have failed to reach many other groups of the heterosexual population at risk for HIV. New public health strategies may be needed for these specific risk groups.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Catania, J A -- Coates, T J -- Stall, R -- Turner, H -- Peterson, J -- Hearst, N -- Dolcini, M M -- Hudes, E -- Gagnon, J -- Wiley, J -- MH43892/MH/NIMH NIH HHS/ -- MH46240/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1101-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439818" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*epidemiology/prevention & control ; Adolescent ; Adult ; Age Factors ; Aged ; Blood Transfusion ; *Condoms ; Continental Population Groups ; Female ; HIV Seropositivity ; Health Surveys ; Hemophilia A/complications ; Humans ; Interviews as Topic ; Male ; Middle Aged ; Regression Analysis ; Risk Factors ; Sexual Behavior ; Sexual Partners ; Substance Abuse, Intravenous ; Time Factors ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, R -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1754.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1535454" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Breast Neoplasms/chemically induced ; *Contraceptive Agents, Female ; Delayed-Action Preparations ; Female ; Humans ; *Legislation, Drug ; Medroxyprogesterone/adverse effects/*analogs & derivatives ; Medroxyprogesterone Acetate ; Osteoporosis/chemically induced ; United States ; United States Food and Drug Administration ; Uterine Neoplasms/prevention & control
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-05-07
    Description: Colorectal tumor DNA was examined for somatic instability at (CA)n repeats on human chromosomes 5q, 15q, 17p, and 18q. Differences between tumor and normal DNA were detected in 25 of the 90 (28 percent) tumors examined. This instability appeared as either a substantial change in repeat length (often heterogeneous in nature) or a minor change (typically two base pairs). Microsatellite instability was significantly correlated with the tumor's location in the proximal colon (P = 0.003), with increased patient survival (P = 0.02), and, inversely, with loss of heterozygosity for chromosomes 5q, 17p, and 18q. These data suggest that some colorectal cancers may arise through a mechanism that does not necessarily involve loss of heterozygosity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibodeau, S N -- Bren, G -- Schaid, D -- CA-15083-18E8.1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484122" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 15 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 5 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Neoplasm/*genetics ; DNA, Satellite/*genetics ; Female ; Heterozygote ; Humans ; Male ; Middle Aged ; *Mutation ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
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  • 71
    Publication Date: 1993-10-22
    Description: The voltage-activated rabbit cardiac calcium channel alpha 1 subunit was expressed in Xenopus oocytes. The charge movement of its voltage sensor was measured and related to the opening of the ion-conducting pore. The half-activation potential for charge movement was 35 millivolts more negative than that for pore opening. Coexpression of the cardiac calcium channel beta subunit reduced this difference without affecting charge movement. Thus, intramolecular coupling between the voltage sensor and the channel pore opening can be facilitated by a regulatory subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neely, A -- Wei, X -- Olcese, R -- Birnbaumer, L -- Stefani, E -- AR38970/AR/NIAMS NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211185" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barium/metabolism ; Calcium Channels/*metabolism ; Electric Conductivity ; *Ion Channel Gating ; Membrane Potentials ; Myocardium/*metabolism ; Oocytes/metabolism ; Rabbits ; Xenopus
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 May 14;260(5110):894.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebellum/drug effects/*physiology ; *Memory/drug effects ; Muscimol/pharmacology ; Rabbits ; Red Nucleus/drug effects/physiology
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  • 73
    Publication Date: 1993-10-15
    Description: In cystic fibrosis (CF), absence or dysfunction of a phosphorylation-regulated chloride channel [CF transmembrane conductance regulator (CFTR)] leads to the loss or reduction of chloride secretion into the airways. Active sodium absorption is also increased in CF, and both of these ion transport changes could alter fluid transport across the airways. Under baseline conditions, cultured human airway epithelia from normal individuals absorbed fluid, and this absorption was increased in epithelia from patients with CF. In normal and CF epithelial cultures fluid absorption was inhibited by amiloride. Adenosine 3',5'-monophosphate stimulated fluid secretion in normal epithelial cultures but not in cultures from individuals with CF. In contrast, fluid secretion induced by nucleotide triphosphates (uridine triphosphate or adenosine triphosphate) was unaltered in cultures of epithelia from patients with CF, suggesting an approach to the treatment of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, C -- Finkbeiner, W E -- Widdicombe, J H -- McCray, P B Jr -- Miller, S S -- HL 42368/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211164" target="_blank"〉PubMed〈/a〉
    Keywords: Absorption ; Adenosine Triphosphate/pharmacology ; Adolescent ; Adult ; Amiloride/pharmacology ; Body Fluids/*metabolism ; Cells, Cultured ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*metabolism ; Epithelial Cells ; Epithelium/metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa/cytology/*metabolism ; Sodium/metabolism ; Sodium Channels/metabolism ; Trachea/cytology/*metabolism ; Uridine Triphosphate/pharmacology
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-01-03
    Description: American children are worse off than those in the previous generation in several important dimensions of mental, physical, and emotional well-being. During the 1960s cultural changes adversely affected children while their material condition improved substantially. By contrast, material conditions deteriorated in the 1980s, especially among children at the lower end of the income distribution. Public policies to improve the material condition of children require a transfer of resources from households that do not have children to those that do. Government programs such as tax credits and child allowances are more efficient and equitable than employer-mandated programs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuchs, V R -- Reklis, D M -- New York, N.Y. -- Science. 1992 Jan 3;255(5040):41-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, CA 94305-8715.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553531" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; *Child Advocacy ; Child Health Services/economics ; Education/*standards ; *Health Policy ; *Health Status ; Humans ; Poverty ; Socioeconomic Factors ; United States
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  • 75
    Publication Date: 1993-09-10
    Description: Activated autoreactive T cells are potentially pathogenic and regulated by clonotypic networks. Experimental autoimmune diseases can be treated by inoculation with autoreactive T cells (T cell vaccination). In the present study, patients with multiple sclerosis were inoculated with irradiated myelin basic protein (MBP)-reactive T cells. T cell responses to the inoculates were induced to deplete circulating MBP-reactive T cells in the recipients. Regulatory T cell lines isolated from the recipients inhibited T cells used for vaccination. The cytotoxicity of the CD8+ T cell lines was restricted by major histocompatibility antigens. Thus, clonotypic interactions regulating autoreactive T cells in humans can be induced by T cell vaccination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Medaer, R -- Stinissen, P -- Hafler, D -- Raus, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Multiple Sclerosis Research Unit, Dr. L. Willems Instituut, Diepenbeek, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690157" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Line ; Epitopes/immunology ; Female ; Humans ; *Immunotherapy, Adoptive ; Lymphocyte Activation ; Male ; Middle Aged ; Multiple Sclerosis/immunology/*therapy ; Myelin Basic Protein/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Vaccination
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leccese, A P -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):665.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8204122" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Adolescent ; Adult ; Female ; Humans ; Male ; Risk-Taking ; *Sexual Behavior ; *Street Drugs ; *Substance-Related Disorders
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1992-08-28
    Description: The extreme sensitivity to initial conditions that chaotic systems display makes them unstable and unpredictable. Yet that same sensitivity also makes them highly susceptible to control, provided that the developing chaos can be analyzed in real time and that analysis is then used to make small control interventions. This strategy has been used here to stabilize cardiac arrhythmias induced by the drug ouabain in rabbit ventricle. By administering electrical stimuli to the heart at irregular times determined by chaos theory, the arrhythmia was converted to periodic beating.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garfinkel, A -- Spano, M L -- Ditto, W L -- Weiss, J N -- KO4 HL01890/HL/NHLBI NIH HHS/ -- R01 HL36729/HL/NHLBI NIH HHS/ -- R01 HL44880/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1230-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Science, University of California, Los Angeles 90024-1527.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519060" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Arrhythmias, Cardiac/chemically induced/*prevention & control ; Calcium/physiology ; Disease Models, Animal ; Electric Stimulation Therapy/*methods ; Electrophysiology ; Epinephrine ; Heart/physiopathology ; Heart Rate ; Ouabain ; Rabbits
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  • 78
    Publication Date: 1993-04-09
    Description: The myotonic dystrophy mutation has recently been identified; however, the molecular mechanism of the disease is still unknown. The sequence of the myotonin-protein kinase gene was determined, and messenger RNA spliced forms were identified in various tissues. Antisera were developed for analytical studies. Quantitative reverse transcription-polymerase chain reaction and radioimmunoassay were used to demonstrate that decreased levels of the messenger RNA and protein expression are associated with the adult form of myotonic dystrophy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y H -- Friedman, D L -- Richards, S -- Pearlman, J A -- Gibbs, R A -- Pizzuti, A -- Ashizawa, T -- Perryman, M B -- Scarlato, G -- Fenwick, R G Jr -- P30-HG00210/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):235-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469976" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alternative Splicing ; Amino Acid Sequence ; Base Sequence ; Gene Expression ; Humans ; Molecular Sequence Data ; Molecular Weight ; Muscles/chemistry/*metabolism ; Myotonic Dystrophy/*genetics/metabolism ; Myotonin-Protein Kinase ; Polymerase Chain Reaction ; Protein Kinases/biosynthesis/chemistry/*genetics ; *Protein-Serine-Threonine Kinases ; RNA, Messenger/*genetics
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  • 79
    Publication Date: 1994-09-09
    Description: Endogenous DNA adducts may contribute to the etiology of human genetic disease and cancer. One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde. A sensitive mass spectrometric method permitted detection and quantitation of the major malondialdehyde-DNA adduct, a pyrimidopurinone derived from deoxyguanosine. DNA from disease-free human liver was found to contain 5400 adducts per cell, a frequency comparable to that of adducts formed by exogenous carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhary, A K -- Nokubo, M -- Reddy, G R -- Yeola, S N -- Morrow, J D -- Blair, I A -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- GM42056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A. B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt University School of Medicine, Nashville, TN 37232-0146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079172" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Carbon Tetrachloride/toxicity ; DNA/*chemistry ; DNA Damage ; Deoxyguanosine/*analogs & derivatives/analysis/*metabolism ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Lipid Peroxidation ; Liver/*chemistry ; Male ; Malondialdehyde/*metabolism ; Rats ; Rats, Sprague-Dawley
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
    Publication Date: 1993-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benhorin, J -- Kalman, Y M -- Medina, A -- Towbin, J -- Rave-Harel, N -- Dyer, T D -- Blangero, J -- MacCluer, J W -- Kerem, B S -- 5R01-HL-33843/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1960-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316839" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Child ; Female ; Genetic Linkage ; Humans ; Long QT Syndrome/*genetics ; Male ; Pedigree ; Phenotype
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  • 81
    Publication Date: 1994-02-18
    Description: Obstruction of airways by viscous sputum causes lung damage in patients with cystic fibrosis (CF). Sputum samples from CF patients were shown to contain filamentous actin. Human plasma gelsolin, a protein that severs actin filaments, rapidly decreased the viscosity of CF sputum samples in vitro. Gc globulin and deoxyribonuclease I, proteins that sequester monomeric actin but do not sever actin filaments, were less efficient than gelsolin in diminishing sputum viscosity. These results suggest that gelsolin may have therapeutic potential as a mucolytic agent in CF patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasconcellos, C A -- Allen, P G -- Wohl, M E -- Drazen, J M -- Janmey, P A -- Stossel, T P -- AR38910/AR/NIAMS NIH HHS/ -- HL19170/HL/NHLBI NIH HHS/ -- HL19429/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):969-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8310295" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*analysis/chemistry ; Adult ; Cystic Fibrosis/*metabolism ; Deoxyribonuclease I/metabolism ; Gelsolin/*pharmacology ; Humans ; In Vitro Techniques ; Sputum/chemistry/*drug effects ; Viscosity ; Vitamin D-Binding Protein/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
    Publication Date: 1993-09-24
    Description: Rheumatoid arthritis is an inflammatory synovial disease thought to involve T cells reacting to an antigen within the joint. Type II collagen is the major protein in articular cartilage and is a potential autoantigen in this disease. Oral tolerization to autoantigens suppresses animal models of T cell-mediated autoimmune disease, including two models of rheumatoid arthritis. In this randomized, double-blind trial involving 60 patients with severe, active rheumatoid arthritis, a decrease in the number of swollen joints and tender joints occurred in subjects fed chicken type II collagen for 3 months but not in those that received a placebo. Four patients in the collagen group had complete remission of the disease. No side effects were evident. These data demonstrate clinical efficacy of an oral tolerization approach for rheumatoid arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trentham, D E -- Dynesius-Trentham, R A -- Orav, E J -- Combitchi, D -- Lorenzo, C -- Sewell, K L -- Hafler, D A -- Weiner, H L -- AG00294/AG/NIA NIH HHS/ -- MO1 RR01032/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1727-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8378772" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Adult ; Aged ; Arthritis, Rheumatoid/*drug therapy/immunology ; Autoimmune Diseases/*drug therapy/immunology ; Collagen/*administration & dosage/adverse effects/therapeutic use ; Double-Blind Method ; Female ; Humans ; Immune Tolerance ; Male ; Middle Aged ; Placebo Effect ; T-Lymphocytes/immunology
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):648-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235581" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Cluster Analysis ; England/epidemiology ; Fathers ; Humans ; Leukemia, Radiation-Induced/epidemiology ; Male ; Neoplasms, Radiation-Induced/*epidemiology ; *Nuclear Reactors ; *Occupational Exposure
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
    Publication Date: 1994-07-15
    Description: A subset of patients who have undergone coronary angioplasty develop restenosis, a vessel renarrowing characterized by excessive proliferation of smooth muscle cells (SMCs). Of 60 human restenosis lesions examined, 23 (38 percent) were found to have accumulated high amounts of the tumor suppressor protein p53, and this correlated with the presence of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the lesions expressed HCMV protein IE84 and high amounts of p53. HCMV infection of cultured SMCs enhanced p53 accumulation, which correlated temporally with IE84 expression. IE84 also bound to p53 and abolished its ability to transcriptionally activate a reporter gene. Thus, HCMV, and IE84-mediated inhibition of p53 function, may contribute to the development of restenosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speir, E -- Modali, R -- Huang, E S -- Leon, M B -- Shawl, F -- Finkel, T -- Epstein, S E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023160" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Angioplasty, Balloon ; Antigens, Viral/*metabolism ; Atherectomy, Coronary ; Base Sequence ; Cells, Cultured ; Coronary Disease/*etiology/pathology/therapy ; Coronary Vessels/cytology/metabolism/microbiology ; Cytomegalovirus/*physiology ; Genes, p53 ; Humans ; Immediate-Early Proteins/*metabolism ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/metabolism/microbiology ; Recurrence ; Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism
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  • 85
    Publication Date: 1994-10-07
    Description: Loss of heterozygosity data from familial tumors suggest that BRCA1, a gene that confers susceptibility to ovarian and early-onset breast cancer, encodes a tumor suppressor. The BRCA1 region is also subject to allelic loss in sporadic breast and ovarian cancers, an indication that BRCA1 mutations may occur somatically in these tumors. The BRCA1 coding region was examined for mutations in primary breast and ovarian tumors that show allele loss at the BRCA1 locus. Mutations were detected in 3 of 32 breast and 1 of 12 ovarian carcinomas; all four mutations were germline alterations and occurred in early-onset cancers. These results suggest that mutation of BRCA1 may not be critical in the development of the majority of breast and ovarian cancers that arise in the absence of a mutant germline allele.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Futreal, P A -- Liu, Q -- Shattuck-Eidens, D -- Cochran, C -- Harshman, K -- Tavtigian, S -- Bennett, L M -- Haugen-Strano, A -- Swensen, J -- Miki, Y -- CA48711/CA/NCI NIH HHS/ -- CA55914/CA/NCI NIH HHS/ -- CA56749/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):120-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939630" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age of Onset ; Alleles ; BRCA1 Protein ; Base Sequence ; Breast Neoplasms/*genetics ; Chromosomes, Human, Pair 17 ; Female ; *Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Middle Aged ; Molecular Sequence Data ; Neoplasm Proteins/*genetics ; Ovarian Neoplasms/*genetics ; Transcription Factors/*genetics
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  • 86
    Publication Date: 1994-07-29
    Description: Rasmussen's encephalitis is a progressive childhood disease of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain. During efforts to raise antibodies to recombinant glutamate receptors (GluRs), behaviors typical of seizures and histopathologic features mimicking Rasmussen's encephalitis were found in two rabbits immunized with GluR3 protein. A correlation was found between the presence of Rasmussen's encephalitis and serum antibodies to GluR3 detected by protein immunoblot analysis and by immunoreactivity to transfected cells expressing GluR3. Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function. Thus, GluR3 is an autoantigen in Rasmussen's encephalitis, and an autoimmune process may underlie this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, S W -- Andrews, P I -- Gahring, L C -- Whisenand, T -- Cauley, K -- Crain, B -- Hughes, T E -- Heinemann, S F -- McNamara, J O -- NS17771/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- NS30990R29/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salt Lake City Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Autoantibodies/blood/*immunology ; Brain/pathology ; Cell Line ; Child ; Disease Models, Animal ; Encephalitis/complications/*immunology/pathology/therapy ; Female ; Humans ; Male ; Plasma Exchange ; Rabbits ; Receptors, Glutamate/*immunology ; Recombinant Fusion Proteins/immunology ; Seizures/etiology/immunology
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-08
    Description: In Thunberg's thermal grill illusion, first demonstrated in 1896, a sensation of strong, often painful heat is elicited by touching interlaced warm and cool bars to the skin. Neurophysiological recordings from two classes of ascending spinothalamic tract neurons that are sensitive to innocuous or noxious cold showed differential responses to the grill. On the basis of these results, a simple model of central disinhibition, or unmasking, predicted a quantitative correspondence between grill-evoked pain and cold-evoked pain, which was verified psychophysically. This integration of pain and temperature can explain the thermal grill illusion and the burning sensation of cold pain and may also provide a basis for the cold-evoked, burning pain of the classic thalamic pain syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Craig, A D -- Bushnell, M C -- DA07402/DA/NIDA NIH HHS/ -- NS25616/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):252-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ 85013.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023144" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cats ; *Cold Temperature ; Female ; Hot Temperature ; Humans ; Male ; Middle Aged ; Models, Biological ; Neurons, Afferent/*physiology ; Pain/*physiopathology ; Spinothalamic Tracts/*physiology
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  • 88
    Publication Date: 1994-09-02
    Description: Theory is linked with data to assess the probability of eradicating human immunodeficiency virus (HIV) in San Francisco through the use of prophylactic vaccines. The necessary vaccine efficacy levels and population coverage levels for eradication are quantified. The likely impact of risk behavior changes on vaccination campaigns is assessed. The results show it is unlikely that vaccines will be able to eradicate HIV in San Francisco unless they are combined with considerable reductions in risk behaviors. Furthermore, if risk behavior increases as the result of a vaccination campaign, then vaccination could result in a perverse outcome by increasing the severity of the epidemic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blower, S M -- McLean, A R -- 1R29DA08153/DA/NIDA NIH HHS/ -- AI33831/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Epidemiology Department, School of Public Health, University of California at Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073289" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Adult ; Disease Outbreaks/prevention & control ; HIV Infections/epidemiology/*prevention & control ; *Homosexuality ; Humans ; Immunization Programs ; Male ; Probability ; *Risk-Taking ; San Francisco/epidemiology
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  • 89
    Publication Date: 1994-05-20
    Description: Sib-pair analysis of 170 individuals from 11 Amish families revealed evidence for linkage of five markers in chromosome 5q31.1 with a gene controlling total serum immunoglobulin E (IgE) concentration. No linkage was found between these markers and specific IgE antibody concentrations. Analysis of total IgE within a subset of 128 IgE antibody-negative sib pairs confirmed evidence for linkage to 5q31.1, especially to the interleukin-4 gene (IL4). A combination of segregation and maximum likelihood analyses provided further evidence for this linkage. These analyses suggest that IL4 or a nearby gene in 5q31.1 regulates IgE production in a nonantigen-specific (noncognate) fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsh, D G -- Neely, J D -- Breazeale, D R -- Ghosh, B -- Freidhoff, L R -- Ehrlich-Kautzky, E -- Schou, C -- Krishnaswamy, G -- Beaty, T H -- 1 P41 RR03655/RR/NCRR NIH HHS/ -- AI20059/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1152-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Asthma and Allergy Center, School of Medicine, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178175" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Allergens/immunology ; Base Sequence ; Child ; Child, Preschool ; *Chromosomes, Human, Pair 5 ; Female ; Genes, MHC Class II ; *Genetic Linkage ; Genetic Markers ; Humans ; Hypersensitivity, Immediate/genetics ; Immunoglobulin E/*blood ; Interleukin-4/*genetics ; Likelihood Functions ; Lod Score ; Male ; Middle Aged ; Molecular Sequence Data
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buehler, L -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1018-9; author reply 1019-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Connexins/metabolism ; Diffusion ; Gap Junctions/*metabolism/ultrastructure ; Ion Channels/metabolism ; Rabbits
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  • 91
    Publication Date: 1993-01-15
    Description: Rab geranylgeranyl transferase (GG transferase) is a two-component enzyme that attaches 20-carbon isoprenoid groups to cysteine residues in Rab proteins, a family of guanosine triphosphate-binding proteins that regulate vesicular traffic. The mutant gene in human choroideremia, an X-linked form of retinal degeneration, encodes a protein that resembles component A of rat Rab GG transferase. Lymphoblasts from choroideremia subjects showed a marked deficiency in the activity of component A, but not component B, of Rab GG transferase. The deficiency was more pronounced when the substrate was Rab3A, a synaptic vesicle protein, than it was when the substrate was Rab1A, a protein of the endoplasmic reticulum. The data imply the existence of multiple component A proteins, one of which is missing in choroideremia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seabra, M C -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380507" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Alkyl and Aryl Transferases ; Cell Line, Transformed ; Cells, Cultured ; Choroid/chemistry ; Choroideremia/*genetics ; Female ; GTP-Binding Proteins/analysis/*metabolism ; Gene Expression Regulation, Enzymologic ; Humans ; Lymphocyte Activation ; Male ; Middle Aged ; Mutation ; Nerve Tissue Proteins/analysis/*metabolism ; Photoreceptor Cells/chemistry ; Pigment Epithelium of Eye/chemistry ; Protein Prenylation ; Retina/chemistry ; Substrate Specificity ; Transferases/*deficiency/genetics ; rab1 GTP-Binding Proteins ; rab3 GTP-Binding Proteins
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  • 92
    Publication Date: 1993-02-05
    Description: Myotonic dystrophy (DM) is an autosomal-dominant disorder that affects 1 in 8000 individuals. Amplification of an unstable trinucleotide CTG repeat, located within the 3' untranslated region of a gene, correlates with a more severe DM phenotype. In three cases, the number of CTG repeats was reduced during the transmission of the DM allele; in one of these cases, the number was reduced to within the normal range and correlated at least with a delay in the onset of clinical signs of DM. Haplotype data of six polymorphic markers in the DM gene region indicate that, in this latter case, two stretches of the affected chromosome had been exchanged with that region of the wild-type chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Hoy, K L -- Tsilfidis, C -- Mahadevan, M S -- Neville, C E -- Barcelo, J -- Hunter, A G -- Korneluk, R G -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Ottawa, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8094260" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Alleles ; Apolipoprotein C-II ; Apolipoproteins C/genetics ; Base Sequence ; *Chromosomes, Human, Pair 19 ; DNA/genetics/isolation & purification ; Female ; Genes, Dominant ; Haplotypes ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Myotonic Dystrophy/*genetics/physiopathology ; Oligodeoxyribonucleotides ; Pedigree ; Polymerase Chain Reaction ; *Polymorphism, Restriction Fragment Length ; *Repetitive Sequences, Nucleic Acid
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  • 93
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):618-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430308" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Aged ; Aged, 80 and over ; Breast Neoplasms/*epidemiology/etiology/mortality/pathology ; *Dietary Fats ; Estrogen Replacement Therapy ; Estrogens/*physiology ; Female ; Humans ; Incidence ; Middle Aged ; Neoplasms/*epidemiology ; Progesterone/*physiology ; Risk Factors ; Socioeconomic Factors ; United States/epidemiology
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caskey, C T -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):48-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211129" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Ethics, Medical ; Federal Government ; Genetic Diseases, Inborn/*diagnosis/therapy ; *Genetic Testing ; Genetic Therapy ; *Genetics, Medical ; *Human Genome Project ; Humans ; Infant, Newborn ; National Institutes of Health (U.S.) ; *Neonatal Screening ; Risk Factors ; United States
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1993 Apr 2;260(5104):13-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465191" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/epidemiology/etiology ; Child ; Electromagnetic Fields/*adverse effects ; Humans ; Leukemia/epidemiology/etiology ; Neoplasms/*etiology ; Sweden
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  • 96
    Publication Date: 1994-11-18
    Description: In April and May 1979, an unusual anthrax epidemic occurred in Sverdlovsk, Union of Soviet Socialist Republics. Soviet officials attributed it to consumption of contaminated meat. U.S. agencies attributed it to inhalation of spores accidentally released at a military microbiology facility in the city. Epidemiological data show that most victims worked or lived in a narrow zone extending from the military facility to the southern city limit. Farther south, livestock died of anthrax along the zone's extended axis. The zone paralleled the northerly wind that prevailed shortly before the outbreak. It is concluded that the escape of an aerosol of anthrax pathogen at the military facility caused the outbreak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meselson, M -- Guillemin, J -- Hugh-Jones, M -- Langmuir, A -- Popova, I -- Shelokov, A -- Yampolskaya, O -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1202-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aerosols ; Aged ; *Air Microbiology ; Animals ; Animals, Domestic ; Anthrax/*epidemiology/history/microbiology/transmission/veterinary ; *Bacillus anthracis/immunology ; Bacterial Vaccines ; Biological Warfare ; *Disease Outbreaks/veterinary ; Female ; History, 20th Century ; Humans ; Male ; Meteorological Concepts ; Middle Aged ; Retrospective Studies ; Spores, Bacterial ; USSR/epidemiology ; Wind
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  • 97
    Publication Date: 1994-11-18
    Description: The T cell antigen receptor (TCR) beta chain regulates early T cell development in the absence of the TCR alpha chain. The developmentally controlled gene described here encodes the pre-TCR alpha (pT alpha) chain, which covalently associates with TCR beta and with the CD3 proteins forms a pre-TCR complex that transduces signals in immature thymocytes. Unlike the lambda 5 pre-B cell receptor protein, the pT alpha chain is a type I transmembrane protein whose cytoplasmic tail contains two potential phosphorylation sites and a Src homology 3 (SH3)-domain binding sequence. Pre-TCR alpha transfection experiments indicated that surface expression of the pre-TCR is controlled by additional developmentally regulated proteins. Identification of the pT alpha gene represents an essential step in the structure-function analysis of the pre-TCR complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saint-Ruf, C -- Ungewiss, K -- Groettrup, M -- Bruno, L -- Fehling, H J -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 373, Institut Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/metabolism ; Base Sequence ; Cell Line ; *Cloning, Molecular ; DNA, Complementary/genetics ; *Gene Expression Regulation, Developmental ; Gene Rearrangement ; Membrane Glycoproteins/chemistry/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Open Reading Frames ; Phosphorylation ; Polymerase Chain Reaction ; Rabbits ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/*genetics/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
    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: 1994-07-29
    Description: Several paradigms of perceptual learning suggest that practice can trigger long-term, experience-dependent changes in the adult visual system of humans. As shown here, performance of a basic visual discrimination task improved after a normal night's sleep. Selective disruption of rapid eye movement (REM) sleep resulted in no performance gain during a comparable sleep interval, although non-REM slow-wave sleep disruption did not affect improvement. On the other hand, deprivation of REM sleep had no detrimental effects on the performance of a similar, but previously learned, task. These results indicate that a process of human memory consolidation, active during sleep, is strongly dependent on REM sleep.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karni, A -- Tanne, D -- Rubenstein, B S -- Askenasy, J J -- Sagi, D -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036518" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Electrodiagnosis ; Female ; Form Perception/*physiology ; Humans ; Learning/*physiology ; Male ; Sleep Deprivation/physiology ; Sleep Stages/physiology ; Sleep, REM/*physiology
    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: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1524, 1526-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Neoplasms/*prevention & control ; *Clinical Trials as Topic ; Coronary Disease/prevention & control ; Endometrial Neoplasms/chemically induced ; Female ; Humans ; Informed Consent ; Lipids/blood ; Middle Aged ; National Institutes of Health (U.S.) ; Risk Factors ; Tamoxifen/adverse effects/*therapeutic use ; 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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  • 100
    Publication Date: 1994-10-14
    Description: Interval mapping of data from two independent samples of sib pairs, at least one member of whom was reading disabled, revealed evidence for a quantitative trait locus (QTL) on chromosome 6. Results obtained from analyses of reading performance from 114 sib pairs genotyped for DNA markers localized the QTL to 6p21.3. Analyses of corresponding data from an independent sample of 50 dizygotic twin pairs provided evidence for linkage to the same region. In combination, the replicate samples yielded a chi 2 value of 16.73 (P = 0.0002). Examination of twin and kindred siblings with more extreme deficits in reading performance yielded even stronger evidence for a QTL (chi 2 = 27.35, P 〈 0.00001). The position of the QTL was narrowly defined with a 100:1 confidence interval to a 2-centimorgan region within the human leukocyte antigen complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardon, L R -- Smith, S D -- Fulker, D W -- Kimberling, W J -- Pennington, B F -- DeFries, J C -- HD-11681/HD/NICHD NIH HHS/ -- HD-27802/HD/NICHD NIH HHS/ -- HG-00085/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Health Sciences Program, SRI International, Menlo Park, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939663" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Child ; Chromosome Mapping ; *Chromosomes, Human, Pair 6 ; Diseases in Twins/*genetics ; Dyslexia/*genetics ; Female ; Genetic Linkage ; Genetic Markers ; HLA Antigens/genetics ; Humans ; Major Histocompatibility Complex ; Male ; Nuclear Family ; Regression Analysis ; Twins, Dizygotic
    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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