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  • Female  (415)
  • American Association for the Advancement of Science (AAAS)  (415)
  • American Physical Society
  • Annual Reviews
  • Cambridge University Press
  • Oxford University Press
  • 2005-2009
  • 1990-1994  (182)
  • 1980-1984  (233)
  • 1993  (114)
  • 1990  (68)
  • 1983  (101)
  • 1980  (132)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (415)
  • American Physical Society
  • Annual Reviews
  • Cambridge University Press
  • Oxford University Press
Years
  • 2005-2009
  • 1990-1994  (182)
  • 1980-1984  (233)
Year
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, K -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1659.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270478" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/diagnosis/*genetics/prevention & control ; Female ; Humans ; Risk Factors
    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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dusheck, J -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1494-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218487" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Congresses as Topic ; Female ; Humans ; Male ; Men ; United States ; *Women
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-09-21
    Description: Nonobese diabetic (NOD) mice develop an autoimmune form of diabetes, becoming hyperglycemic after 3 months of age. This process was accelerated by injecting young NOD mice with CD4+ islet-specific T cell clones derived from NOD mice. Overt diabetes developed in 10 of 19 experimental animals by 7 weeks of age, with the remaining mice showing marked signs of the disease in progress. Control mice did not become diabetic and had no significant pancreatic infiltration. This work demonstrates that a CD4 T cell clone is sufficient to initiate the disease process in the diabetes-prone NOD mouse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haskins, K -- McDuffie, M -- P01 DK40144/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1433-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2205920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Female ; Islets of Langerhans/*immunology/pathology ; Male ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; T-Lymphocytes/*immunology/transplantation
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  • 4
    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
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  • 5
    Publication Date: 1990-08-10
    Description: The interaction of the T cell receptor for antigen (TCR) with its antigen-major histocompatibility complex ligand is difficult to study because both are cell surface multimers. The TCR consists of two chains (alpha and beta) that are complexed to the five or more nonpolymorphic CD3 polypeptides. A soluble form of the TCR was engineered by replacing the carboxyl termini of alpha and beta with signal sequences from lipid-linked proteins, making them susceptible to enzymatic cleavage. In this manner, TCR heterodimers can be expressed independently of the CD3 polypeptides and in significant quantities (0.5 milligram per week). This technique seems generalizable to biochemical and structural studies of many other cell surface molecules as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, A Y -- Devaux, B -- Green, A -- Sagerstrom, C -- Elliott, J F -- Davis, M M -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):677-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University School of Medicine, CA 94305-5402.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1696397" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaline Phosphatase/genetics ; Amino Acid Sequence ; Animals ; Antigens, CD3 ; Antigens, CD55 ; Antigens, Differentiation, T-Lymphocyte/genetics ; Cell Line ; Complement Inactivator Proteins/genetics ; Female ; Humans ; Macromolecular Substances ; Membrane Proteins/genetics ; Molecular Sequence Data ; Placenta/enzymology ; Pregnancy ; Protein Sorting Signals/genetics ; Receptors, Antigen, T-Cell/*genetics ; Transfection
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  • 6
    Publication Date: 1990-12-07
    Description: A molecular clone of the Xenopus laevis ets-2 gene was isolated from an oocyte complementary DNA library. The amount of messenger RNA (mRNA) in each oocyte or embryo was almost constant during oogenesis and was maintained until the blastula stage of embryonic development, indicating that the observed 3.2-kilobase transcript is a maternal message. The only normal adult tissue in which ets-2 mRNA was detected was the ovary. Injection of antisense oligonucleotides homologous to the ets-2 sequence into oocytes led to degradation of the mRNA and blocked hormone-induced germinal vesicle breakdown. The ets-2 product is thus required for the meiotic maturation of Xenopus oocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Z Q -- Burdett, L A -- Seth, A K -- Lautenberger, J A -- Papas, T S -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Oncology, National Cancer Institute, Frederick, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; *DNA-Binding Proteins ; Embryo, Nonmammalian/physiology ; Female ; Gene Expression ; Gene Library ; Oligonucleotides, Antisense/pharmacology ; Oocytes/cytology/drug effects/*physiology ; Oogenesis ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Protein c-ets-2 ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; RNA, Messenger/analysis/genetics ; *Repressor Proteins ; *Trans-Activators ; *Transcription Factors ; Transcription, Genetic ; Xenopus laevis
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  • 7
    Publication Date: 1990-07-20
    Description: Animal lines selected for differences in drug sensitivity can be used to help determine the molecular basis of drug action. Long-sleep (LS) and short-sleep (SS) mice differ markedly in their genetic sensitivity to ethanol. To investigate the molecular basis for this difference, mRNA from brains of LS and SS mice was expressed in Xenopus oocytes and the ethanol sensitivity of gamma-aminobutyric acid A (GABAA)- and N-methyl D-aspartate (NMDA)-activated ion channels was tested. Ethanol facilitated GABA responses in oocytes injected with mRNA from LS mice but antagonized responses in oocytes injected with mRNA from SS animals. Ethanol inhibited NMDA responses equally in the two lines. Thus, genes coding for the GABAA receptor or associated proteins may be critical determinants of individual differences in ethanol sensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wafford, K A -- Burnett, D M -- Dunwiddie, T V -- Harris, R A -- AA03527/AA/NIAAA NIH HHS/ -- AA06399/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Colorado Health Sciences Center, Denver.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Brain/*metabolism ; Chloride Channels ; Chlorides/*physiology ; Diazepam/pharmacology ; Ethanol/*pharmacology ; Female ; Ion Channels/drug effects/physiology ; Membrane Proteins/*physiology ; Mice ; Mice, Inbred Strains ; Microinjections ; N-Methylaspartate ; Oocytes/*drug effects/*physiology ; RNA, Messenger/administration & dosage/genetics ; Receptors, GABA-A/drug effects/*genetics ; Xenopus ; gamma-Aminobutyric Acid/pharmacology
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  • 8
    Publication Date: 1990-05-04
    Description: A cell line has been established in continuous culture of human cerebral cortical neurons obtained from a patient with unilateral megalencephaly, a disorder associated with continued proliferation of immature neuronal cells. When differentiated in the presence of nerve growth factor, 1-isobutyl-3-methylxanthine, and dibutyryl adenosine 3',5'-monophosphate (cAMP), the cells display mature neuronal morphology with numerous long, extensively branched processes with spines and varicosities. The cells stain positively for neurofilament protein and neuron-specific enolase (selective neuronal markers) but are negative for glial markers, such as glial fibrillary acidic protein, S-100, and myelin basic protein. The cells also stain positively for the neurotransmitters gamma-aminobutyric acid (GABA), glutamate, somatostatin, cholecystokinin-8, and vasoactive intestinal polypeptide. These cells may facilitate characterization of neurons in the human central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ronnett, G V -- Hester, L D -- Nye, J S -- Connors, K -- Snyder, S H -- DA 00074/DA/NIDA NIH HHS/ -- DA 00266/DA/NIDA NIH HHS/ -- MH 18501/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 May 4;248(4955):603-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1692158" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Brain Diseases/*pathology ; Bucladesine/pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Cerebral Cortex/*pathology ; Culture Techniques/methods ; Female ; Humans ; Infant ; Nerve Growth Factors/pharmacology ; Nerve Tissue Proteins/analysis ; Neurons/cytology/drug effects/*pathology ; Neurotransmitter Agents/analysis ; gamma-Aminobutyric Acid/analysis
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  • 9
    Publication Date: 1990-09-28
    Description: The erbB2 oncogene encodes a 185-kilodalton transmembrane protein whose sequence is similar to the epidermal growth factor receptor (EGFR). A 30-kilodalton factor (gp30) secreted from MDA-MB-231 human breast cancer cells was shown to be a ligand for p185erbB2. An antibody to EGFR abolished the tyrosine phosphorylation induced by EGF and transforming growth factor-alpha (TGF-alpha) but only partially blocked that produced by gp30 in SK-BR-3 breast cancer cells. In two cell lines that overexpress erbB2 but do not expresss EGFR (MDA-MB-453 breast cancer cells and a Chinese hamster ovary cell line that had been transfected with erbB2), phosphorylation of p185erbB2 was induced only by gp30. The gp30 specifically inhibited the growth of cells that overexpressed p185erbB2. An antibody to EGFR had no effect on the inhibition of SK-BR-3 cell colony formation obtained with gp30. Thus, it appeared that gp30 interacted directly with the EGFR and erbB2. Direct binding of gp30 to p185erbB2 was confirmed by binding competition experiments, where gp30 was found to displace the p185erbB2 binding of a specific antibody to p185erbB2. The evidence described here suggests that gp30 is a ligand for p185erbB2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lupu, R -- Colomer, R -- Zugmaier, G -- Sarup, J -- Shepard, M -- Slamon, D -- Lippman, M E -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1552-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vincent T. Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Binding, Competitive ; Breast Neoplasms ; Cell Line ; Chromatography, Affinity ; Female ; Humans ; Kinetics ; Ligands ; Molecular Weight ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/genetics/immunology/*metabolism ; Proto-Oncogenes ; Receptor, Epidermal Growth Factor/isolation & purification/*metabolism ; Transfection
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galloway, A -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1319.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2078250" target="_blank"〉PubMed〈/a〉
    Keywords: *Congresses as Topic ; Female ; Government Agencies ; Humans ; *Prejudice ; Science ; United States ; *Women
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-05-04
    Description: The amino acid sequences of three fragments of cyanogen bromide-digested human placental inositol 1,2-cyclic phosphate 2-phosphohydrolase, an enzyme of the phosphatidylinositol signaling pathway, are identical to sequences within lipocortin III, a member of a family of homologous calcium- and phospholipid-binding proteins that do not have defined physiological functions. Lipocortin III has also been previously identified as placental anticoagulant protein III (PAP III) and calcimedin 35 alpha. Antibodies to PAP III detected PAP III and inositol 1,2-cyclic phosphate 2-phosphohydrolase with identical reactivity on immunoblotting. In addition, inositol 1,2-cyclic phosphate 2-phosphohydrolase was stimulated by the same acidic phospholipids that bind lipocortins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ross, T S -- Tait, J F -- Majerus, P W -- HLBI 14147/HL/NHLBI NIH HHS/ -- HLBI 16634/HL/NHLBI NIH HHS/ -- HLBI 40801/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 May 4;248(4955):605-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, 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/2159184" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Annexin A3 ; Annexins ; Calcium-Binding Proteins/*genetics ; Female ; Humans ; Immunoblotting ; Kinetics ; Molecular Sequence Data ; Phosphoric Diester Hydrolases/*genetics/isolation & purification/metabolism ; Placenta/*enzymology ; Pregnancy
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  • 12
    Publication Date: 1990-08-10
    Description: Somatic mutations in a subset of growth hormone (GH)-secreting pituitary tumors convert the gene for the alpha polypeptide chain (alpha s) of Gs into a putative oncogene, termed gsp. These mutations, which activate alpha s by inhibiting its guanosine triphosphatase (GTPase) activity, are found in codons for either of two amino acids, each of which is completely conserved in all known G protein alpha chains. The likelihood that similar mutations would activate other G proteins prompted a survey of human tumors for mutations that replace either of these two amino acids in other G protein alpha chain genes. The first gene so far tested, which encodes the alpha chain of Gi2, showed mutations that replaced arginine-179 with either cysteine or histidine in 3 of 11 tumors of the adrenal cortex and 3 of 10 endocrine tumors of the ovary. The mutant alpha i2 gene is a putative oncogene, referred to as gip2. In addition, gsp mutations were found in 18 of 42 GH-secreting pituitary tumors and in an autonomously functioning thyroid adenoma. These findings suggest that human tumors may harbor oncogenic mutations in various G protein alpha chain genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lyons, J -- Landis, C A -- Harsh, G -- Vallar, L -- Grunewald, K -- Feichtinger, H -- Duh, Q Y -- Clark, O H -- Kawasaki, E -- Bourne, H R -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):655-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Cetus Corporation, Emeryville CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2116665" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA, Neoplasm/genetics ; Endocrine System Diseases/*genetics ; Female ; GTP Phosphohydrolases/genetics/metabolism ; GTP-Binding Proteins/*genetics/metabolism ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neoplasms/*genetics ; Oligonucleotide Probes ; *Oncogenes ; Pituitary Neoplasms/*genetics ; Polymerase Chain Reaction
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  • 13
    Publication Date: 1990-07-20
    Description: Minor histocompatibility (H) antigens can be peptides derived from cellular proteins that are presented on the cell surface by major histocompatibility complex (MHC) class I molecules. This is similar to viral antigens, because in both cases cytotoxic T lymphocytes (CTLs) recognize artificially produced peptides loaded on target cells. Naturally processed minor H peptides were found to be similar to those artificial CTL-epitopes, as far as size and hydrophobicity is concerned. The peptides studied were isolated from a transfectant that expressed a model CTL-defined antigen, beta-galactosidase, from male cells that express H-Y, which has been known operationally since 1955, and from cells that express H-4, known since 1961.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rotzschke, O -- Falk, K -- Wallny, H J -- Faath, S -- Rammensee, H G -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):283-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Biologie, Abteilung Immungenetik, Tubingen, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695760" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Epitopes/isolation & purification ; Female ; H-Y Antigen/*analysis/immunology ; Male ; Mice ; Mice, Inbred Strains ; Minor Histocompatibility Antigens/*analysis/immunology ; Molecular Sequence Data ; Peptides/chemical synthesis ; Species Specificity ; Spleen/immunology ; T-Lymphocytes, Cytotoxic/*immunology
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Page, L M -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1320.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Models, Biological ; Reproduction ; Species Specificity ; Zebrafish/genetics/*physiology
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-04-06
    Description: A review of methodologically sound studies of the psychological responses of U.S. women after they obtained legal, nonrestrictive abortions indicates that distress is generally greatest before the abortion and that the incidence of severe negative responses is low. Factors associated with increased risk of negative response are consistent with those reported in research on other stressful life events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adler, N E -- David, H P -- Major, B N -- Roth, S H -- Russo, N F -- Wyatt, G E -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):41-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181664" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Induced/*psychology ; Adaptation, Psychological ; Adolescent ; Emotions ; Female ; Humans ; Pregnancy ; Pregnancy Trimester, First ; *Pregnant Women ; Risk Assessment ; Social Support ; United States
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  • 16
    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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  • 17
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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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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneiderman, M -- Davis, D L -- Wagener, D K -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):228-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2374921" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans ; European Continental Ancestry Group ; Female ; Humans ; Lung Neoplasms/mortality ; Male ; Prevalence ; Smoking/*epidemiology ; United States
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-09
    Description: Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation. An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome. Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia. Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man. Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas. These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation. A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, T -- Lane, J -- Housman, D -- 2 T32 GMO7753-11/GM/NIGMS NIH HHS/ -- GM27882/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):823-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aniridia/*genetics ; Blotting, Southern ; Chromosome Deletion ; Chromosome Mapping ; DNA/analysis ; *Disease Models, Animal ; Eye/embryology/pathology ; Female ; Genes, Wilms Tumor/*genetics ; Genetic Markers ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muridae ; Mutation ; Phenotype ; Polymorphism, Genetic ; Syndrome ; Wilms Tumor/*genetics
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  • 20
    Publication Date: 1990-01-19
    Description: The product of the yeast cell cycle control gene cdc2, and its homologs in higher eukaryotes (p34cdc2), all contain a perfectly conserved sequence of 16 amino acids that has not been found in any other protein sequence. Microinjection of this peptide triggers a specific increase in the concentration of intracellular free Ca2+ that originates from intracellular stores in both starfish and Xenopus oocytes. Thus, p34cdc2 might interact through its conserved peptide domain with some component of the Ca2(+)-regulatory system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Picard, A -- Cavadore, J C -- Lory, P -- Bernengo, J C -- Ojeda, C -- Doree, M -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):327-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS and INSERM, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2153316" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *CDC2 Protein Kinase ; Calcium/*metabolism ; Chloride Channels ; Chlorides/metabolism ; Cytoplasmic Granules/physiology ; Egtazic Acid/pharmacology ; Exocytosis/drug effects ; Female ; Genes, Fungal ; Growth Substances/*genetics ; Maturation-Promoting Factor ; Membrane Proteins/metabolism ; Microinjections ; Molecular Sequence Data ; Oocytes/drug effects/*physiology ; *Peptide Fragments ; Peptides/*pharmacology ; Starfish ; Xenopus
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  • 21
    Publication Date: 1990-06-08
    Description: X-linked Alport syndrome is a hereditary glomerulonephritis in which progressive loss of kidney function is often accompanied by progressive loss of hearing. Ultrastructural defects in glomerular basement membranes (GBM) of Alport syndrome patients implicate an altered structural protein as the cause of nephritis. The product of COL4A5, the alpha 5(IV) collagen chain, is a specific component of GBM within the kidney, and the gene maps to the same X chromosomal region as does Alport syndrome. Three structural aberrations were found in COL4A5, in intragenic deletion, a Pst I site variant, and an uncharacterized abnormality, which appear to cause nephritis and deafness, with allele-specific severity, in three Alport syndrome kindreds in Utah.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, D F -- Hostikka, S L -- Zhou, J -- Chow, L T -- Oliphant, A R -- Gerken, S C -- Gregory, M C -- Skolnick, M H -- Atkin, C L -- Tryggvason, K -- DK 36200/DK/NIDDK NIH HHS/ -- DK 39497/DK/NIDDK NIH HHS/ -- M01 RR 00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Informatics, 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/2349482" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Southern ; Cloning, Molecular ; Collagen/*genetics ; DNA/genetics/isolation & purification ; Exons ; Female ; *Genes ; Humans ; Male ; Molecular Weight ; *Mutation ; Nephritis, Hereditary/*genetics ; Pedigree ; Restriction Mapping ; X Chromosome
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  • 22
    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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  • 23
    Publication Date: 1990-04-13
    Description: The alpha chain of the human histocompatibility antigen HLA-G was identified as an array of five 37- to 39-kilodalton isoforms by the use of two-dimensional gel electrophoresis. Both cell-associated and secreted HLA-G antigens are prominent in first trimester villous cytotrophoblasts and are greatly reduced in third trimester cytotrophoblasts. Allelic variation was not detected, an indication that HLA-G is not obviously polymorphic in cytotrophoblasts. Among the following choriocarcinoma cell lines studied, HLA-G is expressed in JEG but not in Jar or BeWo. Expression of endogenous HLA-G genes has not been found in normal lymphoid cells. Thus, HLA-G is subject to both cell type-specific and developmental regulation and is expressed in early gestation human cytotrophoblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovats, S -- Main, E K -- Librach, C -- Stubblebine, M -- Fisher, S J -- DeMars, R -- AI-15586/AI/NIAID NIH HHS/ -- HD-24495/HD/NICHD NIH HHS/ -- P0I HD-24180/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Apr 13;248(4952):220-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Oncology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326636" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Line ; Choriocarcinoma/immunology ; Female ; Gene Expression ; *Genes, MHC Class I ; HLA Antigens/*genetics ; HLA-G Antigens ; Histocompatibility Antigens Class I/*genetics ; Humans ; Macromolecular Substances ; Pregnancy ; Pregnancy Trimester, First ; Trophoblasts/*immunology ; Tumor Cells, Cultured/immunology ; Uterine Neoplasms/immunology
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-30
    Description: Mice have an olfactory (pheromone) recognition memory located at the first relay in the sensory system. It is acquired with one-trial learning, contingent upon norepinephrine activation at mating, and lasts for several weeks. The mechanism involves Hebbian (association-dependent) changes in synaptic efficacy at dendrodendritic synapses in the accessory olfactory bulb. As a result of this memory, males made familiar by mating are recognized by the females, thereby mitigating pregnancy block. Such a memory function is biologically important to the female, as it is required to sustain pregnancy in the presence of her stud male's odors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brennan, P -- Kaba, H -- Keverne, E B -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sub-Department of Animal Behaviour, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147078" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/physiology ; Animals ; Female ; Hypothalamus/physiology ; Lidocaine/pharmacology ; Male ; Memory/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; N-Methylaspartate/antagonists & inhibitors/physiology ; Norepinephrine/physiology ; Olfactory Bulb/drug effects/physiology ; Olfactory Pathways/drug effects/physiology ; *Pheromones/urine ; Pregnancy ; Pregnancy, Animal/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Reproduction/physiology ; Smell/*physiology ; Synapses/physiology
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-01-19
    Description: The mevalonate-derived portion of a prenylated protein from Chinese hamster ovary cells has been established as diterpenoid (C20). This group is linked to a carboxyl-terminal cysteine as a thioether. It was removed from the protein by hydrazinolysis followed by Raney nickel desulfurization, and the resulting hydrocarbon fraction was analyzed by gas chromatography-mass spectrometry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rilling, H C -- Breunger, E -- Epstein, W W -- Crain, P F -- GM 29812/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):318-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Utah, Salt Lake City 84112.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2296720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Diterpenes/*metabolism ; Female ; Gas Chromatography-Mass Spectrometry ; Mevalonic Acid/metabolism ; Molecular Structure ; Ovary ; Protein Precursors/metabolism ; *Protein Processing, Post-Translational ; Proteins/*metabolism
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carson, H L -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):191.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Female ; Genetic Variation ; *Genetics, Population ; Male ; Recombination, Genetic ; Selection, Genetic
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-03-30
    Description: Population growth in the United States and the Soviet Union is slowing. Since the 1970s, labor force growth in both countries is slowing even more than population growth, and both countries are aging. Economic effects of slowing growth can be compensated for by increased participation in the labor force and increased productivity and by adjustments in the military forces. Economic flexibility and policy choices will determine how successfully the trend to slower population growth will be accommodated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torrey, B B -- Kingkade, W W -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1548-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Research, U.S. Bureau of the Census, Washington DC 20233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321015" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Aged ; Female ; Fertility ; Humans ; Male ; Middle Aged ; *Population Dynamics ; Ussr ; United States
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  • 28
    Publication Date: 1990-06-01
    Description: An amyloid protein that precipitates in the cerebral vessel walls of Dutch patients with hereditary cerebral hemorrhage with amyloidosis is similar to the amyloid protein in vessel walls and senile plaques in brains of patients with Alzheimer's disease, Down syndrome, and sporadic cerebral amyloid angiopathy. Cloning and sequencing of the two exons that encode the amyloid protein from two patients with this amyloidosis revealed a cytosine-to-guanine transversion, a mutation that caused a single amino acid substitution (glutamine instead of glutamic acid) at position 22 of the amyloid protein. The mutation may account for the deposition of this amyloid protein in the cerebral vessel walls of these patients, leading to cerebral hemorrhages and premature death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, E -- Carman, M D -- Fernandez-Madrid, I J -- Power, M D -- Lieberburg, I -- van Duinen, S G -- Bots, G T -- Luyendijk, W -- Frangione, B -- AG 05891/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1124-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University Medical Center, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2111584" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease/*genetics ; Amino Acid Sequence ; Amyloid/*genetics ; Amyloid beta-Protein Precursor ; Amyloidosis/complications/*genetics ; Base Sequence ; Brain Chemistry ; Cerebral Hemorrhage/etiology/*genetics ; Cerebrovascular Disorders/complications/*genetics ; Dna ; Deoxyribonucleases, Type II Site-Specific ; Exons ; Female ; Genes, Dominant ; Humans ; Middle Aged ; Molecular Sequence Data ; *Mutation ; Netherlands ; Polymerase Chain Reaction ; Protein Precursors/*genetics
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  • 29
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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〉Cherfas, J -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1240.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2399460" target="_blank"〉PubMed〈/a〉
    Keywords: Fatigue Syndrome, Chronic/*etiology/microbiology/psychology ; Female ; Humans ; Male
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cherfas, J -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):852-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Female ; Growth Hormone/*standards ; Humans ; Milk ; Recombinant Proteins/standards ; United States ; United States Food and Drug Administration
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  • 31
    Publication Date: 1990-11-02
    Description: The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, M -- Coirini, H -- Pfaff, D W -- McEwen, B S -- HD-05751/HD/NICHD NIH HHS/ -- NS-07080/NS/NINDS NIH HHS/ -- TWO4103/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):691-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/pharmacology ; Female ; Oxytocin/pharmacology ; Progesterone/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Oxytocin ; Sexual Behavior, Animal/*drug effects ; Ventromedial Hypothalamic Nucleus/*drug effects
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-01-19
    Description: In a pedigree derived from a mouse treated with the mutagen ethylnitrosourea, a mutation has been identified that predisposes to spontaneous intestinal cancer. The mutant gene was found to be dominantly expressed and fully penetrant. Affected mice developed multiple adenomas throughout the entire intestinal tract at an early age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, A R -- Pitot, H C -- Dove, W F -- CA07175/CA/NCI NIH HHS/ -- CA50585/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):322-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2296722" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/complications/*genetics ; Alleles ; Anemia/complications/genetics ; Animals ; Ethylnitrosourea ; Female ; Intestinal Neoplasms/complications/*genetics/pathology ; Male ; Mice ; Mice, Inbred AKR ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Feb 9;247(4943):620-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300818" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; Neoplasms, Radiation-Induced/*epidemiology ; Occupational Diseases/*epidemiology ; Radiation Injuries/*epidemiology ; Risk Factors
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-16
    Description: Activin, a member of the transforming growth factor beta protein family, was originally isolated from gonadal fluids and stimulates the release of pituitary follicle-stimulating hormone (FSH). Activin has numerous functions in both normal and neoplastic cells. Various cells synthesize activin and have a specific binding site for this peptide. However, the molecular basis for its actions is unknown. A binding protein for activin was purified from rat ovary and was identical to follistatin, a specific inhibitor of FSH release. It is likely that the binding protein participates in the diverse regulatory actions of activin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, T -- Takio, K -- Eto, Y -- Shibai, H -- Titani, K -- Sugino, H -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Frontier Research Program, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2106159" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Animals ; *Carrier Proteins ; Cells, Cultured ; Female ; Follicle Stimulating Hormone/secretion ; Inhibins/isolation & purification/*metabolism/pharmacology ; Kinetics ; Molecular Weight ; Ovary/*metabolism ; Pituitary Gland/drug effects/secretion ; Protein Binding ; Rats
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-08-17
    Description: The major small nuclear ribonucleoprotein particles (snRNPs) U1, U2, U4 + U6, and U5 have to be transported from the cytoplasm, where they are synthesized, to the nucleus, where they splice pre-messenger RNAs. Since the free core snRNP proteins in the cytoplasm do not enter the nucleus on their own, the nuclear location signal must either reside on the snRNA or be created as a result of snRNA-protein interaction. Here the involvement by the 5'-terminal cap of snRNA molecules in the nucleo-cytoplasmic transport of UsnRNPs has been studied by microinjection of synthetic U1 RNA molecules into frog oocytes; the U1 RNA bore either the normal cap (m3G) or a chemical derivative. Antibodies in the cytoplasm against the m3G cap inhibited the nuclear uptake of U1 snRNP. U1 RNA that was uncapped or contained an unnatural ApppG cap did not enter the nucleus, even though it carried a normal complement of protein molecules. When the ribose ring of the m3G cap was oxidized with periodate, nuclear transport of U1 snRNPs was severely inhibited. Finally, microinjection of m3G cap alone (but not m7G cap) into oocytes severely inhibited the transport of U1 snRNPs to the nucleus. These data suggest that one step in the nuclear uptake of U1 snRNPs involves the m3G cap structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, U -- Luhrmann, R -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):786-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie und Tumorforschung, Phillipps-Universitat Marburg, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2143847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Nucleus/*metabolism ; Cytoplasm/metabolism ; Female ; Guanosine/*analogs & derivatives/physiology ; Kinetics ; Mutation ; Oocytes/*ultrastructure ; RNA Caps/*physiology ; Ribonucleoproteins/genetics/*metabolism ; Ribonucleoproteins, Small Nuclear ; Signal Transduction/*physiology ; Xenopus laevis
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  • 36
    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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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):909.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305259" target="_blank"〉PubMed〈/a〉
    Keywords: Contraceptive Agents ; Contraceptive Devices ; Family Planning Services/*legislation & jurisprudence/trends ; Female ; Humans ; Male ; Sterilization, Reproductive ; United States
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-15
    Description: The alpha beta T cell receptor (TCR) recognizes antigens that are presented by major histocompatibility complex (MHC)-encoded cell surface molecules by binding to both the antigen and the MHC molecules. Discrimination of self from nonself antigens and MHC molecules is achieved by negative and positive selection of T cells in the thymus: potentially harmful T cells with receptors that bind to self antigens plus self MHC molecules are deleted before they can mount immune responses. In contrast, the maturation of useful T cells with receptors that bind foreign antigens plus self MHC molecules requires the binding of their receptor to MHC molecules on thymic epithelium in the absence of foreign antigen. The binding of the TCR to either class I or class II MHC molecules directs differentiation of the selected cells into either CD4-8+ (killer) or CD4+8- (helper) T cells, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, H -- Kisielow, P -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Cell Survival ; Female ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; *Immune Tolerance ; Killer Cells, Natural/immunology ; Male ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, C K -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):612.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382137" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; National Institutes of Health (U.S.) ; *Physicians, Women ; *Research Support as Topic ; United States
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  • 40
    Publication Date: 1990-10-26
    Description: The role of defective glucose transport in the pathogenesis of noninsulin-dependent diabetes (NIDDM) was examined in Zucker diabetic fatty rats, a model of NIDDM. As in human NIDDM, insulin secretion was unresponsive to 20 mM glucose. Uptake of 3-O-methylglucose by islet cells was less than 19% of controls. The beta cell glucose transporter (GLUT-2) immunoreactivity and amount of GLUT-2 messenger RNA were profoundly reduced. Whenever fewer than 60% of beta cells were GLUT-2-positive, the response to glucose was absent and hyperglycemia exceeded 11 mM plasma glucose. We conclude that in NIDDM underexpression of GLUT-2 messenger RNA lowers high Km glucose transport in beta cells, and thereby impairs glucose-stimulated insulin secretion and prevents correction of hyperglycemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, J H -- Ogawa, A -- Chen, L -- Orci, L -- Newgard, C B -- Alam, T -- Unger, R H -- DK02700-30/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 26;250(4980):546-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Diabetes Research, University of Texas, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237405" target="_blank"〉PubMed〈/a〉
    Keywords: 3-O-Methylglucose ; Animals ; Biological Transport ; Diabetes Mellitus/metabolism ; Diabetes Mellitus, Experimental/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Female ; *Gene Expression ; Glucose/pharmacology ; Immunoblotting ; Insulin/secretion ; Islets of Langerhans/drug effects/*metabolism ; Kinetics ; Male ; Methylglucosides/metabolism ; Monosaccharide Transport Proteins/*genetics/metabolism ; Obesity ; RNA, Messenger/metabolism ; Rats ; Rats, Inbred Strains ; Rats, Zucker
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  • 41
    Publication Date: 1990-02-16
    Description: Transfection of Chinese hamster ovary cells with complementary DNA encoding the RIIA sodium channel alpha subunit from rat brain led to expression of functional sodium channels with the rapid, voltage-dependent activation and inactivation characteristic of sodium channels in brain neurons. The sodium currents mediated by these transfected channels were inhibited by tetrodotoxin, persistently activated by veratridine, and prolonged by Leiurus alpha-scorpion toxin, indicating that neurotoxin receptor sites 1 through 3 were present in functional form. The RIIA sodium channel alpha subunit cDNA alone is sufficient for stable expression of functional sodium channels with the expected kinetic and pharmacological properties in mammalian somatic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheuer, T -- Auld, V J -- Boyd, S -- Offord, J -- Dunn, R -- Catterall, W A -- NS 15751/NS/NINDS NIH HHS/ -- NS 25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):854-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Cell Line ; Cricetinae ; Cricetulus ; Electric Conductivity ; Female ; Membrane Potentials/drug effects ; Membrane Proteins/genetics/*physiology ; Ovary ; Rats ; Sodium Channels/drug effects/*physiology ; Tetrodotoxin/pharmacology ; *Transfection
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1503-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2274777" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Breast Neoplasms/*prevention & control ; Dietary Fats/administration & dosage ; Ethics ; Female ; Humans ; Middle Aged ; *National Institutes of Health (U.S.) ; Patient Compliance ; Research Support as Topic/economics ; United States ; *Women's Health
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  • 43
    Publication Date: 1990-07-20
    Description: Angiotensin II (AII) stimulates rapid increases in the concentration of cytosolic calcium in follicular oocytes from Xenopus laevis. This calcium response was not present in denuded oocytes, indicating that it is mediated by AII receptors on the adherent follicular cells. The endogenous AII receptors differed in their binding properties from mammalian AII receptors expressed on the oocyte surface after injection of rat adrenal messenger RNA. Also, the calcium responses to activation of the amphibian AII receptor, but not the expressed mammalian AII receptor, were blocked reversibly by octanol and intracellular acidification, treatments that inhibit cell coupling through gap junctions. In addition, AII increased the rate of progesterone-induced maturation. Thus, an AII-induced calcium-mobilizing signal is transferred from follicle cells to the oocyte through gap junctions and may play a physiological role in oocyte maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, K -- Bor, M -- Ji, H -- Markwick, A -- Millan, M A -- Catt, K J -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):298-301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2374929" target="_blank"〉PubMed〈/a〉
    Keywords: Aequorin ; Angiotensin II/*analogs & derivatives/metabolism/*pharmacology ; Animals ; Calcium/*metabolism ; Cytosol/drug effects/metabolism ; Female ; Intercellular Junctions/drug effects/*physiology ; Kinetics ; Luminescence ; Oocytes/drug effects/*physiology ; Progesterone/pharmacology ; Receptors, Angiotensin/metabolism ; *Signal Transduction/drug effects ; Structure-Activity Relationship ; Xenopus laevis
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  • 44
    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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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1372.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402633" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*deficiency/genetics ; Child, Preschool ; Female ; *Genetic Therapy ; Humans ; National Institutes of Health (U.S.) ; Nucleoside Deaminases/*deficiency ; United States
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  • 46
    Publication Date: 1990-08-03
    Description: Chronic endobronchial infection with mucoid Pseudomonas aeruginosa accounts for much of the morbidity and mortality in patients with cystic fibrosis (CF). Reduced morbidity is observed when infection is absent. Clinical investigations have implicated opsonizing antibody specific for the mucoid exopolysaccharide (MEP) surrounding these bacteria as a potential immunologic protective mechanism, whereas nonopsonizing antibody to MEP is not protective. Mice and rats immunized with doses of MEP that elicited opsonizing antibody had reduced levels of infection compared with nonimmune controls after intratracheal challenge with mucoid P. aeruginosa enmeshed in agar beads. Doses of MEP that elicited nonopsonizing antibody were not protective. Parallel experiments in which passive transfer of polyclonal and monoclonal opsonizing and nonopsonizing antibody were used yielded similar results. These data indicate that MEP-specific opsonizing antibody can protect against chronic P. aeruginosa infection in this model of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pier, G B -- Small, G J -- Warren, H B -- AI 22534/AI/NIAID NIH HHS/ -- AI 22806/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):537-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Animal Resource Center, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2116663" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*therapeutic use ; Cystic Fibrosis/complications ; Disease Models, Animal ; Female ; Immunization, Passive ; Lung/pathology ; Polysaccharides, Bacterial/*immunology ; Pseudomonas Infections/*immunology/pathology/prevention & control ; Pseudomonas aeruginosa/immunology ; Rats
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-09
    Description: Immunoglobulin rearrangement is central to generating antibody diversity because of heterogeneity generated during recombination by deletion or addition of nucleotides at coding joints by the recombinase machinery. Examination of these junctional modifications revealed that the addition of nongermline-encoded nucleotides was more prevalent in adult versus fetal B cells, thus partially limiting the fetal antibody repertoire. In contrast, deletion of nucleotides occurs equivalently in B cells at different stages of development and at different points in B cell ontogeny. Finally, the bias in murine immunoglobulins for one DH segment reading frame occurs at the DHJH intermediate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meek, K -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):820-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, 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/2237433" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/immunology ; Animals ; Animals, Newborn ; *Antibody Diversity ; B-Lymphocytes/*immunology ; Blotting, Southern ; Electrophoresis, Polyacrylamide Gel ; Female ; *Gene Rearrangement, B-Lymphocyte ; Immunoglobulin Joining Region/*genetics ; Mice ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Pregnancy ; Restriction Mapping
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-23
    Description: A founder transgenic mouse harbored two different integration patterns of a transgene at the same locus, each of which gave rise to a similar autosomal recessive mutation. Mice of the mutant phenotype were of small stature but had normal levels of growth hormone. The disrupted locus was cloned, and a genetic and molecular analysis showed that the insertional mutants were allelic to a spontaneous mutant, pygmy. The mice should be a useful model for the growth hormone-resistant human dwarf syndromes and could lead to a greater understanding of the pathways involved in growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, X -- Benson, K F -- Chada, K -- GM38731/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Disease Models, Animal ; Dwarfism/*genetics ; Female ; Growth Hormone/blood ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Nucleic Acid Hybridization ; Pedigree ; Restriction Mapping
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  • 49
    Publication Date: 1990-05-11
    Description: Female green turtles exhibit strong nest-site fidelity as adults, but whether the nesting beach is the natal site is not known. Under the natal homing hypothesis, females return to their natal beach to nest, whereas under the social facilitation model, virgin females follow experienced breeders to nesting beaches and after a "favorable" nesting experience, fix on that site for future nestings. Differences shown in mitochondrial DNA genotype frequency among green turtle colonies in the Caribbean Sea and Atlantic Ocean are consistent with natal homing expectations and indicate that social facilitation to nonnatal sites is rare.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meylan, A B -- Bowen, B W -- Avise, J C -- New York, N.Y. -- Science. 1990 May 11;248(4956):724-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Natural Resources, Florida Marine Research Institute, Petersburgh 33701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333522" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/*genetics ; Female ; Genotype ; Models, Psychological ; *Orientation ; *Social Facilitation ; Turtles/genetics/*physiology
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  • 50
    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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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-04-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pool, R -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):29-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321025" target="_blank"〉PubMed〈/a〉
    Keywords: *Cells/ultrastructure ; Female ; Fertilization in Vitro ; Humans ; Infertility/surgery ; *Laser Therapy ; Male
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-03-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, R W -- Brent, R L -- New York, N.Y. -- Science. 1990 Mar 9;247(4947):1166.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2315688" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Intellectual Disability/*etiology ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Radiation Dosage ; *Radiation Injuries
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  • 53
    Publication Date: 1990-01-19
    Description: Target cells are thought to regulate the survival of afferent neurons during development by supplying limiting amounts of neurotrophic factors, but the degree to which afferent neurons remain dependent on target-derived support in the adult is uncertain. In this study, uninjured basal forebrain cholinergic neurons did not die after excitotoxic ablation of their target neurons in young adult rats, indicating that they are either not dependent on neurotrophic factors for survival or can obtain trophic support from other sources after target neurons are lost. This finding suggests that cholinergic cell death in neurodegenerative conditions such as Alzheimer's disease is not due solely to a loss of target neurons or factors provided by them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sofroniew, M V -- Galletly, N P -- Isacson, O -- Svendsen, C N -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):338-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of Cambridge, England.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1688664" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/analysis ; Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Axonal Transport ; Cell Survival ; Choline/*physiology ; Diencephalon/*cytology ; Female ; Hippocampus/cytology/drug effects ; Immunohistochemistry ; N-Methylaspartate ; Nerve Growth Factors/physiology ; Neurons, Afferent/*physiology ; Rats ; Septal Nuclei/cytology ; Telencephalon/*cytology
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-03-23
    Description: Estrogen and luteinizing hormone-releasing hormone (LH-RH) interact to influence both behavior and gonadotropin release. However, little is known about the biochemical mechanisms that mediate the effects of these hormones or their interactions. The most prominent protein induced by estrogen in the ventromedial hypothalamus has the same amino-terminal sequence as the most prominent protein induced by LH-RH in the pituitary in vitro and in vivo; these proteins comigrate on two-dimensional gels. Furthermore, the hormonal induction may be caused by modification of a constitutive protein with the same molecular weight (70,000) but a slightly more acidic isoelectric point, whose level is inversely related to the level of the induced form after estrogen treatment. Thus estrogen and LH-RH may interact by additively or synergistically inducing this protein, which is called HIP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobbs, C V -- Fink, G -- Pfaff, D W -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1477-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Behavior, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Electrophoresis, Gel, Two-Dimensional ; Estrogens/*pharmacology ; Female ; Gonadotropin-Releasing Hormone/*pharmacology ; Hypothalamus/drug effects/*metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*biosynthesis ; Ovariectomy ; Pituitary Gland/drug effects/*metabolism ; *Protein Biosynthesis ; Rats
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  • 55
    Publication Date: 1990-12-21
    Description: The progesterone receptor (PR) in the chicken oviduct is a phosphoprotein that regulates gene transcription in the presence of progesterone. Treatment with progesterone in vivo stimulates phosphorylation of the progesterone receptor. With transient transfection assays, the present work has tested whether phosphorylation participates in the regulation of PR-mediated transcription. Treatment with 8-bromo-cyclic adenosine monophosphate (8-Br cAMP), a stimulator of cAMP-dependent protein kinase [protein kinase A (PKA)], mimicked progesterone-dependent, receptor-mediated transcription in the absence of progesterone. Inhibition of PKA blocked hormone action. Treatment with okadaic acid, an inhibitor of protein phosphatases 1 and 2A, stimulated transcription in a manner similar to that of progesterone. These observations suggest that phosphorylation of the PR or other proteins in the transcription complex can modulate PR-mediated transcription in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denner, L A -- Weigel, N L -- Maxwell, B L -- Schrader, W T -- O'Malley, B W -- HD-07857/HD/NICHD NIH HHS/ -- HD-22061/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1740-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2176746" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cell Line ; Chickens ; Female ; Gene Expression Regulation ; Kinetics ; Oviducts/metabolism ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphorylation ; Progesterone/*pharmacology ; Receptors, Progesterone/*metabolism ; *Transcription, Genetic/drug effects ; Transfection
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-08-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, D P -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):469.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2200119" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Female ; Health Services/*legislation & jurisprudence ; Health Services Administration ; Humans ; Medicaid ; Oregon ; United States
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-01
    Description: The identification of ras oncogenes in human and animal cancers including precancerous lesions indicates that these genes participate in the early stages of neoplastic development. Yet, these observations do not define the timing of ras oncogene activation in the multistep process of carcinogenesis. To ascertain the timing of ras oncogene activation, an animal model system was devised that involves the induction of mammary carcinomas in rats exposed at birth to the carcinogen nitrosomethylurea. High-resolution restriction fragment length polymorphism analysis of polymerase chain reaction-amplified ras sequences revealed the presence of both H-ras and K-ras oncogenes in normal mammary glands 2 weeks after carcinogen treatment and at least 2 months before the onset of neoplasia. These ras oncogenes can remain latent within the mammary gland until exposure to estrogens, demonstrating that activation of ras oncogenes can precede the onset of neoplasia and suggesting that normal physiological proliferative processes such as estrogen-induced mammary gland development may lead to neoplasia if the targeted cells harbor latent ras oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, R -- Sukumar, S -- Barbacid, M -- 1-RO1-CA48943/CA/NCI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Squibb Institute for Medical Research, Princeton, NJ 08543.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188364" target="_blank"〉PubMed〈/a〉
    Keywords: Adenofibroma/genetics ; Animals ; Animals, Newborn ; Base Sequence ; Carcinoma/genetics ; Cell Transformation, Neoplastic/*genetics ; Estrogens/physiology ; Female ; Gene Expression Regulation, Neoplastic/*physiology ; Genes, ras/*physiology ; Mammary Glands, Animal/growth & development ; Mammary Neoplasms, Experimental/chemically induced/*genetics ; Methylnitrosourea ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; Rats ; Rats, Inbred Strains ; Sexual Maturation ; Time Factors
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Jul 20;249(4966):228.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2374920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens/*physiology ; *Eggs ; Energy Metabolism ; Female ; Thermodynamics
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  • 59
    Publication Date: 1990-12-21
    Description: Human breast cancer is usually caused by genetic alterations of somatic cells of the breast, but occasionally, susceptibility to the disease is inherited. Mapping the genes responsible for inherited breast cancer may also allow the identification of early lesions that are critical for the development of breast cancer in the general population. Chromosome 17q21 appears to be the locale of a gene for inherited susceptibility to breast cancer in families with early-onset disease. Genetic analysis yields a lod score (logarithm of the likelihood ratio for linkage) of 5.98 for linkage of breast cancer susceptibility to D17S74 in early-onset families and negative lod scores in families with late-onset disease. Likelihood ratios in favor of linkage heterogeneity among families ranged between 2000:1 and greater than 10(6):1 on the basis of multipoint analysis of four loci in the region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, J M -- Lee, M K -- Newman, B -- Morrow, J E -- Anderson, L A -- Huey, B -- King, M C -- CA27632/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1684-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270482" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/diagnosis/etiology/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Female ; Humans ; Male ; Pedigree ; Polymorphism, Genetic ; Pregnancy ; Risk Factors
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  • 60
    Publication Date: 1990-06-29
    Description: The presence of endothelin, a vasoconstrictor peptide, in the hypothalamus and posterior pituitary suggests that it also regulates neural and other nonvascular target cells. In pituitary gonadotrophs, low doses of endothelin evoked oscillations in the intracellular calcium concentration, and high doses induced a biphasic calcium response. Mobilization of intracellular calcium predominated during the spike phase of the calcium response to endothelin, whereas calcium entry through dihydropyridine-sensitive channels contributed to both the spike and plateau phases of the calcium response. Endothelin was a potent as hypothalamic gonadotropin-releasing hormone (GnRH) in stimulation of gonadotropin release in perifused pituitary cells. Endothelin bound specifically to pituitary cells with a dissociation constant of 70 picomolar, and induced rapid formation of inositol trisphosphate and diacyglycerol. Although intracellular calcium concentration and gonadotropin secretory responses to endothelin were independent to the GnRH receptor, endothelin and GnRH appeared to have a common signal transduction mechanism. These observations suggest that endothelin can act as a neuropeptide to regulate anterior pituitary function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stojilkovic, S S -- Merelli, F -- Iida, T -- Krsmanovic, L Z -- Catt, K J -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1663-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Endothelins ; Endothelium, Vascular ; Female ; Follicle Stimulating Hormone/*secretion ; Gonadotropin-Releasing Hormone/pharmacology ; Kinetics ; Luteinizing Hormone/*secretion ; Male ; Nifedipine/pharmacology ; Orchiectomy ; Peptides/metabolism/*pharmacology ; Pituitary Gland, Anterior/drug effects/*metabolism/secretion ; Rats ; Rats, Inbred Strains ; Receptors, Cell Surface/metabolism ; Receptors, Endothelin ; Reference Values
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djerassi, C -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1061-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2343313" target="_blank"〉PubMed〈/a〉
    Keywords: Biomarkers/analysis ; Estradiol/analysis ; Female ; Humans ; Menstrual Cycle/physiology ; *Natural Family Planning Methods ; Ovulation Detection/*methods ; Progesterone/analysis ; Reagent Strips
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  • 62
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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〉Holden, C -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2363048" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*therapy ; Female ; Humans ; National Institutes of Health (U.S.) ; Prognosis ; Recurrence ; Risk Factors ; United States
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-02
    Description: Estimates of the upper limits to human longevity have important policy implications that directly affect forecasts of life expectancy, active life expectancy, population aging, and social and medical programs tied to the size and health status of the elderly population. In the past, investigators have based speculations about the upper limits of human longevity on observations of past trends in mortality. Here the estimate of the upper bound is based on hypothesized reductions in current mortality rates necessary to achieve a life expectancy at birth from 80 to 120 years and an expectation of life at age 50 from 30 to 70 years. With the use of conditional probabilities of death from complete life tables for the United States, reductions in mortality required to achieve extreme longevity (that is, 80 to 120 years) were compared with those resulting from hypothetical cures for all cardiovascular diseases, ischemic heart disease, diabetes, and cancer. Results indicate that in order for life expectancy at birth to increase from present levels to what has been referred to as the average biological limit to life (age 85), mortality rates from all causes of death would need to decline at all ages by 55%, and at ages 50 and over by 60%. Given that hypothetical cures for major degenerative diseases would reduce overall mortality by 75%, it seems highly unlikely that life expectancy at birth will exceed the age of 85.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olshansky, S J -- Carnes, B A -- Cassel, C -- AG06996-01/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):634-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, IL.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237414" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Life Expectancy ; *Longevity ; Male ; Mortality ; Survival Rate ; Terminology as Topic
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  • 64
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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〉Palca, J -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1484.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360043" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*transmission ; Female ; Humans ; Male ; *Prostitution ; Substance Abuse, Intravenous/*complications
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  • 65
    Publication Date: 1990-05-04
    Description: The Drosophila Shaker gene on the X chromosome has three sister genes, Shal, Shab, and Shaw, which map to the second and third chromosomes. This extended gene family encodes voltage-gated potassium channels with widely varying kinetics (rate of macroscopic current activation and inactivation) and voltage sensitivity of steady-state inactivation. The differences in the currents of the various gene products are greater than the differences produced by alternative splicing of the Shaker gene. In Drosophila, the transient (A current) subtype of the potassium channel (Shaker and Shal) and the delayed-rectifier subtype (Shab and Shaw) are encoded by homologous genes, and there is more than one gene for each subtype of channel. Homologs of Shaker, Shal, Shab, and Shaw are present in mammals; each Drosophila potassium-channel gene may be represented as a multigene subfamily in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, A -- Covarrubias, M -- Butler, A -- Baker, K -- Pak, M -- Salkoff, L -- 1 RO1-NS24785-01/NS/NINDS NIH HHS/ -- GMO 7200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 May 4;248(4955):599-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, 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/2333511" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Chromosome Mapping ; Drosophila/*genetics ; Drosophila Proteins ; Female ; Membrane Proteins/*genetics/physiology ; Mice/*genetics ; Molecular Sequence Data ; *Multigene Family ; Oocytes/physiology ; Potassium Channels/*physiology ; Sequence Homology, Nucleic Acid ; Shab Potassium Channels ; Transcription, Genetic ; *X Chromosome ; Xenopus
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  • 66
    Publication Date: 1990-04-27
    Description: In Drosophila three maternal pattern organizing activities, the anterior, the posterior, and the terminal, establish the anterior-posterior body pattern of the embryo by initiating the spatially restricted activities of the gap class of zygotic segmentation genes. The activities of tailless (tll) and the newly identified gap gene huckebein (hkb) are specifically involved in mediating the maternal terminal information at the posterior end of the blastoderm embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weigel, D -- Jurgens, G -- Klingler, M -- Jackle, H -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universitat Munchen, Institut fur Genetik und Mikrobiologie, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2158673" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastoderm/*physiology ; Cell Differentiation ; Drosophila/embryology/*genetics ; Female ; Gene Expression ; Genes/*physiology ; Genotype ; Mutation ; Phenotype ; Protein-Tyrosine Kinases/genetics ; Receptors, Cell Surface/genetics ; Suppression, Genetic
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-07-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):117-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371558" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Diptera ; Female ; Government Agencies ; Libya ; Male ; Myiasis/*prevention & control ; *Pest Control, Biological ; Screw Worm Infection/*prevention & control ; United States
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):522.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300810" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Child ; Female ; *Government Agencies ; Humans ; Infant ; *Nutritional Physiological Phenomena ; *Public Assistance ; United States
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  • 69
    Publication Date: 1993-03-05
    Description: Fertilization depends on cell surface recognition proteins that interact and thereby mediate binding and subsequent fusion of the sperm and egg. Overlapping complementary DNA's encoding the egg plasma membrane receptor for sperm from the sea urchin Strongylocentrotus purpuratus were cloned and sequenced. Analysis of the deduced primary structure suggests that the receptor is a transmembrane protein with a short cytoplasmic domain. This domain showed no sequence similarity to known protein sequences. In contrast, the extracellular, sperm binding domain of the receptor did show sequence similarity to the heat shock protein 70 (hsp70) family of proteins. Recombinant protein representing this portion of the receptor bound to the sperm protein, binding, and also inhibited fertilization in a species-specific manner; beads coated with the protein became specifically bound to acrosome-reacted sperm. These data provide a basis for detailed investigations of molecular interactions that occur in gamete recognition and egg activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foltz, K R -- Partin, J S -- Lennarz, W J -- HD18590/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1421-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of California, Santa Barbara 93106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383878" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Female ; Fertilization ; Heat-Shock Proteins/*genetics ; Humans ; Male ; Molecular Sequence Data ; Ovum/physiology ; Receptors, Cell Surface/*genetics/metabolism ; Recombinant Proteins/metabolism ; Restriction Mapping ; Sea Urchins ; Sequence Homology, Amino Acid ; Sperm-Ovum Interactions ; Spermatozoa/cytology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1712-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8390093" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/therapeutic use ; *Acquired Immunodeficiency Syndrome/drug therapy/immunology/prevention & control ; Drug Therapy, Combination ; Female ; Humans ; Immunity, Cellular ; Male ; Sexually Transmitted Diseases/prevention & control ; Zalcitabine/therapeutic use ; Zidovudine/therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barash, D P -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):491.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Child ; Child Abuse ; Female ; Humans ; Male ; *Sexual Behavior ; Sexual Behavior, Animal ; Sociology ; *Violence
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  • 72
    Publication Date: 1993-08-27
    Description: The gene encoding alpha 6(IV) collagen, COL4A6, was identified on the human X chromosome in a head-to-head arrangement and within 452 base pairs of the alpha 5(IV) collagen gene, COL4A5. In earlier studies, intragenic deletions of COL4A5 were detected in a subset of patients with Alport syndrome (AS), a hereditary defect of basement membranes. In some families, AS cosegregates with diffuse leiomyomatosis (DL), a benign smooth muscle tumor diathesis. Here it is shown that patients with AS-DL harbor deletions that disrupt both COL4A5 and COL4A6. Thus, type IV collagen may regulate smooth muscle differentiation and morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, J -- Mochizuki, T -- Smeets, H -- Antignac, C -- Laurila, P -- de Paepe, A -- Tryggvason, K -- Reeders, S T -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1167-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06536-0812.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356449" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Differentiation ; Collagen/chemistry/*genetics ; Exons ; Female ; Fetus/metabolism ; *Gene Deletion ; Genetic Linkage ; Humans ; Leiomyoma/*genetics ; Male ; Molecular Sequence Data ; Morphogenesis ; Muscle, Smooth/cytology ; Mutation ; Nephritis, Hereditary/*genetics ; RNA, Messenger/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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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〉Lippman, M E -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):631-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vincent T. Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430312" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Factors/*therapeutic use ; Breast Neoplasms/*therapy ; Female ; Growth Substances/*therapeutic use ; Humans ; Prognosis
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  • 74
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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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  • 75
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
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  • 76
    Publication Date: 1993-06-25
    Description: CD4+ T cells play a major role in protective immunity against the blood stage of malaria, but the mechanism of protection is unclear. By adoptive transfer of cloned T cell lines, direct evidence is provided that both TH1 and TH2 subsets of CD4+ T cells can protect mice against Plasmodium chabaudi chabaudi infection. TH1 cells protect by a nitric oxide-dependent mechanism, whereas TH2 cells protect by the enhancement and accelerated production of specific immunoglobulin G1 antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor-Robinson, A W -- Phillips, R S -- Severn, A -- Moncada, S -- Liew, F Y -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Laboratories for Experimental Parasitology, University of Glasgow, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/biosynthesis ; Arginine/analogs & derivatives/pharmacology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Female ; Immunoglobulin G/*biosynthesis ; Lymphocyte Depletion ; Malaria/*immunology ; Mice ; Mice, Inbred Strains ; Nitrates/blood ; Nitric Oxide/*metabolism ; Plasmodium chabaudi/*immunology ; T-Lymphocyte Subsets/*immunology ; omega-N-Methylarginine
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  • 77
    Publication Date: 1993-07-30
    Description: Anopheles gambiae, the primary vector of human malaria in Africa, is responsible for approximately a million deaths per year, mostly of children. Despite its significance in disease transmission, this mosquito has not been studied extensively by genetic or molecular techniques. To facilitate studies on this vector, a genetic map has been developed that covers the X chromosome at an average resolution of 2 centimorgans. This map has been integrated with the chromosome banding pattern and used to localize a recessive, sex-linked mutation (white eye) to within 1 centimorgan of flanking markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, L -- Collins, F H -- Kumar, V -- Kafatos, F C -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):605-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342025" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles/*genetics ; Base Sequence ; Chromosome Banding ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Satellite/genetics ; Female ; *Genes, Insect ; Genes, Recessive ; Genetic Markers ; Insect Vectors/*genetics ; Malaria/transmission ; Male ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; *X Chromosome
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  • 78
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-07-09
    Description: Direct gene transfer into adult animals resulting in generalized or tissue-specific expression would facilitate rapid analysis of transgene effects and allow precise in vivo manipulation of biologic processes at the molecular level. A single intravenous injection of expression plasmid:cationic liposome complexes into adult mice efficiently transfected virtually all tissues. In addition to vascular endothelial cells, most of the extravascular parenchymal cells present in many tissues including the lung, spleen, lymph nodes, and bone marrow expressed the transgene without any apparent treatment-related toxicity. The transgene was still expressed in large numbers of cells in multiple tissues for at least 9 weeks after a single injection. Expression could be targeted to specific tissues and cell types, depending on the promoter element used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, N -- Liggitt, D -- Liu, Y -- Debs, R -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):209-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Institute, University of California, San Francisco 94143-0128.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7687073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bone Marrow/metabolism ; Chloramphenicol O-Acetyltransferase/genetics ; Cystic Fibrosis/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator ; Cytomegalovirus/genetics ; Female ; *Gene Expression ; Injections, Intravenous ; Liposomes ; Liver/metabolism ; Lung/metabolism ; Lung Neoplasms/genetics ; Lymphoid Tissue/metabolism ; Membrane Proteins/genetics ; Mice ; Mice, Inbred ICR ; Mice, Transgenic ; Molecular Sequence Data ; Myocardium/metabolism ; Oligodeoxyribonucleotides ; Phosphatidylethanolamines/chemistry ; Plasmids ; Quaternary Ammonium Compounds ; *Transfection
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  • 79
    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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  • 80
    Publication Date: 1993-12-17
    Description: Intracellular recordings from simple cells of the cat visual cortex were used to test linear models for the generation of selectivity for the direction of visual motion. Direction selectivity has been thought to arise in part from nonlinear processes, as suggested by previous experiments that were based on extracellular recordings of action potentials. In intracellular recordings, however, the fluctuations in membrane potential evoked by moving stimuli were accurately predicted by the linear summation of responses to stationary stimuli. Nonlinear mechanisms were not required.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jagadeesh, B -- Wheat, H S -- Ferster, D -- R01 EY04726/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1901-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Female ; Mathematics ; Membrane Potentials ; *Motion Perception ; Neurons/physiology ; *Synaptic Transmission ; Visual Cortex/*physiology
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-10-08
    Description: The amino acid at position 160 of the ligand-binding subunit, alpha 1, is an important determinant of agonist and antagonist binding to the glycine receptor. Exchange of the neighboring residues, phenylalanine at position 159 and tyrosine at position 161, increased the efficacy of amino acid agonists. Whereas wild-type alpha 1 channels expressed in Xenopus oocytes required 0.7 millimolar beta-alanine for a half-maximal response, the doubly mutated (F159Y,Y161F) alpha 1 subunit had an affinity for beta-alanine (which was more potent than glycine) that was 110-fold that of the wild type. Also, gamma-aminobutyric acid and D-serine, amino acids that do not activate wild-type alpha 1 receptors, efficiently gated the mutant channel. Thus, aromatic hydroxyl groups are crucial for ligand discrimination at inhibitory amino acid receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmieden, V -- Kuhse, J -- Betz, H -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211147" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Female ; Glycine/metabolism ; Ion Channel Gating/drug effects ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oocytes ; Receptors, GABA/chemistry/metabolism ; Receptors, Glycine/chemistry/genetics/*metabolism ; Serine/pharmacology ; Taurine/pharmacology ; Xenopus ; beta-Alanine/*metabolism/pharmacology ; gamma-Aminobutyric Acid/*metabolism/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-02-12
    Description: The analysis of the differences between two complex genomes holds promise for the discovery of infectious agents and probes useful for genetic studies. A system was developed in which subtractive and kinetic enrichment was used to purify restriction endonuclease fragments present in one population of DNA fragments but not in another. Application of this method to DNA populations of reduced complexity ("representations") resulted in the isolation of probes to viral genomes present as single copies in human DNA, and probes that detect polymorphisms between two individuals. In principle, this system, called representational difference analysis (RDA), may also be used for isolating probes linked to sites of genomic rearrangements, whether occurring spontaneously and resulting in genetic disorders or cancer, or programmed during differentiation and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lisitsyn, N -- Wigler, M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):946-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438152" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Bacteriophage lambda/genetics ; Base Sequence ; *Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; DNA, Viral ; Female ; Gene Deletion ; Genetic Diseases, Inborn/genetics ; Humans ; Male ; Molecular Sequence Data ; Neoplasms/genetics ; Nucleic Acid Hybridization/methods ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Sequence Homology, Nucleic Acid
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  • 83
    Publication Date: 1993-06-25
    Description: Female spotted hyenas exhibit male-like genitalia and dominance over males. Hyena ovarian tissues incubated in vitro produced large quantities of the steroid hormone precursor androstenedione. The activity of aromatase, which converts androstenedione to estrogen, was one-twentieth as great in hyena versus human placental homogenates. In comparison, the activity of 17 beta-hydroxysteroid dehydrogenase, which converts androstenedione to testosterone, was equal in the two homogenates. The limited aromatase activity may allow the hyena placenta to convert high circulating concentrations of androstenedione to testosterone, which results in virilization of the fetal external genitalia and possibly destruction of fetal ovarian follicles. Androstenedione production by residual ovarian stromal cells during reproductive life accounts for the epigenetic transmission of virilization in female spotted hyenas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcinkaya, T M -- Siiteri, P K -- Vigne, J L -- Licht, P -- Pavgi, S -- Frank, L G -- Glickman, S E -- CA-39825/CA/NCI NIH HHS/ -- MH-39917/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1929-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics, Gynecology, University of California School of Medicine, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391165" target="_blank"〉PubMed〈/a〉
    Keywords: 17-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Aromatase/*metabolism ; Carnivora/embryology/*metabolism ; Corpus Luteum/metabolism ; Estradiol/biosynthesis ; Female ; Humans ; In Vitro Techniques ; Luteinizing Hormone/pharmacology ; Male ; Ovary/*metabolism ; Placenta/enzymology/*metabolism ; Pregnancy ; Progesterone/biosynthesis ; *Sex Differentiation ; Testosterone/*biosynthesis
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-07-16
    Description: Fertilization is accompanied by a transient increase in the concentration of intracellular Ca2+, which serves as a signal for initiating development. Some of the Ca2+ appears to be released from intracellular stores by the binding of inositol trisphosphate (IP3) to its receptor. However, in sea urchin eggs, other mechanisms appear to participate. Cyclic adenosine diphosphate--ribose (cADPR), a naturally occurring metabolite of nicotinamide adenine dinucleotide, is as potent as IP3 in mobilizing Ca2+ in sea urchin eggs. Experiments with antagonists of the cADPR and IP3 receptors revealed that both Ca2+ mobilizing systems were activated during fertilization. Blockage of either of the systems alone was not sufficient to prevent the sperm-induced Ca2+ transient. This study provides direct evidence for a physiological role of cADPR in the Ca2+ signaling process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, H C -- Aarhus, R -- Walseth, T F -- HD17484/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Minnesota, Minneapolis 55455.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8392749" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate Ribose/analogs & derivatives/pharmacology ; Animals ; Calcium/*metabolism ; *Calcium Channels ; Cyclic ADP-Ribose ; Cyclic AMP/analogs & derivatives/pharmacology ; Female ; *Fertilization ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/pharmacology ; Inositol 1,4,5-Trisphosphate Receptors ; Ovum/*metabolism ; Receptors, Cell Surface/*physiology ; *Receptors, Cytoplasmic and Nuclear ; Sea Urchins ; Signal Transduction
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  • 85
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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〉Morell, V -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):683-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342036" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Australia ; Contraception, Immunologic/*veterinary ; Ecology ; Female ; *Foxes/microbiology ; *Genetic Engineering ; Male ; Myxoma virus/genetics ; Pest Control, Biological/*methods ; *Rabbits/microbiology ; Viruses/*genetics
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  • 86
    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1722-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511575" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Female ; *Genes, Recessive ; Genetic Diseases, Inborn ; Humans ; Male ; Monoamine Oxidase/deficiency/*genetics ; Mutation ; Pedigree ; *X Chromosome
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  • 88
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, L -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):452.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424165" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Bioethics ; Brain Neoplasms/*therapy ; DNA, Recombinant ; Death ; *Ethical Review ; Federal Government ; Female ; *Genetic Therapy ; *Government Regulation ; Humans ; Middle Aged ; National Institutes of Health (U.S.) ; *Therapeutic Human Experimentation ; United States
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, L -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):172.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421780" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Ethical Review ; Federal Government ; Female ; Genetic Therapy/*legislation & jurisprudence ; *Government Regulation ; Humans ; Interleukin-2/*genetics ; Middle Aged ; National Institutes of Health (U.S.) ; Neoplasms/*therapy ; Patient Selection ; Research Subjects ; United States
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friend, S H -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):774-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetics, Massachusetts General Hospital Cancer Center, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Cyprinodontiformes/*genetics ; Female ; Fish Diseases/*genetics ; Genes, Tumor Suppressor ; *Genetic Predisposition to Disease ; Male ; Melanoma/genetics/*veterinary ; Models, Genetic ; Neoplasms/*genetics ; Proto-Oncogenes
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frisch, R E -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1103-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356441" target="_blank"〉PubMed〈/a〉
    Keywords: *Adipose Tissue ; Body Composition ; Body Weight ; Female ; Humans ; *Menarche ; *Menstrual Cycle
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  • 93
    Publication Date: 1993-08-27
    Description: Better characterization of human immunodeficiency virus-type 1 (HIV-1) in patients with primary infection has important implications for the development of an acquired immunodeficiency syndrome (AIDS) vaccine because vaccine strategies should target viral isolates with the properties of transmitted viruses. In five HIV-1 seroconverters, the viral phenotype was found to be uniformly macrophage-tropic and non-syncytium-inducing. Furthermore, the viruses were genotypically homogeneous within each patient, but a common signature sequence was not discernible among transmitted viruses. In the two cases where the sexual partners were also studied, the sequences of the transmitted viruses matched best with minor variants in the blood of the transmitters. There was also a stronger pressure to conserve sequences in gp120 than in gp41, nef, and p17, suggesting that a selective mechanism is involved in transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, T -- Mo, H -- Wang, N -- Nam, D S -- Cao, Y -- Koup, R A -- Ho, D D -- AI24030/AI/NIAID NIH HHS/ -- AI25541/AI/NIAID NIH HHS/ -- AI27742/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Female ; Gene Products, gag/chemistry/genetics ; Genes, Viral ; Genotype ; Giant Cells/physiology ; HIV Antigens/chemistry/genetics ; HIV Envelope Protein gp120/chemistry/*genetics ; HIV Envelope Protein gp41/chemistry/genetics ; HIV Infections/*microbiology/transmission ; HIV Seropositivity/microbiology ; HIV-1/chemistry/*genetics/*physiology ; Humans ; Macrophages ; Male ; Molecular Sequence Data ; Phenotype ; Sequence Alignment ; Sexual Partners ; *Viral Proteins ; Virus Replication ; gag Gene Products, Human Immunodeficiency Virus
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  • 94
    Publication Date: 1993-05-07
    Description: A predisposition to colorectal cancer is shown to be linked to markers on chromosome 2 in some families. Molecular features of "familial" cancers were compared with those of sporadic colon cancers. Neither the familial nor sporadic cancers showed loss of heterozygosity for chromosome 2 markers, and the incidence of mutations in KRAS, P53, and APC was similar in the two groups of tumors. Most of the familial cancers, however, had widespread alterations in short repeated DNA sequences, suggesting that numerous replication errors had occurred during tumor development. Thirteen percent of sporadic cancers had identical abnormalities and these cancers shared biologic properties with the familial cases. These data suggest a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aaltonen, L A -- Peltomaki, P -- Leach, F S -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Powell, S M -- Jen, J -- Hamilton, S R -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):812-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484121" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Female ; Genetic Markers ; Humans ; Lod Score ; Male ; Mutation ; Pedigree ; Polymorphism, Genetic ; Rectal Neoplasms/genetics ; Repetitive Sequences, Nucleic Acid
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):942-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco 94143-0444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8094900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; Female ; Gene Deletion ; Humans ; Male ; Nucleic Acid Hybridization/*methods ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length
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  • 96
    Publication Date: 1993-02-19
    Description: The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCR beta and TCR alpha beta transgenic NOD mice the beta chain transgene was expressed by 〉 98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V beta genes. Nonetheless, NOD animals transgenic for TCR beta and TCR alpha beta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipes, M A -- Rosenzweig, A -- Tan, K N -- Tanigawa, G -- Ladd, D -- Seidman, J G -- Eisenbarth, G S -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267690" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 2/genetics/immunology/*physiopathology ; Female ; Gene Rearrangement, T-Lymphocyte ; Islets of Langerhans/immunology/pathology ; Male ; Mice ; Mice, Inbred NOD/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Pancreatic Diseases/genetics/immunology/pathology ; Polymerase Chain Reaction/methods ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; T-Lymphocytes/*immunology/pathology
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  • 97
    Publication Date: 1993-08-13
    Description: The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corder, E H -- Saunders, A M -- Strittmatter, W J -- Schmechel, D E -- Gaskell, P C -- Small, G W -- Roses, A D -- Haines, J L -- Pericak-Vance, M A -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346443" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; *Alleles ; Alzheimer Disease/*genetics/metabolism/mortality ; Amyloid beta-Peptides/metabolism ; Apolipoprotein E4 ; Apolipoproteins E/*genetics/physiology ; Female ; *Gene Frequency ; Genotype ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Risk Factors ; Survival Rate
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  • 98
    Publication Date: 1993-07-16
    Description: Propagating Ca2+ waves are a characteristic feature of Ca(2+)-linked signal transduction pathways. Intracellular Ca2+ waves are formed by regenerative stimulation of Ca2+ release from intracellular stores by Ca2+ itself. Mechanisms that rely on either inositol trisphosphate or ryanodine receptor channels have been proposed to account for Ca2+ waves in various cell types. Both channel types contributed to the Ca2+ wave during fertilization of sea urchin eggs. Alternative mechanisms of Ca2+ release imply redundancy but may also allow for modulation and diversity in the generation of Ca2+ waves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galione, A -- McDougall, A -- Busa, W B -- Willmott, N -- Gillot, I -- Whitaker, M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):348-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Oxford University, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8392748" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate Ribose/analogs & derivatives/pharmacology ; Adenosine Triphosphate/metabolism ; Animals ; Caffeine/pharmacology ; Calcium/*metabolism/pharmacology ; *Calcium Channels ; Cyclic ADP-Ribose ; Female ; *Fertilization ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/pharmacology ; Inositol 1,4,5-Trisphosphate Receptors ; Muscle Proteins/drug effects/*physiology ; Ovum/drug effects/*metabolism ; Receptors, Cell Surface/drug effects/*physiology ; *Receptors, Cytoplasmic and Nuclear ; Ryanodine/pharmacology ; Ryanodine Receptor Calcium Release Channel ; Sea Urchins ; Signal Transduction ; Thimerosal/pharmacology ; Xenopus
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  • 99
    Publication Date: 1993-01-15
    Description: A variety of tumors are potentially immunogenic but do not stimulate an effective anti-tumor immune response in vivo. Tumors may be capable of delivering antigen-specific signals to T cells, but may not deliver the costimulatory signals necessary for full activation of T cells. Expression of the costimulatory ligand B7 on melanoma cells was found to induce the rejection of a murine melanoma in vivo. This rejection was mediated by CD8+ T cells; CD4+ T cells were not required. These results suggest that B7 expression renders tumor cells capable of effective antigen presentation, leading to their eradication in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Townsend, S E -- Allison, J P -- CA57986/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):368-70.〈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/7678351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD80 ; Antigens, Surface/genetics/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cross Reactions ; Female ; Gene Expression Regulation ; Genetic Vectors ; Ligands ; *Lymphocyte Activation ; Melanoma/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; T-Lymphocytes, Regulatory/*immunology ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barlow, D P -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):309-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/genetics/*metabolism ; *Dosage Compensation, Genetic ; Embryo, Mammalian/metabolism ; Fathers ; Female ; *Gene Expression Regulation ; Insulin-Like Growth Factor II/genetics ; Male ; Methylation ; Mice ; Models, Genetic ; Mothers ; Oocytes/metabolism ; Receptor, IGF Type 2/genetics ; Spermatozoa/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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