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  • United States  (133)
  • Cells, Cultured  (106)
  • American Association for the Advancement of Science (AAAS)  (239)
  • Nature Publishing Group
  • 1990-1994  (162)
  • 1980-1984  (77)
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  • 1935-1939
  • 1925-1929
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  • American Association for the Advancement of Science (AAAS)  (239)
  • Nature Publishing Group
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  • 1
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    A new arbovirus from Aedes albopictus, an Asian mosquito established in the United States (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Ten strains of a new arbovirus belonging to the Bunyamwera group (Bunyaviridae) were recovered from field-collected Aedes albopictus mosquitoes in Potosi, Missouri. This evidence indicates that this species may serve as an arbovirus vector in the United States. The urban-suburban distribution, aggressive biting behavior, and broad viral susceptibility of Ae. albopictus may lead to the transmission of viruses of known public health importance and perhaps of viruses hitherto not transmitted to humans because of the feeding pattern of their usual vectors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Francy, D B -- Karabatsos, N -- Wesson, D M -- Moore, C G Jr -- Lazuick, J S -- Niebylski, M L -- Tsai, T F -- Craig, G B Jr -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1738-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Vector-Borne Infectious Diseases, Centers for Disease Control, U.S. Public Health Service, Fort Collins, CO 80522.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270489" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*microbiology ; Animals ; Arboviruses/*isolation & purification ; Asia ; Humans ; Insect Vectors ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Smokers: black and white (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Selective activation of the B natriuretic peptide receptor by C-type natriuretic peptide (CNP) (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-05
    Description: The natriuretic peptides are hormones that can stimulate natriuretic, diuretic, and vasorelaxant activity in vivo, presumably through the activation of two known cell surface receptor guanylyl cyclases (ANPR-A and ANPR-B). Although atrial natriuretic peptide (ANP) and, to a lesser extent, brain natriuretic peptide (BNP) are efficient activators of the ANPR-A guanylyl cyclase, neither hormone can significantly stimulate ANPR-B. A member of this hormone family, C-type natriuretic peptide (CNP), potently and selectively activated the human ANPR-B guanylyl cyclase. CNP does not increase guanosine 3',5'-monophosphate accumulation in cells expressing human ANPR-A. The affinity of CNP for ANPR-B is 50- or 500-fold higher than ANP or BNP, respectively. This ligand-receptor pair may be involved in the regulation of fluid homeostasis by the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, K J -- Lowe, D G -- Bennett, G L -- Minamino, N -- Kangawa, K -- Matsuo, H -- Goeddel, D V -- New York, N.Y. -- Science. 1991 Apr 5;252(5002):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/*physiology ; Cells, Cultured ; Cercopithecus aethiops ; Cloning, Molecular ; Dose-Response Relationship, Drug ; Guanylate Cyclase/metabolism ; Humans ; Natriuretic Peptide, Brain ; Natriuretic Peptide, C-Type ; Nerve Tissue Proteins/*pharmacology ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Recombinant Proteins ; Signal Transduction
    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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  • 4
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    Rel-associated pp40: an inhibitor of the rel family of transcription factors (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-23
    Description: The Rel-associated protein pp40 is functionally related to I kappa B, an inhibitor of the transcription factor NF-kappa B. Purified pp40 inhibits the DNA binding activity of the NF-kappa B protein complex (p50:p65 heterodimers), p50:c-Rel heteromers, and c-Rel homodimers. The sequence of the complementary DNA encoding pp40 revealed similarity to the gene encoding MAD-3, a protein with mammalian I kappa B-like activity. Protein sequencing of I kappa B purified from rabbit lung confirmed that MAD-3 encodes a protein similar to I kappa B. The sequence similarity between MAD-3 and pp40 includes a casein kinase II and consensus tyrosine phosphorylation site, as well as five repeats of a sequence found in the human erythrocyte protein ankyrin. These results suggest that rel-related transcription factors, which are capable of cytosolic to nuclear translocation, may be held in the cytosol by interaction with related cytoplasmic anchor molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, N -- Ghosh, S -- Simmons, D L -- Tempst, P -- Liou, H C -- Baltimore, D -- Bose, H R Jr -- CA09583/CA/NCI NIH HHS/ -- CA2616/CA/NCI NIH HHS/ -- CA33192/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1891714" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Chick Embryo ; Cloning, Molecular ; DNA Probes ; Molecular Sequence Data ; NF-kappa B/*antagonists & inhibitors ; Oligonucleotide Probes ; Oncogene Proteins v-rel ; Open Reading Frames ; Phosphoproteins/*genetics/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors ; RNA, Messenger/genetics ; Retroviridae Proteins, Oncogenic/*antagonists & inhibitors ; Sequence Homology, Nucleic Acid ; Transcription Factors/*antagonists & inhibitors
    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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  • 5
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    The readers' NIH (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, D D -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):529.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411549" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Government/*methods ; National Institutes of Health (U.S.)/*economics ; Research Design ; *Research Support as Topic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Activation-induced ubiquitination of the T cell antigen receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: The zeta subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta molecules were modified, and at least one other TCR subunit, CD3 delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cenciarelli, C -- Hou, D -- Hsu, K C -- Rellahan, B L -- Wiest, D L -- Smith, H T -- Fried, V A -- Weissman, A M -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology/metabolism ; Cells, Cultured ; Hybridomas/immunology ; Lymphocyte Activation/*physiology ; Macromolecular Substances ; Mice ; Mice, Inbred C57BL ; Molecular Weight ; *Protein Processing, Post-Translational ; Receptors, Antigen, T-Cell/immunology/isolation & purification/*metabolism ; Spleen/immunology ; T-Lymphocytes/*immunology ; Ubiquitins/isolation & purification/*metabolism
    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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  • 7
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
    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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  • 8
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    Biodiversity entreaty (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tobin, J E -- Goldburg, R -- Hopkins, D D -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):13-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211119" target="_blank"〉PubMed〈/a〉
    Keywords: *Biotechnology ; *Conservation of Natural Resources ; Developing Countries ; *Genetic Variation ; *International Cooperation ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Neuroprotective effects of glutamate antagonists and extracellular acidity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Glutamate antagonists protect neurons from hypoxic injury both in vivo and in vitro, but in vitro studies have not been done under the acidic conditions typical of hypoxia-ischemia in vivo. Consistent with glutamate receptor antagonism, extracellular acidity reduced neuronal death in murine cortical cultures that were deprived of oxygen and glucose. Under these acid conditions, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate antagonists further reduced neuronal death, such that some neurons tolerated prolonged oxygen and glucose deprivation almost as well as did astrocytes. Neuroprotection induced by this combination exceeded that induced by glutamate antagonists alone, suggesting that extracellular acidity has beneficial effects beyond the attenuation of ionotropic glutamate receptor activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaku, D A -- Giffard, R G -- Choi, D W -- NS 01425/NS/NINDS NIH HHS/ -- NS 26907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1516-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cerebral Cortex/cytology ; *Excitatory Amino Acid Antagonists ; Extracellular Space/*metabolism ; Glucose/deficiency ; *Hydrogen-Ion Concentration ; L-Lactate Dehydrogenase/metabolism ; Mice ; Nerve Degeneration/drug effects ; Neurons/*drug effects/enzymology ; Receptors, AMPA ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
    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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  • 10
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    Proliferation of human smooth muscle cells promoted by lipoprotein(a) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Elevated blood concentrations of lipoprotein(a) [Lp(a)] and its constituent, apolipoprotein(a) [apo(a)], constitute a major risk factor for atherosclerosis, but their physiological activities remain obscure. Lp(a) and purified apo(a) stimulated the growth of human smooth muscle cells in culture. This effect resulted from inhibition of plasminogen activation, and consequently the activation by plasmin of latent transforming growth factor-beta, which is an inhibitor of smooth muscle cell growth. Because smooth muscle proliferation is one of the hallmarks of atherosclerotic lesions, these results point to a plausible mechanism for the atherogenic activity of Lp(a).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grainger, D J -- Kirschenlohr, H L -- Metcalfe, J C -- Weissberg, P L -- Wade, D P -- Lawn, R M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/physiology ; Apoprotein(a) ; Cell Division/drug effects/physiology ; Cells, Cultured ; Fibrinolysin/physiology ; Humans ; Lipoprotein(a)/*physiology ; Muscle, Smooth, Vascular/*cytology/metabolism ; Plasminogen Activators/metabolism ; Rats ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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