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  • Articles  (229)
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  • Articles  (229)
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  • American Association for the Advancement of Science (AAAS)  (229)
  • American Association of Petroleum Geologists (AAPG)
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  • 101
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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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  • 102
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
    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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  • 103
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    Developmental regulation of neural response to FGF-1 and FGF-2 by heparan sulfate proteoglycan (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Murine neural precursor cells and cell lines derived from them are stimulated by members of the heparin-binding fibroblast growth factor (FGF) family. The activity of FGF is regulated by heparan sulfate proteoglycans (HSPGs), and this interaction is an essential prerequisite for the binding of growth factor to the signal transducing receptors. Messenger RNA for FGF-2 was detectable in the neuroepithelium at embryonic day 9, and the HSPGs produced by these cells at this time preferentially bound FGF-2. However, at embryonic day 11, when messenger RNA for FGF-1 was first detectable, there was a switch in the binding specificity of the HSPG to FGF-1. Thus, a single species of HSPG undergoes a rapid, tightly controlled change in growth factor-binding specificity concomitant with the temporal expression of the FGFs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nurcombe, V -- Ford, M D -- Wildschut, J A -- Bartlett, P F -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Culture Media, Conditioned ; Epithelium/chemistry/embryology ; Fibroblast Growth Factor 1/genetics/*pharmacology ; Fibroblast Growth Factor 2/genetics/*pharmacology ; Gene Expression ; Gestational Age ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/*pharmacology ; Mice ; Molecular Weight ; Nervous System/chemistry/*embryology/metabolism ; Neurons/cytology ; Polysaccharide-Lyases/metabolism ; Proteoglycans/*pharmacology ; RNA, Messenger/analysis ; Signal Transduction/physiology ; Stem Cells/cytology
    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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  • 104
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    AIDS theories (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, T -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418488" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*transmission ; Animals ; Cells, Cultured ; *Hiv-1 ; Haplorhini ; Humans ; Kidney ; Male
    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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  • 105
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    Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, T M -- Arriza, J L -- Jaworsky, D E -- Borisy, F F -- Attramadal, H -- Lefkowitz, R J -- Ronnett, G V -- NS 01578-01/NS/NINDS NIH HHS/ -- NS-02131/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8381559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*metabolism ; *Arrestins ; Cells, Cultured ; Cyclic AMP/metabolism ; *Cyclic AMP-Dependent Protein Kinases ; Cytosol/metabolism ; Dendrites/physiology ; Eye Proteins/*metabolism ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Proteins/*metabolism ; Isoenzymes/metabolism ; Male ; Mechanoreceptors/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Bulb/*physiology ; Protein Kinases/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; *Smell ; Testis/physiology ; Turbinates/*physiology ; beta-Adrenergic Receptor Kinases
    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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  • 106
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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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  • 107
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    A Ca-dependent early step in the release of catecholamines from adrenal chromaffin cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: Intense stimuli, such as trains of depolarizing pulses or the caffeine-induced release of calcium from intracellular stores, readily depress the secretory response in neuroendocrine cells. Secretory responses are restored by rest periods of minutes in duration. This recovery was accelerated when the concentration of cytosolic calcium was moderately increased and probably resulted from calcium-dependent replenishment of a pool of release-ready granules. Continuously increased concentrations of calcium led the over-filling of such a pool. Subsequently, secretory responses to stronger calcium stimuli were augmented. Hormone-induced calcium transients with a plateau phase of increased concentration of calcium may enhance the secretory response in this way.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Ruden, L -- Neher, E -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1061-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane Biophysics, Max-Planck-Institut fur biophysikalische Chemie, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235626" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/cytology/drug effects/metabolism/*secretion ; Animals ; Bradykinin/pharmacology ; Caffeine/pharmacology ; Calcium/*metabolism ; Catecholamines/metabolism/*secretion ; Cattle ; Cells, Cultured ; Chromaffin Granules/drug effects/*secretion ; Electric Conductivity ; Histamine ; Membrane Potentials ; Models, Biological ; Nystatin/pharmacology
    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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  • 108
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    Translocation of repetitive RNA sequences with the germ plasm in Xenopus oocytes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Xlsirts are a family of interspersed repeat RNAs from Xenopus laevis that contain from 3 to 13 repeat units (each 79 to 81 nucleotides long) flanked by unique sequences. They are homologous to the mammalian Xist gene that is involved in X chromosome inactivation. Xlsirt RNA appears first in the mitochondrial cloud (Balbiani body) in stage 2 oocytes and is then translocated as island-like structures to the vegetal cortex at early stage 3 coincident with the localization of the germ plasm. Exogenous Xlsirt RNA injected into oocytes translocates to the location of the endogenous RNA at that particular stage. The Xlsirt RNA repeat sequences are required for translocation and can cause the translocation of heterologous unique RNAs to the vegetal cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Spohr, G -- Etkin, L D -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1712-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Female ; In Situ Hybridization ; Molecular Sequence Data ; Nucleic Acid Conformation ; Oocytes/*metabolism ; Oogenesis ; RNA/chemistry/*metabolism ; *Repetitive Sequences, Nucleic Acid ; Xenopus laevis
    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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  • 109
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    Switch of CD8 T cells to noncytolytic CD8-CD4- cells that make TH2 cytokines and help B cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: CD8+ T cells are a major defense against viral infections and intracellular parasites. Their production of interferon-gamma (IFN-gamma) and their cytolytic activity are key elements in the immune response to these pathogens. Mature mouse CD8+ T cells that were activated in the presence of interleukin-4 (IL-4) developed into a CD8-CD4- population that was not cytolytic and did not produce IFN-gamma. However, these CD8- cells produced large amounts of IL-4, IL-5, and IL-10 and helped activate resting B cells. Thus, CD8 effector functions are potentially diverse and could be exploited by infectious agents that switch off host protective cytolytic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erard, F -- Wild, M T -- Garcia-Sanz, J A -- Le Gros, G -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Allergy/Immunology, Ciba-Geigy Ltd., Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Cytotoxicity, Immunologic ; Immunophenotyping ; Interleukin-10/biosynthesis ; Interleukin-2/pharmacology ; Interleukin-4/biosynthesis/pharmacology ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Ionomycin/pharmacology ; *Lymphocyte Activation ; Membrane Glycoproteins/genetics ; Mice ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Tetradecanoylphorbol Acetate/pharmacology
    Print ISSN: 0036-8075
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  • 110
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    Potential role of human cytomegalovirus and p53 interaction in coronary restenosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: A subset of patients who have undergone coronary angioplasty develop restenosis, a vessel renarrowing characterized by excessive proliferation of smooth muscle cells (SMCs). Of 60 human restenosis lesions examined, 23 (38 percent) were found to have accumulated high amounts of the tumor suppressor protein p53, and this correlated with the presence of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the lesions expressed HCMV protein IE84 and high amounts of p53. HCMV infection of cultured SMCs enhanced p53 accumulation, which correlated temporally with IE84 expression. IE84 also bound to p53 and abolished its ability to transcriptionally activate a reporter gene. Thus, HCMV, and IE84-mediated inhibition of p53 function, may contribute to the development of restenosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speir, E -- Modali, R -- Huang, E S -- Leon, M B -- Shawl, F -- Finkel, T -- Epstein, S E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023160" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Angioplasty, Balloon ; Antigens, Viral/*metabolism ; Atherectomy, Coronary ; Base Sequence ; Cells, Cultured ; Coronary Disease/*etiology/pathology/therapy ; Coronary Vessels/cytology/metabolism/microbiology ; Cytomegalovirus/*physiology ; Genes, p53 ; Humans ; Immediate-Early Proteins/*metabolism ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/metabolism/microbiology ; Recurrence ; Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism
    Print ISSN: 0036-8075
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  • 111
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    Cell suicide: by ICE, not fire (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
    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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  • 112
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    A molecular determinant for submillisecond desensitization in glutamate receptors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The decay of excitatory postsynaptic currents in central neurons mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors is likely to be shaped either by receptor desensitization or by offset after removal of glutamate from the synaptic cleft. Native AMPA receptors show desensitization time constants of 1 to about 10 milliseconds, but the underlying molecular determinants of these large differences are unknown. Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower. Cerebellar granule cells switch their expression of GluR-D splice variants from mostly flip forms in early stages to predominantly flop forms in the adult rat brain. These findings suggest that rapid desensitization of AMPA receptors can be regulated by the expression and alternative splicing of GluR-D gene transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosbacher, J -- Schoepfer, R -- Monyer, H -- Burnashev, N -- Seeburg, P H -- Ruppersberg, J P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1059-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973663" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cloning, Molecular ; Glutamic Acid/*pharmacology ; In Situ Hybridization ; Oocytes ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/drug effects/genetics/*physiology ; Recombinant Proteins ; Synaptic Transmission ; Xenopus laevis
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  • 113
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Visualization of quantal synaptic transmission by dendritic calcium imaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: As changes in synaptic strength are thought to be critical for learning and memory, it would be useful to monitor the activity of individual identified synapses on mammalian central neurons. Calcium imaging of cortical neurons grown in primary culture was used to visualize the activation of individual postsynaptic elements by miniature excitatory synaptic currents elicited by spontaneous quantal release. This approach revealed that the probability of spontaneous activity differed among synapses on the same dendrite. Furthermore, synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, T H -- Baraban, J M -- Wier, W G -- Blatter, L A -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):529-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7904774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cerebral Cortex ; Dendrites/*metabolism ; Glutamates/pharmacology ; Glutamic Acid ; Kinetics ; Microelectrodes ; Neuronal Plasticity ; Neurons/*physiology ; Phorbol Esters/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Direct signaling from astrocytes to neurons in cultures of mammalian brain cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, M -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/*metabolism ; Calcium/*metabolism ; Cell Communication ; Cells, Cultured ; Electric Stimulation ; Excitatory Amino Acid Antagonists ; Gap Junctions/physiology ; Kynurenic Acid/pharmacology ; Neurons/drug effects/*metabolism ; Nifedipine/pharmacology ; Octanols/pharmacology ; Prosencephalon/*cytology/embryology ; Rats ; *Signal Transduction ; Synapses/metabolism ; Tetrodotoxin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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    Regulation of melanin biosynthesis in the human epidermis by tetrahydrobiopterin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The participation of (6R) 5,6,7,8-tetrahydrobiopterin (6-BH4) in regulating the tyrosine supply for melanin biosynthesis was investigated by the examination of human keratinocytes, melanocytes, and epidermal suction blisters from normal human skin and from patients with the depigmentation disorder vitiligo. Cells, as well as total epidermis, contained high phenylalanine hydroxylase activities and also displayed the capacity to synthesize and recycle 6-BH4, the essential cofactor for this enzyme. In vitiligo, 4a-hydroxy-BH4 dehydratase activity was extremely low or absent, yielding an accumulation of the nonenzymatic by-product 7-tetrahydrobiopterin (7-BH4) at concentrations up to 8 x 10(-6) M in the epidermis. This by-product is a potent competitive inhibitor in the phenylalanine hydroxylase reaction with an inhibition constant of 10(-6) M. Thus, 6-BH4 seems to control melanin biosynthesis in the human epidermis, whereas 7-BH4 may initiate depigmentation in patients with vitiligo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schallreuter, K U -- Wood, J M -- Pittelkow, M R -- Gutlich, M -- Lemke, K R -- Rodl, W -- Swanson, N N -- Hitzemann, K -- Ziegler, I -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1444-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128228" target="_blank"〉PubMed〈/a〉
    Keywords: Biopterin/*analogs & derivatives/biosynthesis/metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Epidermis/*metabolism ; GTP Cyclohydrolase/metabolism ; Humans ; Keratinocytes/metabolism ; Melanins/*biosynthesis ; Melanocytes/metabolism ; Phenylalanine Hydroxylase/antagonists & inhibitors/metabolism ; Tyrosine/biosynthesis ; Vitiligo/*metabolism
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    Padlock probes: circularizing oligonucleotides for localized DNA detection (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Nucleotide sequence information derived from DNA segments of the human and other genomes is accumulating rapidly. However, it frequently proves difficult to use such short DNA segments to identify clones in genomic libraries or fragments in blots of the whole genome or for in situ analysis of chromosomes. Oligonucleotide probes, consisting of two target-complementary segments, connected by a linker sequence, were designed. Upon recognition of the specific nucleic acid molecule the ends of the probes were joined through the action of a ligase, creating circular DNA molecules catenated to the target sequence. These probes thus provide highly specific detection with minimal background.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsson, M -- Malmgren, H -- Samiotaki, M -- Kwiatkowski, M -- Chowdhary, B P -- Landegren, U -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2085-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beijer Laboratory, Department of Medical Genetics, Biomedical Center, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522346" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cells, Cultured ; Chromosomes, Human, Pair 12 ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA/*analysis ; DNA, Circular/*analysis ; Genetic Vectors ; Humans ; In Situ Hybridization ; Lymphocytes ; Membrane Proteins/genetics ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Oligonucleotide Probes/chemistry ; Repetitive Sequences, Nucleic Acid ; Templates, Genetic
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    Cloning of a T cell growth factor that interacts with the beta chain of the interleukin-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: A cytokine was identified that stimulated the proliferation of T lymphocytes, and a complementary DNA clone encoding this new T cell growth factor was isolated. The cytokine, designated interleukin-15 (IL-15), is produced by a wide variety of cells and tissues and shares many biological properties with IL-2. Monoclonal antibodies to the beta chain of the IL-2 receptor inhibited the biological activity of IL-15, and IL-15 competed for binding with IL-2, indicating that IL-15 uses components of the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Eisenman, J -- Shanebeck, K -- Rauch, C -- Srinivasan, S -- Fung, V -- Beers, C -- Richardson, J -- Schoenborn, M A -- Ahdieh, M -- New York, N.Y. -- Science. 1994 May 13;264(5161):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Research and Development Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; *Cloning, Molecular ; Haplorhini ; Humans ; Interleukin-15 ; Interleukin-2/immunology/metabolism/pharmacology ; Interleukins/chemistry/*genetics/metabolism/pharmacology ; Killer Cells, Lymphokine-Activated/immunology ; Leukocytes, Mononuclear/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Molecular Sequence Data ; Protein Structure, Secondary ; Receptors, Interleukin-2/immunology/*metabolism ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology
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    T cells and suppression in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, B -- Kaye, J -- Lo, D -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):464-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Clonal Anergy ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; T-Lymphocytes, Regulatory/*immunology
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    Noradrenergic regulation of cholinergic differentiation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: When the sympathetic nerves that innervate rat sweat glands reach their targets, they are induced to switch from using norepinephrine as their neurotransmitter to acetylcholine. Catecholamines (such as norepinephrine) released by nerves growing to the sweat gland induce this phenotypic conversion by stimulating production of a cholinergic differentiation factor [sweat gland factor (SGF)] by gland cells. Here, culture of gland cells with sympathetic, but not sensory, neurons induced SGF production. Blockage of alpha 1- or beta-adrenergic receptors prevented acquisition of the cholinergic phenotype in sympathetic neurons co-cultured with sweat glands, and sweat glands from sympathectomized animals lacked SGF. Thus, reciprocal instructive interactions, mediated in part by small molecule neurotransmitters, direct the development of this synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habecker, B A -- Landis, S C -- NS-023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1602-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4975.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Glycoproteins/*biosynthesis ; Molecular Sequence Data ; Neuregulins ; Neurons/cytology/physiology ; Neurons, Afferent/cytology/physiology ; Parasympathetic Nervous System/cytology/*physiology ; Phenotype ; Rats ; Receptors, Adrenergic/*physiology ; Sweat Glands/cytology/*innervation/metabolism ; Sympathectomy ; Sympathetic Nervous System/cytology/*physiology
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    Glia: the brain's other cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):970-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973679" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/physiology ; Brain/*cytology/physiology ; Calcium/metabolism ; Cell Communication ; Cells, Cultured ; Humans ; Nerve Growth Factors/biosynthesis ; Neuroglia/*physiology ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Synapses/metabolism
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    Genetic engineering. Safety concerns halt U.K. study (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):748.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303287" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Advisory Committees ; Cells, Cultured ; *Containment of Biohazards ; *Genetic Engineering ; *Government Regulation ; Great Britain ; Humans ; *Oncogenes ; Simian virus 40/*genetics
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    Activity-dependent changes in the intrinsic properties of cultured neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Learning and memory arise through activity-dependent modifications of neural circuits. Although the activity dependence of synaptic efficacy has been studied extensively, less is known about how activity shapes the intrinsic electrical properties of neurons. Lobster stomatogastric ganglion neurons fire in bursts when receiving synaptic and modulatory input but fire tonically when pharmacologically isolated. Long-term isolation in culture changed their intrinsic activity from tonic firing to burst firing. Rhythmic stimulation reversed this transition through a mechanism that was mediated by a rise in intracellular calcium concentration. These data suggest that neurons regulate their conductances to maintain stable activity patterns and that the intrinsic properties of a neuron depend on its recent history of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turrigiano, G -- Abbott, L F -- Marder, E -- MH46742/MH/NIMH NIH HHS/ -- NS17813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 13;264(5161):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cells, Cultured ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Electrophysiology ; Ganglia, Invertebrate/cytology ; Membrane Potentials ; Nephropidae ; Neurites/physiology ; Neurons/cytology/*physiology ; Synapses/physiology
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    CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: A proportion of developing oligodendrocytes undergo natural cell death by apoptosis, and mature oligodendrocytes die, either by apoptosis or necrosis, in response to injurious signals such as cytotoxic cytokines and complement. Ciliary neurotrophic factor (CNTF), a trophic factor found in astrocytes in the central nervous system (CNS), promoted the survival and maturation of cultured oligodendrocytes. This trophic factor also protected oligodendrocytes from death induced by tumor necrosis factors (apoptosis) but not against complement (necrosis). These results suggest that CNTF functions in the survival of oligodendrocytes during development and may lead to therapeutic approaches for degenerative diseases of the CNS that involve oligodendrocyte destruction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Louis, J C -- Magal, E -- Takayama, S -- Varon, S -- NS16349/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430320" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology ; Cell Death/*drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Central Nervous System/physiology ; Ciliary Neurotrophic Factor ; Dose-Response Relationship, Drug ; Humans ; Kinetics ; Lymphotoxin-alpha/*pharmacology ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/*pharmacology ; Oligodendroglia/cytology/drug effects/*physiology ; Recombinant Proteins/pharmacology ; Time Factors ; Tumor Necrosis Factor-alpha/*pharmacology
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    Retinal degeneration in choroideremia: deficiency of rab geranylgeranyl transferase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Rab geranylgeranyl transferase (GG transferase) is a two-component enzyme that attaches 20-carbon isoprenoid groups to cysteine residues in Rab proteins, a family of guanosine triphosphate-binding proteins that regulate vesicular traffic. The mutant gene in human choroideremia, an X-linked form of retinal degeneration, encodes a protein that resembles component A of rat Rab GG transferase. Lymphoblasts from choroideremia subjects showed a marked deficiency in the activity of component A, but not component B, of Rab GG transferase. The deficiency was more pronounced when the substrate was Rab3A, a synaptic vesicle protein, than it was when the substrate was Rab1A, a protein of the endoplasmic reticulum. The data imply the existence of multiple component A proteins, one of which is missing in choroideremia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seabra, M C -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380507" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Alkyl and Aryl Transferases ; Cell Line, Transformed ; Cells, Cultured ; Choroid/chemistry ; Choroideremia/*genetics ; Female ; GTP-Binding Proteins/analysis/*metabolism ; Gene Expression Regulation, Enzymologic ; Humans ; Lymphocyte Activation ; Male ; Middle Aged ; Mutation ; Nerve Tissue Proteins/analysis/*metabolism ; Photoreceptor Cells/chemistry ; Pigment Epithelium of Eye/chemistry ; Protein Prenylation ; Retina/chemistry ; Substrate Specificity ; Transferases/*deficiency/genetics ; rab1 GTP-Binding Proteins ; rab3 GTP-Binding Proteins
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    The skipping of constitutive exons in vivo induced by nonsense mutations (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: Nonsense mutations create a premature signal for the termination of translation of messenger RNA. Such mutations have been observed to cause a severe reduction in the amount of mutant allele transcript or to generate a peptide truncated at the carboxyl end. Analysis of fibrillin transcript from a patient with Marfan syndrome revealed the skipping of a constitutive exon containing a nonsense mutation. Similar results were observed for two nonsense mutations in the gene encoding ornithine delta-aminotransferase from patients with gyrate atrophy. All genomic DNA sequences flanking these exons that are known to influence RNA splicing were unaltered, which suggests that nonsense mutations can alter splice site selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dietz, H C -- Valle, D -- Francomano, C A -- Kendzior, R J Jr -- Pyeritz, R E -- Cutting, G R -- AR-41135/AR/NIAMS NIH HHS/ -- HG-00373/HG/NHGRI NIH HHS/ -- RR-00722/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):680-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, 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/8430317" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cells, Cultured ; DNA/*genetics/isolation & purification ; *Exons ; Female ; Fibroblasts/physiology ; Humans ; Male ; Marfan Syndrome/*genetics ; Microfilament Proteins/*genetics ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Reference Values
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    Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Genetic and metabolic studies have been done on a large kindred in which several males are affected by a syndrome of borderline mental retardation and abnormal behavior. The types of behavior that occurred include impulsive aggression, arson, attempted rape, and exhibitionism. Analysis of 24-hour urine samples indicated markedly disturbed monoamine metabolism. This syndrome was associated with a complete and selective deficiency of enzymatic activity of monoamine oxidase A (MAOA). In each of five affected males, a point mutation was identified in the eighth exon of the MAOA structural gene, which changes a glutamine to a termination codon. Thus, isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunner, H G -- Nelen, M -- Breakefield, X O -- Ropers, H H -- van Oost, B A -- NS 21921/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):578-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University Hospital Nijmegen, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211186" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Cell Line ; Cells, Cultured ; Female ; *Genes ; Humans ; Intellectual Disability/enzymology/*genetics ; Male ; Monoamine Oxidase/deficiency/*genetics ; Pedigree ; Phenotype ; *Point Mutation ; Skin/enzymology ; Syndrome ; X Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Modulation of anxiety and neuropeptide Y-Y1 receptors by antisense oligodeoxynucleotides (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-22
    Description: The function of neuropeptide Y, one of the most abundant peptide transmitters of the mammalian brain, remains unclear because of a lack of specific receptor antagonists. An antisense oligodeoxynucleotide corresponding to the NH2-terminus of the rat Y1 receptor was constructed and added to cultures of rat cortical neurons. This treatment resulted in a reduced density of Y1 (but not Y2) receptors and diminished the decrease in adenosine 3',5'-monophosphate (cAMP) usually seen after Y1 receptor activation. Repeated injection of the same oligodeoxynucleotide into the lateral cerebral ventricle of rats was followed by a similar reduction of cortical Y1 (but not Y2) receptors. Such antisense-treated animals displayed behavioral signs of anxiety. Thus, specific inhibition of neurotransmitter receptor expression can be accomplished in the living brain and demonstrates that altered central neuropeptide Y transmission produces an anxiety-like state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wahlestedt, C -- Pich, E M -- Koob, G F -- Yee, F -- Heilig, M -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Anxiety ; Base Sequence ; Cells, Cultured ; Cerebral Cortex/*physiology ; Cyclic AMP/metabolism ; Down-Regulation ; Embryo, Mammalian ; Learning ; Male ; Molecular Sequence Data ; Neurons/drug effects/*physiology ; Neuropeptide Y/*physiology ; Oligodeoxyribonucleotides ; Oligonucleotides, Antisense/*pharmacology ; Polymerase Chain Reaction ; Rats ; Rats, Wistar ; Receptors, Neuropeptide Y/*drug effects/*genetics/metabolism
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    A transglutaminase that converts interleukin-2 into a factor cytotoxic to oligodendrocytes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Regenerating optic nerves from fish produce a factor that is cytotoxic to oligodendrocytes. The cytotoxic factor is recognized by antibodies to interleukin-2 (IL-2) and has the apparent molecular size of a dimer of IL-2. An enzyme, identified as a nerve transglutaminase, was purified from regenerating optic nerves of fish and was found to catalyze dimerization of human IL-2. The dimerized IL-2, unlike monomeric IL-2, is cytotoxic to oligodendrocytes from rat brain in culture. The results suggest that posttranslational modification of a cytokine can alter its activity. Under conditions in which oligodendrocytes inhibit neuronal regeneration, dimerization of IL-2 might provide a mechanism to permit nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eitan, S -- Schwartz, M -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):106-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100369" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Newborn ; Brain/cytology ; Cell Survival/drug effects ; Cells, Cultured ; Fishes ; Interleukin-2/*metabolism/pharmacology ; Molecular Sequence Data ; *Nerve Regeneration ; Oligodendroglia/cytology/*drug effects ; Optic Nerve/enzymology/*physiology ; Transglutaminases/isolation & purification/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Alzheimer's pathology begins to yield its secrets (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):457-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424167" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/etiology/genetics/*metabolism ; Amyloid beta-Peptides/biosynthesis/genetics/*metabolism ; Brain/*metabolism ; Cells, Cultured ; Humans ; Lysosomes/metabolism
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  • 133
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    Phosphorylation and modulation of a kainate receptor (GluR6) by cAMP-dependent protein kinase (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-19
    Description: Ligand-gated ion channels gated by glutamate constitute the major excitatory neurotransmitter system in the mammalian brain. The functional modulation of GluR6, a kainate-activated glutamate receptor, by adenosine 3',5'-monophosphate-dependent protein kinase A (PKA) was examined with receptors expressed in human embryonic kidney cells. Kainate-evoked currents underwent a rapid desensitization that was blocked by lectins. Kainate currents were potentiated by intracellular perfusion of PKA, and this potentiation was blocked by co-application of an inhibitory peptide. Site-directed mutagenesis was used to identify the site or sites of phosphorylation on GluR6. Although mutagenesis of two serine residues, Ser684 and Ser666, was required for complete abolition of the PKA-induced potentiation, Ser684 may be the preferred site of phosphorylation in native GluR6 receptor complexes. These results indicate that glutamate receptor function can be directly modulated by protein phosphorylation and suggest that a dynamic regulation of excitatory receptors could be associated with some forms of learning and memory in the mammalian brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, L Y -- Taverna, F A -- Huang, X P -- MacDonald, J F -- Hampson, D R -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1173-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8382377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding Sites ; Brain/*physiology ; Cells, Cultured ; Concanavalin A/pharmacology ; Evoked Potentials/drug effects ; Humans ; Kainic Acid/*pharmacology ; Kidney ; Kinetics ; Membrane Potentials/drug effects ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oligodeoxyribonucleotides ; Protein Kinases/*metabolism ; Receptors, Glutamate/drug effects/genetics/*physiology ; Receptors, Kainic Acid ; Serine ; Wheat Germ Agglutinins/pharmacology
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    Mechanotransduction across the cell surface and through the cytoskeleton (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: Mechanical stresses were applied directly to cell surface receptors with a magnetic twisting device. The extracellular matrix receptor, integrin beta 1, induced focal adhesion formation and supported a force-dependent stiffening response, whereas nonadhesion receptors did not. The cytoskeletal stiffness (ratio of stress to strain) increased in direct proportion to the applied stress and required intact microtubules and intermediate filaments as well as microfilaments. Tensegrity models that incorporate mechanically interdependent struts and strings that reorient globally in response to a localized stress mimicked this response. These results suggest that integrins act as mechanoreceptors and transmit mechanical signals to the cytoskeleton. Mechanotransduction, in turn, may be mediated simultaneously at multiple locations inside the cell through force-induced rearrangements within a tensionally integrated cytoskeleton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, N -- Butler, J P -- Ingber, D E -- CA45548/CA/NCI NIH HHS/ -- HL-33009/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 21;260(5111):1124-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Respiratory Biology Program, Harvard School of Public Health, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7684161" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/physiology ; Amino Acid Sequence ; Antigens, CD29 ; Cell Membrane/*physiology ; Cells, Cultured ; Cytoskeleton/*physiology ; Endothelium, Vascular/*cytology ; Integrins/*physiology ; Intermediate Filaments/physiology ; Magnetics ; Microspheres ; Microtubules/physiology ; Molecular Sequence Data ; Oligopeptides/metabolism ; *Signal Transduction ; Stress, Mechanical
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    Prevention of vertebrate neuronal death by the crmA gene (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-11
    Description: Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gagliardini, V -- Fernandez, P A -- Lee, R K -- Drexler, H C -- Rotello, R J -- Fishman, M C -- Yuan, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):826-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1 ; Cells, Cultured ; Chickens ; Ganglia, Spinal ; Gene Expression ; Metalloendopeptidases/*genetics/physiology ; Microinjections ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/*cytology/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Serpins/*genetics/physiology ; *Viral Proteins
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    Stimulation of human gamma delta T cells by nonpeptidic mycobacterial ligands (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-08
    Description: Most human peripheral blood gamma delta T lymphocytes respond to hitherto unidentified mycobacterial antigens. Four ligands from Mycobacterium tuberculosis strain H37Rv that stimulated proliferation of a major human gamma delta T cell subset were isolated and partially characterized. One of these ligands, TUBag4, is a 5' triphosphorylated thymidine-containing compound, to which the three other stimulatory molecules are structurally related. These findings support the hypothesis that some gamma delta T cells recognize nonpeptidic ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constant, P -- Davodeau, F -- Peyrat, M A -- Poquet, Y -- Puzo, G -- Bonneville, M -- Fournie, J J -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department III, Laboratoire de Pharmacologie et de Toxicologie Fondamentales du CNRS, Toulouse, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146660" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Bacterial/chemistry/*immunology/isolation & purification ; Cells, Cultured ; Chromatography, Ion Exchange ; Humans ; Ligands ; *Lymphocyte Activation ; Magnetic Resonance Spectroscopy ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; Thymine Nucleotides/analysis/chemistry/*immunology/isolation & purification
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    DNA repair rates mapped along the human PGK1 gene at nucleotide resolution (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-11
    Description: The repair of cyclobutane pyrimidine dimers (CPDs), DNA lesions induced by ultraviolet light, was studied at nucleotide resolution. Human fibroblasts were irradiated with ultraviolet light and allowed to repair. The DNA was enzymatically cleaved at the CPDs, and the induced breaks along the promoter and exon 1 of the PGK1 gene were mapped by ligation-mediated polymerase chain reaction. Repair rates within the nontranscribed strand varied as much as 15-fold, depending on nucleotide position. Preferential repair of the transcribed strand began just downstream of the transcription start site but was most pronounced beginning at nucleotide +140 in exon 1. The promoter contained two slowly repaired regions that coincided with two transcription factor binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, S -- Drouin, R -- Holmquist, G P -- CA54773/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1438-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Research Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128226" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cells, Cultured ; *DNA Repair ; Exons ; *Genes ; HeLa Cells ; Humans ; Kinetics ; Phosphoglycerate Kinase/*genetics ; Promoter Regions, Genetic ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Transcription Factors/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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    T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-25
    Description: Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Critchfield, J M -- Racke, M K -- Zuniga-Pflucker, J C -- Cannella, B -- Raine, C S -- Goverman, J -- Lenardo, M J -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1139-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Apoptosis ; CD4-Positive T-Lymphocytes/*immunology ; Cell Division ; Cells, Cultured ; Cytochrome c Group/immunology ; Dose-Response Relationship, Immunologic ; Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology/therapy ; *Immune Tolerance ; Immunotherapy ; Interleukin-2/immunology/pharmacology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Myelin Basic Protein/immunology ; Myelin Sheath/immunology/pathology ; Spinal Cord/pathology ; T-Lymphocytes/*immunology
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    Requirement for BDNF in activity-dependent survival of cortical neurons (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-18
    Description: Cultured embryonic cortical neurons from rats were used to explore mechanisms of activity-dependent neuronal survival. Cell survival was increased by the activation of voltage-sensitive calcium channels (VSCCs) but not by activation of N-methyl-D-aspartate receptors. These effects correlated with the expression of brain-derived neurotrophic factor (BDNF) induced by these two classes of calcium channels. Antibodies to BDNF (which block intracellular signaling by BDNF, but not by nerve growth factor, NT3, or NT4/5) reduced the survival of cortical neurons and reversed the VSCC-mediated increase in survival. Thus, endogenous BDNF is a trophic factor for cortical neurons whose expression is VSCC-regulated and that functions in the VSCC-dependent survival of these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, A -- Carnahan, J -- Greenberg, M E -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1618-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Brain-Derived Neurotrophic Factor ; Calcium Channels/*physiology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cerebral Cortex/*cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Embryo, Mammalian ; Glutamates/pharmacology ; Glutamic Acid ; N-Methylaspartate/pharmacology ; Nerve Growth Factors/biosynthesis/genetics/immunology/*physiology ; Nerve Tissue Proteins/biosynthesis/genetics/immunology/*physiology ; Neurons/*cytology ; Phosphorylation ; Potassium Chloride/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Signal Transduction
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    Involvement of the IRF-1 transcription factor in antiviral responses to interferons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: The mechanisms underlying interferon (IFN)-induced antiviral states are not well understood. Interferon regulatory factor-1 (IRF-1) is an IFN-inducible transcriptional activator, whereas IRF-2 suppresses IRF-1 action. The inhibition of encephalomyocarditis virus (EMCV) replication by IFN-alpha and especially by IFN-gamma was impaired in cells from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice). The IRF-1-/- mice were less resistant than normal mice to EMCV infection, as revealed by accelerated mortality and a larger virus titer in target organs. The absence of IRF-1 did not clearly affect replication of two other types of viruses. Thus, IRF-1 is necessary for the antiviral action of IFNs against some viruses, but IFNs activate multiple activation pathways through diverse target genes to induce the antiviral state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, T -- Nakayama, K -- Penninger, J -- Kitagawa, M -- Harada, H -- Matsuyama, T -- Tanaka, N -- Kamijo, R -- Vilcek, J -- Mak, T W -- R35CA49731/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovirus Infections/*immunology/microbiology ; Cells, Cultured ; DNA-Binding Proteins/genetics/*physiology ; Encephalomyocarditis virus/physiology ; Gene Expression Regulation ; Interferon Regulatory Factor-1 ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Mice ; Mutation ; Phosphoproteins/genetics/*physiology ; Simplexvirus/physiology ; Transcription Factors/genetics/*physiology ; Vesicular stomatitis Indiana virus/physiology ; *Virus Replication
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    Putting antibodies to work inside cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356445" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/therapy ; Cells, Cultured ; Endoplasmic Reticulum/*metabolism ; Gene Products, env/metabolism ; Genetic Therapy/*methods ; HIV/*metabolism ; HIV Antibodies/*genetics/metabolism ; HIV Envelope Protein gp120/*immunology ; HIV Envelope Protein gp160 ; Humans ; *Protein Engineering ; Protein Precursors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Betacellulin: a mitogen from pancreatic beta cell tumors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Betacellulin, a member of the epidermal growth factor family, has been identified in the conditioned medium of cell lines derived from mouse pancreatic beta cell tumors. Betacellulin is a 32-kilodalton glycoprotein that appears to be processed from a larger transmembrane precursor by proteolytic cleavage. The carboxyl-terminal domain of betacellulin has 50 percent sequence similarity with that of rat transforming growth factor alpha. Betacellulin is a potent mitogen for retinal pigment epithelial cells and vascular smooth muscle cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shing, Y -- Christofori, G -- Hanahan, D -- Ono, Y -- Sasada, R -- Igarashi, K -- Folkman, J -- CA 70118/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1604-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456283" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Base Sequence ; Betacellulin ; Cell Division/drug effects ; Cells, Cultured ; DNA Replication/drug effects ; Endothelium, Vascular/cytology/drug effects ; Epidermal Growth Factor/pharmacology ; Growth Substances/*genetics/isolation & purification/pharmacology ; Humans ; *Intercellular Signaling Peptides and Proteins ; Islets of Langerhans/physiopathology ; Kinetics ; Mice ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/drug effects ; Oligodeoxyribonucleotides ; Pancreatic Neoplasms/*physiopathology ; Pigment Epithelium of Eye/cytology/drug effects ; Polymerase Chain Reaction/methods ; Protein Precursors/genetics ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Proteins/pharmacology ; Sequence Homology, Amino Acid ; Thymidine/metabolism ; Transforming Growth Factor alpha/genetics
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    Sequestration from immune CD4+ T cells of mycobacteria growing in human macrophages (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: CD4+ helper T cells mediate resistance to tuberculosis, presumably by enhancing the antimicrobial activity of macrophages within which the Mycobacterium tuberculosis organism grows. A first step in resistance should be the presentation of mycobacterial antigens by macrophages to CD4+ T cells. However, when the antigenic stimulus is limited to organisms growing in human monocytes, the organisms become sequestered from immune CD4+ T cells. This block in presentation is selective for growing mycobacteria and not for other stimuli. Sequestration would allow replicating organisms to persist in infected individuals and may contribute to virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pancholi, P -- Mirza, A -- Bhardwaj, N -- Steinman, R M -- AI24775/AI/NIAID NIH HHS/ -- AR39552/AR/NIAMS NIH HHS/ -- MOI-RR00102/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1993 May 14;260(5110):984-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8098550" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/*immunology ; BCG Vaccine/immunology ; CD4-Positive T-Lymphocytes/*immunology ; Cells, Cultured ; Humans ; Macrophages/immunology/*microbiology ; Monocytes/immunology/*microbiology ; Mycobacterium bovis/growth & development/*immunology ; Tuberculin/immunology ; Tuberculosis/immunology
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    Characterization of a presynaptic glutamate receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: Glutamate receptors mediate excitatory neurotransmission in the brain and are important in the formation of memory and in some neurodegenerative disorders. A complementary DNA clone that encoded a 33-kilodalton protein (GR33) was obtained by screening a library with an antibody generated against glutamate binding proteins. The sequence of GR33 is identical to that of the recently reported presynaptic protein syntaxin. When GR33 was expressed in Xenopus oocytes, it formed glutamate-activated ion channels that are pharmacologically similar to those of N-methyl-D-aspartate receptors but with different electrophysiological properties. Mutation of the leucine 278 residue in the single putative transmembrane segment of GR33 affects the properties of the channel. Thus, in vivo GR33 may be a presynaptic glutamate receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smirnova, T -- Stinnakre, J -- Mallet, J -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):430-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de genetique moleculaire de la neurotransmission et des processus neurodegeneratifs, Centre National de la Recherche Scientifique (CNRS), Gif sur Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8105537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/chemistry ; Brain/embryology ; Brain Chemistry ; Calcium/metabolism ; Cells, Cultured ; Cloning, Molecular ; Glutamates/pharmacology ; Glutamic Acid ; Humans ; Membrane Potentials ; Mutagenesis, Site-Directed ; N-Methylaspartate/pharmacology ; Nerve Tissue Proteins/chemistry ; Neurons/chemistry ; Oocytes ; Rats ; Rats, Wistar ; Receptors, Glutamate/chemistry/genetics/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Presynaptic/chemistry/genetics/*metabolism ; Syntaxin 1 ; Xenopus
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    Carbon monoxide: a putative neural messenger (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Carbon monoxide, an activator of guanylyl cyclase, is formed by the action of the enzyme heme oxygenase. By in situ hybridization in brain slices, discrete neuronal localization of messenger RNA for the constitutive form of heme oxygenase throughout the brain has been demonstrated. This localization is essentially the same as that for soluble guanylyl cyclase messenger RNA. In primary cultures of olfactory neurons, zinc protoporphyrin-9, a potent selective inhibitor of heme oxygenase, depletes endogenous guanosine 3',5'-monophosphate (cGMP). Thus, carbon monoxide, like nitric oxide, may be a physiologic regulator of cGMP. These findings, together with the neuronal localizations of heme oxygenase, suggest that carbon monoxide may function as a neurotransmitter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verma, A -- Hirsch, D J -- Glatt, C E -- Ronnett, G V -- Snyder, S H -- DA00266/DA/NIDA NIH HHS/ -- MH18501/MH/NIMH NIH HHS/ -- NS02131/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):381-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Walter Reed Army Medical Center, Washington, DC 20307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678352" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Aminolevulinate Synthetase/analysis/genetics ; Amino Acid Oxidoreductases/analysis/genetics ; Animals ; Animals, Newborn ; Base Sequence ; Brain/*enzymology ; Carbon Monoxide/*metabolism ; Cells, Cultured ; Cyclic GMP/*metabolism ; Guanylate Cyclase/analysis/genetics ; Heme Oxygenase (Decyclizing)/*analysis/genetics ; In Situ Hybridization ; Molecular Sequence Data ; NADPH-Ferrihemoprotein Reductase/analysis/genetics ; Neurons/*enzymology ; Neurotransmitter Agents/*metabolism ; Nitric Oxide Synthase ; Oligodeoxyribonucleotides/chemistry ; RNA, Messenger/analysis ; Rats
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    A nonpeptidyl growth hormone secretagogue (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-11
    Description: A nonpeptidyl secretagogue for growth hormone of the structure 3-amino-3-methyl-N-(2,3,4,5-tetrahydro-2-oxo-1-([2'-(1H-tetrazol-5 -yl) (1,1'-biphenyl)-4-yl]methyl)-1H-1-benzazepin-3(R)-yl)-butanamid e (L-692,429) has been identified. L-692,429 synergizes with the natural growth hormone secretagogue growth hormone-releasing hormone and acts through an alternative signal transduction pathway. The mechanism of action of L-692,429 and studies with peptidyl and nonpeptidyl antagonists suggest that this molecule is a mimic of the growth hormone-releasing hexapeptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6). L-692,429 is an example of a nonpeptidyl specific secretagogue for growth hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, R G -- Cheng, K -- Schoen, W R -- Pong, S S -- Hickey, G -- Jacks, T -- Butler, B -- Chan, W W -- Chaung, L Y -- Judith, F -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Animal Science Research, Merck Research Laboratories, Rahway, NJ 07065.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503009" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Benzazepines/*pharmacology ; Cells, Cultured ; Dogs ; Growth Hormone/*drug effects/secretion ; Male ; Membrane Potentials/drug effects ; Molecular Sequence Data ; Oligopeptides/chemistry/pharmacology ; Pituitary Gland, Anterior/drug effects/secretion ; Rats ; Second Messenger Systems/drug effects ; Stereoisomerism ; Structure-Activity Relationship ; Tetrazoles/*pharmacology
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    Transient transfection and expression in the obligate intracellular parasite Toxoplasma gondii (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: Toxoplasma gondii is a protozoan pathogen that produces severe disease in humans and animals. This obligate intracellular parasite provides an excellent model for the study of how such pathogens are able to invade, survive, and replicate intracellularly. DNA encoding chloramphenicol acetyltransferase was introduced into T. gondii and transiently expressed with the use of three vectors based on different Toxoplasma genes. The ability to introduce genes and have them efficiently and faithfully expressed is an essential tool for understanding the structure-function relation of genes and their products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soldati, D -- Boothroyd, J C -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chloramphenicol O-Acetyltransferase/genetics ; *Gene Expression ; *Genes, Protozoan ; Genetic Vectors ; Humans ; Toxoplasma/*genetics ; *Transfection
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    Control of topographic retinal axon branching by inhibitory membrane-bound molecules (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-08-05
    Description: Retinotopic map development in nonmammalian vertebrates appears to be controlled by molecules that guide or restrict retinal axons to correct locations in their targets. However, the retinotopic map in the superior colliculus (SC) of the rat is developed instead by a topographic bias in collateral branching and arborization. Temporal retinal axons extending across alternating membranes from the topographically correct rostral SC or the incorrect caudal SC of embryonic rats preferentially branch on rostral membranes. Branching preference is due to an inhibitory phosphatidylinositol-linked molecule in the caudal SC. Thus, position-encoding membrane-bound molecules may establish retinotopic maps in mammals by regulating axon branching, not by directing axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roskies, A L -- O'Leary, D D -- NEI RO1 EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):799-803.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carbocyanines ; Cells, Cultured ; Embryonic and Fetal Development/physiology ; Fluorescent Dyes ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*physiology ; Superior Colliculi/embryology
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    Anergic T cells as suppressor cells in vitro (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-10
    Description: T cell-mediated suppression is an established phenomenon, but its underlying mechanisms are obscure. An in vitro system was used to test the possibility that anergic T cells can act as specific suppressor cells. Anergic human T cells caused inhibition of antigen-specific and allospecific T cell proliferation. In order for the inhibition to occur, the anergic T cells had to be specific for the same antigen-presenting cells (APCs) as the T cells that were suppressed. The mechanism of this suppression appears to be competition for the APC surface and for locally produced interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombardi, G -- Sidhu, S -- Batchelor, R -- Lechler, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1587-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Royal Postgraduate Medical School, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202711" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Line ; Cells, Cultured ; *Clonal Anergy ; Humans ; Interleukin-10/immunology ; Interleukin-2/immunology/secretion ; Interleukin-4/immunology ; Lymphocyte Activation ; Recombinant Proteins/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Transforming Growth Factor beta/immunology
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    Generation of lymphohematopoietic cells from embryonic stem cells in culture (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: An efficient system was developed that induced the differentiation of embryonic stem (ES) cells into blood cells of erythroid, myeloid, and B cell lineages by coculture with the stromal cell line OP9. This cell line does not express functional macrophage colony-stimulating factor (M-CSF). The presence of M-CSF had inhibitory effects on the differentiation of ES cells to blood cells other than macrophages. Embryoid body formation or addition of exogenous growth factors was not required, and differentiation was highly reproducible even after the selection of ES cells with the antibiotic G418. Combined with the ability to genetically manipulate ES cells, this system will facilitate the study of molecular mechanisms involved in development and differentiation of hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University Yoshida, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology ; Base Sequence ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Culture Media ; Erythrocytes/cytology ; Erythropoiesis ; Gene Rearrangement ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology ; Lymphocytes/*cytology ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/cytology ; Mesoderm/cytology ; Mice ; Molecular Sequence Data ; Recombinant Proteins/pharmacology ; Stromal Cells/cytology
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    Differential effects of apolipoproteins E3 and E4 on neuronal growth in vitro (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-05-06
    Description: Apolipoprotein E4 (apoE4), one of the three common isoforms of apoE, has been implicated in Alzheimer's disease. The effects of apoE on neuronal growth were determined in cultures of dorsal root ganglion neurons. In the presence of beta-migrating very low density lipoproteins (beta-VLDL), apoE3 increased neurite outgrowth, whereas apoE4 decreased outgrowth. The effects of apoE3 or apoE4 in the presence of beta-VLDL were prevented by incubation with a monoclonal antibody to apoE or by reductive methylation of apoE, both of which block the ability of apoE to interact with lipoprotein receptors. The data suggest that receptor-mediated binding or internalization (or both) of apoE-enriched beta-VLDL leads to isoform-specific differences in interactions with cellular proteins that affect neurite outgrowth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, B P -- Bellosta, S -- Sanan, D A -- Weisgraber, K H -- Mahley, R W -- Pitas, R E -- HL 41633/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 May 6;264(5160):850-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171342" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein E3 ; Apolipoprotein E4 ; Apolipoproteins E/metabolism/*pharmacology ; Cells, Cultured ; Culture Media, Serum-Free ; Fetus ; Ganglia, Spinal ; Lipoproteins, VLDL/pharmacology ; Neurites/*drug effects/ultrastructure ; Neurons/cytology/*drug effects ; Rabbits ; Receptors, LDL/metabolism
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    Control of angiogenesis in fibroblasts by p53 regulation of thrombospondin-1 (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-09-09
    Description: As normal cells progress toward malignancy, they must switch to an angiogenic phenotype to attract the nourishing vasculature that they depend on for their growth. In cultured fibroblasts from Li-Fraumeni patients, this switch was found to coincide with loss of the wild-type allele of the p53 tumor suppressor gene and to be the result of reduced expression of thrombospondin-1 (TSP-1), a potent inhibitor of angiogenesis. Transfection assays revealed that p53 can stimulate the endogenous TSP-1 gene and positively regulate TSP-1 promoter sequences. These data indicate that, in fibroblasts, wild-type p53 inhibits angiogenesis through regulation of TSP-1 synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dameron, K M -- Volpert, O V -- Tainsky, M A -- Bouck, N -- CA52750/CA/NCI NIH HHS/ -- CA64239/CA/NCI NIH HHS/ -- P01 CA34936/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1582-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521539" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cells, Cultured ; Fibroblasts/*metabolism ; *Gene Expression Regulation ; *Genes, p53 ; Humans ; Li-Fraumeni Syndrome ; Membrane Glycoproteins/biosynthesis/*genetics/physiology ; *Neovascularization, Pathologic ; Phenotype ; Promoter Regions, Genetic ; Thrombospondins ; Transfection
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    Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: Both interferon gamma (IFN-gamma) produced by T helper 1 (TH1) lymphocytes and interleukin-4 (IL-4) produced by TH2 lymphocytes were reduced in either bulk circulating mononuclear cells or mitogen-induced CD4+ T cell clones from the peripheral blood of individuals infected with human immunodeficiency virus (HIV). There was a preferential reduction in clones producing IL-4 and IL-5 in the advanced phases of infection. However, enhanced proportions of CD4+ T cell clones producing both TH1-type and TH2-type cytokines (TH0 clones) were generated from either skin-infiltrating T cells that had been activated in vivo or peripheral blood T cells stimulated by antigen in vitro when cells were isolated from HIV-infected individuals. All TH2 and most TH0 clones supported viral replication, although viral replication was not detected in any of the TH1 clones infected in vitro with HIV. These results suggest that HIV (i) does not induce a definite TH1 to TH2 switch, but can favor a shift to the TH0 phenotype in response to recall antigens, and (ii) preferentially replicates in CD4+ T cells producing TH2-type cytokines (TH2 and TH0).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maggi, E -- Mazzetti, M -- Ravina, A -- Annunziato, F -- de Carli, M -- Piccinni, M P -- Manetti, R -- Carbonari, M -- Pesce, A M -- del Prete, G -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):244-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Immunology and Allergy, University of Florence, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023142" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Cell Line ; Cells, Cultured ; HIV/*physiology ; HIV Infections/*immunology/microbiology ; HIV Seropositivity/immunology ; Humans ; Immunologic Memory ; Interferon-gamma/*biosynthesis ; Interleukin-4/biosynthesis ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Lymphocyte Activation ; Phenotype ; T-Lymphocytes, Helper-Inducer/*immunology/microbiology ; Virus Replication
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  • 154
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    c-Fos: a key regulator of osteoclast-macrophage lineage determination and bone remodeling (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression overcame this differentiation block. The lack of Fos also caused a lineage shift between osteoclasts and macrophages that resulted in increased numbers of bone marrow macrophages. These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grigoriadis, A E -- Wang, Z Q -- Cecchini, M G -- Hofstetter, W -- Felix, R -- Fleisch, H A -- Wagner, E F -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):443-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Transplantation ; Bone Remodeling/*physiology ; Cell Differentiation ; Cells, Cultured ; Genes, fos ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Macrophages/*cytology ; Mice ; Mice, Mutant Strains ; Osteoclasts/*cytology ; Osteogenesis ; Osteopetrosis/metabolism/pathology ; Proto-Oncogene Proteins c-fos/genetics/*physiology
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  • 155
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    Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in the p53 tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tornaletti, S -- Pfeifer, G P -- ES06070/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1436-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Rsearch Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128225" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; *DNA Repair ; Exons ; *Genes, p53 ; HeLa Cells ; Humans ; Mutation ; Phosphoglycerate Kinase/genetics ; Polymerase Chain Reaction ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Skin Neoplasms/*genetics/metabolism ; Ultraviolet Rays
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  • 156
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    Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Although beta-amyloid is the main constituent of neurite plaques and may play a role in the pathophysiology of Alzheimer's disease, mechanisms by which soluble beta-amyloid might produce early symptoms such as memory loss before diffuse plaque deposition have not been implicated. Treatment of fibroblasts with beta-amyloid (10 nM) induced the same potassium channel dysfunction previously shown to occur specifically in fibroblasts from patients with Alzheimer's disease--namely, the absence of a 113-picosiemen potassium channel. A tetraethylammonium-induced increase of intracellular concentrations of calcium, [Ca2+]i, a response that depends on functional 113-picosiemen potassium channels, was also eliminated or markedly reduced by 10 nM beta-amyloid. Increased [Ca2+]i induced by high concentrations of extracellular potassium and 166-picosiemen potassium channels were unaffected by 10 nM beta-amyloid. In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etcheberrigaray, R -- Ito, E -- Kim, C S -- Alkon, D L -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146663" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid beta-Peptides/*pharmacology ; Bombesin/pharmacology ; Calcium/metabolism ; Cell Line ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Female ; Fibroblasts/*drug effects/metabolism ; Humans ; Male ; Phenotype ; Potassium Channel Blockers ; Potassium Channels/*drug effects/metabolism ; Potassium Chloride/pharmacology ; Solubility ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology
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    Aberrant neurites and synaptic vesicle protein deficiency in synapsin II-depleted neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals. After depletion of synapsin II by antisense oligonucleotides, rat hippocampal neurons in culture were unable to consolidate their minor processes and did not elongate axons. These aberrant morphological changes were accompanied by an abnormal distribution of intracellular filamentous actin (F-actin). In addition, synapsin II suppression resulted in a selective decrease in the amounts of several synaptic vesicle-associated proteins. These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Kosik, K S -- Greengard, P -- Han, H Q -- New York, N.Y. -- Science. 1994 May 13;264(5161):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178158" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Base Sequence ; *Calcium-Binding Proteins ; Cells, Cultured ; Hippocampus/cytology ; Membrane Glycoproteins/*metabolism ; Microtubule-Associated Proteins/metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Neurites/*physiology ; Neurons/*cytology/metabolism/ultrastructure ; Oligonucleotides, Antisense/pharmacology ; Rats ; Synapsins/genetics/*metabolism ; Synaptophysin/*metabolism ; Synaptotagmins ; Tubulin/metabolism ; tau Proteins/metabolism
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    Post-transcriptional regulation of early T cell development by T cell receptor signals (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-27
    Description: During differentiation in the thymus, immature T cells progress through an ordered sequence of developmental stages that are best characterized by variable expression of the co-receptor molecules CD4 and CD8. Crosslinking of T cell receptor (TCR) molecules on precursor thymocytes was found to block their differentiation into CD4+CD8+ cells by eliminating messenger RNA's encoding two families of developmentally important molecules: the co-receptor molecules CD4 and CD8 and the recombination activating genes 1 and 2. TCR-induced post-transcriptional regulation in early thymocytes was specific for selective messenger RNA's, required protein synthesis, and was itself developmentally regulated. These data identify a post-transcriptional mechanism that is influenced by TCR signals and that regulates early thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahama, Y -- Singer, A -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1456-62.〈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/1439838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8/genetics ; Cell Differentiation/physiology ; Cells, Cultured ; Fetus/cytology ; Gene Rearrangement, T-Lymphocyte/genetics ; Genes, RAG-1/genetics ; Mice ; Protein Synthesis Inhibitors/pharmacology ; Protein-Tyrosine Kinases/genetics ; RNA Processing, Post-Transcriptional/physiology ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; Signal Transduction/physiology ; T-Lymphocytes/*cytology/drug effects ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/cytology/embryology
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  • 159
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    Serotonin-mediated endocytosis of apCAM: an early step of learning-related synaptic growth in Aplysia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-01
    Description: The long-term facilitation of synaptic efficacy that is induced by serotonin in dissociated cell cultures of sensory and motor neurons of Aplysia is accompanied by the growth of new synaptic connections. This growth is associated with a down-regulation in the sensory neuron of Aplysia cell adhesion molecules (apCAMs). To examine the mechanisms of this down-regulation, thin-section electron microscopy was combined with immunolabeling by gold-conjugated monoclonal antibodies specific to apCAM. Within 1 hour, serotonin led to a 50% decrease in the density of gold-labeled complexes at the surface membrane of the sensory neuron. This down-regulation was achieved by a heterologous, protein synthesis-dependent activation of the endosomal pathway, which leads to internalization and apparent degradation of apCAM. The internalization is particularly prominent at sites where the processes of the sensory neurons contact one another and may act there to destabilize process-to-process contacts that normally inhibit growth. In turn, the endocytic activation may lead to a redistribution of membrane components to sites where new synapses form.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bailey, C H -- Chen, M -- Keller, F -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- MH37134/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 May 1;256(5057):645-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1585177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Antibodies, Monoclonal ; Aplysia/*physiology ; Cell Adhesion Molecules/*metabolism ; Cell Membrane/metabolism/ultrastructure ; Cells, Cultured ; Coated Pits, Cell-Membrane/metabolism/ultrastructure ; Endocytosis/*drug effects ; Immunohistochemistry ; Microscopy, Electron ; Motor Neurons/physiology/ultrastructure ; Neurons, Afferent/physiology/ultrastructure ; Serotonin/*pharmacology ; Synapses/*physiology/ultrastructure ; Wheat Germ Agglutinins/metabolism
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    Polyamine depletion and drug-induced chromosomal damage: new results (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tofilon, P J -- Deen, D F -- Marton, L J -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1378.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455236" target="_blank"〉PubMed〈/a〉
    Keywords: Carmustine/toxicity ; Cell Death ; Cells, Cultured ; *DNA Damage ; In Vitro Techniques ; Polyamines/*metabolism ; Sister Chromatid Exchange/drug effects
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    Inhibition of development of Kaposi's sarcoma-related lesions by a bacterial cell wall complex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: In vitro and in vivo model systems for the study of human immunodeficiency virus (HIV)-associated Kaposi's sarcoma (KS) were used to evaluate compounds for their potential as therapeutic agents. A sulfated polysaccharide-peptidoglycan compound (SP-PG) produced by bacteria controlled the in vitro growth of acquired immunodeficiency syndrome (AIDS)-associated, KS-derived spindle-shaped cells (AIDS-KS cells) at noncytotoxic concentrations. Angiogenesis induced by AIDS-KS cells in the chicken chorioallantoic membrane assay was blocked by SP-PG, which also inhibited the vascular hyperpermeability response and the angiogenesis associated with the induction of KS-like lesions that develop after subcutaneous inoculation of AIDS-KS cells into nude mice. Suramin, pentosan polysulfate, and interferon alpha, which are currently in use for therapy of KS, were either less effective than SP-PG or much more cytotoxic, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, S -- Sakurada, S -- Salahuddin, S Z -- Osada, Y -- Tanaka, N G -- Sakamoto, N -- Sekiguchi, M -- Gallo, R C -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1437-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Southern California, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1371891" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Arthrobacter ; Arylsulfatases ; Capillary Permeability/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Endothelium, Vascular/cytology/drug effects ; Fibroblasts/drug effects ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Pathologic/*prevention & control ; *Peptidoglycan ; Polysaccharides/*pharmacology ; Sarcoma, Kaposi/etiology/*pathology ; Tumor Cells, Cultured
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    No requirement for p56lck in the antigen-stimulated clonal deletion of thymocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Activation of protein-tyrosine kinases (PTKs) is required for signal transduction during T cell activation, although the pathway used during thymic selection is unknown. An in vitro system was established in which T cell receptor transgenic thymocytes underwent clonal deletion in response to peptide antigen. The effects of two PTK-specific inhibitors, herbimycin A and genistein, on the clonal deletion of immature thymocytes and the activation of mature thymocytes were examined. Clonal deletion occurred while T cell activation was inhibited and when no p56lck activity was evident. Thus, p56lck is not required for the antigen-stimulated step of clonal deletion of immature thymocytes, and negative selection proceeds via a distinct pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Loh, D Y -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of 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/1621101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzoquinones ; Cells, Cultured ; Chickens ; DNA Replication ; Genistein ; Isoflavones/pharmacology ; L Cells (Cell Line) ; Lactams, Macrocyclic ; *Lymphocyte Activation/drug effects ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Quinones/pharmacology ; Receptors, Antigen, T-Cell/*genetics/immunology ; Rifabutin/analogs & derivatives ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/drug effects/*immunology ; Transfection
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  • 163
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    GnRH-induced Ca2+ oscillations and rhythmic hyperpolarizations of pituitary gonadotropes (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-24
    Description: Secretion of gonadotropic hormones from pituitary gonadotropes in response to gonadotropin-releasing hormone (GnRH) is essential for regulation of reproductive potential. Gonadotropes from male rats exhibited an unusual form of cellular excitation that resulted from periodic membrane hyperpolarization. GnRH induced an oscillatory release of intracellular Ca2+ via a guanosine triphosphate (GTP) binding protein-coupled phosphoinositide pathway and hyperpolarized the gonadotrope periodically by opening apamin-sensitive Ca(2+)-activated K+ (SK) channels. Each hyperpolarization was terminated by firing of a few action potentials that may result from removal of inactivation from voltage-gated Na+ and Ca2+ channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, A -- Hille, B -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apamin/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; GTP-Binding Proteins/physiology ; Gonadotropin-Releasing Hormone/*physiology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate/physiology ; Membrane Potentials ; Periodicity ; Pituitary Gland, Anterior/cytology/*physiology ; Potassium Channels/physiology ; Rats
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    Identification of envelope V3 loop as the major determinant of CD4 neutralization sensitivity of HIV-1 (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-24
    Description: Laboratory isolates of human immunodeficiency virus type-1 (HIV-1) such as HTLV-IIIB are generally T cell line-tropic and highly sensitive to neutralization by soluble CD4 (sCD4), a potential antiviral agent that is undergoing clinical trial. However, many primary HIV-1 isolates are macrophage-tropic and sCD4-resistant. Envelope V3 loop sequences derived from primary HIV-1 isolates were sufficient to confer on HTLV-IIIB not only the tissue tropism but also the degree of sCD4 neutralization resistance characteristic of their HIV-1 strains of origin. Single amino acid changes in the V3 loop enhanced sCD4 resistance by up to tenfold. These observations suggest that the tissue tropism and sCD4 neutralization sensitivity of HIV-1 isolates are regulated by similar mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, S S -- Boyle, T J -- Lyerly, H K -- Cullen, B R -- AI28233/AI/NIAID NIH HHS/ -- AI28662/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636088" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Cell Line ; Cells, Cultured ; Gene Products, gag/*immunology ; HIV Envelope Protein gp120/*immunology ; HIV-1/*immunology/isolation & purification ; Humans ; Kinetics ; Molecular Sequence Data ; Neutralization Tests ; Proviruses/immunology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virion/immunology
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    Encoding of a homolog of the IFN-gamma receptor by myxoma virus (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: Many poxvirus-encoded virulence factors have been identified as proteins that are secreted from infected cells. The major secreted protein (37 kilodaltons) from cells infected with myxoma virus is encoded by the M-T7 open reading frame. This protein has significant sequence similarity to the human and mouse receptors for interferon-gamma (IFN-gamma). Furthermore, the myxoma M-T7 protein specifically binds rabbit IFN-gamma and inhibits the biological activity of extracellular IFN-gamma, one of the key regulatory cytokines in the host immune response against viral infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, C -- Mossman, K -- McFadden, G -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1369-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Alberta, Edmonton, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cloning, Molecular ; *Genes, Viral ; In Vitro Techniques ; Interferon-gamma/metabolism ; Molecular Sequence Data ; Myxoma virus/*genetics/pathogenicity ; Protein Binding ; Rabbits ; Receptors, Interferon/*genetics ; Restriction Mapping ; Sequence Alignment ; Sequence Homology, Amino Acid ; Viral Interference ; Viral Proteins/*genetics ; Viral Structural Proteins/*genetics
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    An antiviral soluble form of the LDL receptor induced by interferon (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: Interferons, which induce several intracellular antiviral proteins, also induce an extracellular soluble protein that inhibits vesicular stomatitis virus (VSV) infection. This 28-kilodalton soluble protein was purified to homogeneity and identified by protein sequencing as the ligand-binding domain of the human 160-kilodalton low density lipoprotein receptor (LDLR). The existence of an antiviral soluble LDLR was confirmed by immunoaffinity chromatography with monoclonal antibody to LDLR. This soluble receptor mediates most of the interferon-triggered antiviral activity against VSV, apparently by interfering with virus assembly or budding, and not by inhibiting virus attachment to cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, D G -- Tal, N -- Novick, D -- Barak, S -- Rubinstein, M -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):250-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211145" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antiviral Agents/*biosynthesis/chemistry/isolation & purification ; Cell Line ; Cells, Cultured ; Chromatography, Affinity ; Culture Media, Serum-Free ; Cytopathogenic Effect, Viral ; HeLa Cells ; Humans ; Interferon-beta/pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Molecular Weight ; Receptors, LDL/*biosynthesis/chemistry/isolation & purification ; Solubility ; Vesicular stomatitis Indiana virus/growth & development
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  • 167
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    Restoration of HIV-specific cell-mediated immune responses by interleukin-12 in vitro (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Peripheral blood mononuclear cells (PBMCs) from many asymptomatic individuals infected with human immunodeficiency virus-type 1 (HIV) are unresponsive as measured by in vitro T cell proliferation and interleukin-2 (IL-2) production to influenza virus and synthetic peptides of HIV envelope (Env). Strong influenza virus- and Env-stimulated IL-2 responses and T cell proliferation were restored when cultures were stimulated in the presence of IL-12. Interferon-gamma production by PBMCs from HIV seropositive (HIV+) patients was also restored with IL-12. Furthermore, in vitro antigen-specific production of IL-2 and proliferation of PBMCs from HIV- donors were suppressed by antibody to IL-12, but were not enhanced by addition of exogenous IL-12. Thus, IL-12 may be limiting in PBMCs from HIV+ but not HIV- individuals. These findings demonstrate that IL-12 can restore HIV-specific cell-mediated immunity in vitro in HIV-infected individuals and suggest a potential use of IL-12 in augmenting the diminished immunologic functions associated with HIV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clerici, M -- Lucey, D R -- Berzofsky, J A -- Pinto, L A -- Wynn, T A -- Blatt, S P -- Dolan, M J -- Hendrix, C W -- Wolf, S F -- Shearer, G M -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1721-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7903123" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Gene Products, env/immunology ; HIV Infections/*immunology ; HIV-1/*immunology ; Humans ; Immunity, Cellular ; Influenza A virus/immunology ; Interferon-gamma/biosynthesis ; Interleukin-12 ; Interleukin-2/biosynthesis/pharmacology ; Interleukins/immunology/*pharmacology ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/immunology ; Lymphocyte Activation ; Phytohemagglutinins/immunology ; Recombinant Proteins/pharmacology ; T-Lymphocytes, Helper-Inducer/*immunology
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  • 168
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    Cloning of an M. tuberculosis DNA fragment associated with entry and survival inside cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Mycobacterium tuberculosis infects one-third of the world's human population. This widespread infection depends on the organism's ability to escape host defenses by gaining entry and surviving inside the macrophage. DNA sequences of M. tuberculosis have been cloned; these confer on a nonpathogenic Escherichia coli strain an ability to invade HeLa cells, augment macrophage phagocytosis, and survive for at least 24 hours inside the human macrophage. This capacity to gain entry into mammalian cells and survive inside the macrophage was localized to two distinct loci on the cloned M. tuberculosis DNA fragment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arruda, S -- Bomfim, G -- Knights, R -- Huima-Byron, T -- Riley, L W -- TW00018/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1454-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of International Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367727" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/genetics ; Cells, Cultured ; *Cloning, Molecular ; DNA, Bacterial/genetics ; Escherichia coli/*genetics/physiology ; *Genes, Bacterial ; HeLa Cells ; Humans ; Macrophages/*microbiology ; Molecular Sequence Data ; Mycobacterium tuberculosis/*genetics/pathogenicity/physiology ; Virulence
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  • 169
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    Targeted insertion of a variable region gene into the immunoglobulin heavy chain locus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: A mutant mouse strain has been generated in which a rearranged immunoglobulin heavy (H) chain variable (V) region gene is placed into the heavy chain locus in its natural position, replacing the JH elements. In homozygous mutant mice, essentially all B cells in the spleen express the transgenic VH region in their antibodies. The proper location of the transgene relative to the constant region genes allows it to participate in isotype switching and undergo somatic hypermutation. Immunoglobulin transgenic mice generated in this fashion by gene targeting should prove useful for the exploration of immunoregulatory mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taki, S -- Meiering, M -- Rajewsky, K -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235657" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Sequence ; Cells, Cultured ; *Genes, Immunoglobulin ; Homozygote ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin Variable Region/*genetics ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation
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  • 170
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    Yin and yang of phosphorylation in cytokine signaling (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, Y H -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cell Biology, National University of Singapore, Republic of Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7692598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cytokines/*metabolism/pharmacology ; Humans ; Interferons/metabolism/pharmacology ; Interleukins/metabolism/pharmacology ; Mice ; Models, Biological ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; *Signal Transduction ; T-Lymphocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
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  • 171
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    Spatially resolved dynamics of cAMP and protein kinase A subunits in Aplysia sensory neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-09
    Description: Cyclic adenosine monophosphate (cAMP)-dependent protein kinase, labeled with fluorescein and rhodamine on the catalytic and regulatory subunits, respectively, was injected into Aplysia sensory neurons either in culture or in intact cell clusters. Energy transfer between the subunits, a measure of cytosolic cAMP concentration ([cAMP]), and compartmentation of the dissociated subunits were monitored by confocal fluorescence microscopy. Bath application of serotonin produced a much greater elevation of [cAMP] in the processes than in the central bodies of the neurons. The resulting gradients must drive a sizable centripetal flux of cAMP because direct microinjection of cAMP showed that it diffused readily. Perinuclear increases in [cAMP] slowly caused the translocation of the freed catalytic subunit into the nucleus to an extent proportional to the percentage of its dissociation from the regulatory subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bacskai, B J -- Hochner, B -- Mahaut-Smith, M -- Adams, S R -- Kaang, B K -- Kandel, E R -- Tsien, R Y -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Diego, La Jolla 92093-0647.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682336" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Aplysia ; Cell Compartmentation ; Cell Nucleus/enzymology/metabolism ; Cells, Cultured ; Cyclic AMP/*metabolism ; Cytoplasm/enzymology/metabolism ; Diffusion ; Fluorescein ; Fluoresceins ; Microinjections ; Neurons, Afferent/drug effects/enzymology/*metabolism ; Protein Kinases/*metabolism ; Rhodamines ; Serotonin/pharmacology
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  • 172
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    Regulation of gene expression in hippocampal neurons by distinct calcium signaling pathways (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-09
    Description: Calcium ions (Ca2+) act as an intracellular second messenger and can enter neurons through various ion channels. Influx of Ca2+ through distinct types of Ca2+ channels may differentially activate biochemical processes. N-Methyl-D-aspartate (NMDA) receptors and L-type Ca2+ channels, two major sites of Ca2+ entry into hippocampal neurons, were found to transmit signals to the nucleus and regulated gene transcription through two distinct Ca2+ signaling pathways. Activation of the multifunctional Ca(2+)-calmodulin-dependent protein kinase (CaM kinase) was evoked by stimulation of either NMDA receptors or L-type Ca2+ channels; however, activation of CaM kinase appeared to be critical only for propagating the L-type Ca2+ channel signal to the nucleus. Also, the NMDA receptor and L-type Ca2+ channel pathways activated transcription by means of different cis-acting regulatory elements in the c-fos promoter. These results indicate that Ca2+, depending on its mode of entry into neurons, can activate two distinct signaling pathways. Differential signal processing may provide a mechanism by which Ca2+ controls diverse cellular functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bading, H -- Ginty, D D -- Greenberg, M E -- 2F32 NS 08764/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases ; Cells, Cultured ; DNA-Binding Proteins/genetics ; *Gene Expression Regulation ; Genes, fos ; Glutamates/pharmacology ; Glutamic Acid ; Hippocampus/*metabolism ; Neurons/*metabolism ; Nuclear Proteins/genetics ; Protein Kinases/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Regulatory Sequences, Nucleic Acid ; Second Messenger Systems ; Serum Response Factor ; *Signal Transduction ; Transcription Factors/genetics ; Transfection
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  • 173
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    Tissue engineering (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-05-14
    Description: The loss or failure of an organ or tissue is one of the most frequent, devastating, and costly problems in human health care. A new field, tissue engineering, applies the principles of biology and engineering to the development of functional substitutes for damaged tissue. This article discusses the foundations and challenges of this interdisciplinary field and its attempts to provide solutions to tissue creation and repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langer, R -- Vacanti, J P -- New York, N.Y. -- Science. 1993 May 14;260(5110):920-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge 02319.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Engineering ; *Bioprosthesis ; Cells, Cultured ; Culture Techniques ; Ectoderm ; Endoderm ; Humans ; Mesoderm ; *Tissue Transplantation
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  • 174
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    Development of TH1 CD4+ T cells through IL-12 produced by Listeria-induced macrophages (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-23
    Description: Development of the appropriate CD4+ T helper (TH) subset during an immune response is important for disease resolution. With the use of naive, ovalbumin-specific alpha beta T cell receptor transgenic T cell, it was found that heat-killed Listeria monocytogenes induced TH1 development in vitro through macrophage production of interleukin-12 (IL-12). Moreover, inhibition of macrophage production of IL-12 may explain the ability of IL-10 to suppress TH1 development. Murine immune responses to L. monocytogenes in vivo are of the appropriate TH1 phenotype. Therefore, this regulatory pathway may have evolved to enable innate immune cells, through interactions with microbial pathogens, to direct development of specific immunity toward the appropriate TH phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, C S -- Macatonia, S E -- Tripp, C S -- Wolf, S F -- O'Garra, A -- Murphy, K M -- 1 PO1 A131238-01/PHS HHS/ -- 5 T32 GM07200-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):547-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/8097338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Cell Differentiation ; Cells, Cultured ; Interferon-gamma/secretion ; Interleukin-10/pharmacology ; Interleukin-12 ; Interleukin-2/biosynthesis ; Interleukins/biosynthesis/*immunology/pharmacology ; Listeria monocytogenes/*immunology ; Macrophages/*immunology ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell, alpha-beta/immunology
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  • 175
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    Nonuniform probability of glutamate release at a hippocampal synapse (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-29
    Description: A change in the probability of neurotransmitter release (Pr) is an important mechanism underlying synaptic plasticity. Although Pr is often assumed to be the same for all terminals at a single synapse, this assumption is difficult to reconcile with the nonuniform size and structure of synaptic terminals in the central nervous system. Release probability was measured at excitatory synapses on cultured hippocampal neurons by analysis of the progressive block of N-methyl-D-aspartate receptor-mediated synaptic currents by the irreversible open channel blocker MK-801. Release probability was nonuniform (range of 0.09 to 0.54) for terminals arising from a single axon, the majority of which had a low Pr. However, terminals with high Pr are more likely to be affected by the activity-dependent modulation that occurs in long-term potentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenmund, C -- Clements, J D -- Westbrook, G L -- MH46613/MH/NIMH NIH HHS/ -- NS26494/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):754-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7901909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baclofen/pharmacology ; Cells, Cultured ; Dizocilpine Maleate/pharmacology ; Glutamates/*metabolism ; Glutamic Acid ; Hippocampus/metabolism/*physiology ; Neuronal Plasticity/physiology ; Neurotransmitter Agents/*metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/drug effects/physiology ; Synapses/metabolism ; Synaptic Transmission/drug effects/*physiology
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  • 176
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    Rabies viruses increase in virulence when propagated in neuroblastoma cell culture (1978)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1978-03-10
    Description: Several strains of attenuated rabies virus lacking the capacity to kill adult mice acquired a high lethal potential for mice after one to five serial passages in murine or human neuroblastoma cells. The virulence acquired after passage in neuroblastoma cells is a stable genetic trait retained during subsequent passage of viruses in nonneuroblastoma cell systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, H F -- New York, N.Y. -- Science. 1978 Mar 10;199(4333):1072-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/628831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Mice ; Neuroblastoma/*microbiology ; Neurons/microbiology ; Rabies Vaccines/toxicity ; Rabies virus/genetics/*pathogenicity ; Vaccines, Attenuated/toxicity ; Virus Replication
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  • 177
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    Murine lymphoma-induced immunosuppression: requirement for direct tumour cell contact (1978)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1978-04-07
    Description: The FBL-3 lymphoma cell line caused impaired antibody formation in vivo when injected into mice intraperitoneally, and in vitro when added to normal syngeneic spleen cells immunized in vitro with sheep erythrocytes. Immunosuppression occurred only when intact viable tumor cells were cocultivated with the normal spleen cells. As few as 10(5) FBL-3 cells, when added to 5 X 10(6) normal cells, impaired antibody formation. However, cell-free extracts of filtrates from even much larger numbers of tumor cells did not affect antibody formation, either in vitro or in vivo. Heating the tumor cells at 56 degrees C or irradiation with as little as 1000 rads completely abolished immunosuppressive activity, both in vitro and in vivo. Separation of viable tumor cells from target antibody-forming cells by cell-impermeable membranes prevented immunosuppression, showing that direct cell-to-cell contact is required for immunosuppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cimprich, R S -- Specter, S -- Friedman, H -- New York, N.Y. -- Science. 1978 Apr 7;200(4337):60-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/635572" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibody Formation ; Cell Communication ; Cells, Cultured ; *Immunosuppression ; Lymphoma/*immunology ; Neoplasms, Experimental/immunology
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  • 178
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    Diazepam inhibits myoblast fusion and expression of muscle specific protein synthesis (1978)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1978-05-05
    Description: The presence of diazepam in culutres of chicken embryo myoblasts arrests normal muscle cell differentiation. High concentrations of the drug reversibly prevent myoblasts from fusing to form multinucleated myotubes. Lower concentrations of diazepam allow cell fusion to occur, but inhibit the synthesis and accumulation of myosin heavy chain, implying that cell fusion does not obligate myoblasts to synthesize and accumulate large quantities of muscle specific protein. The effect of diazepam on muscle cells in culture is direct and specific.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandman, E -- Walker, C R -- Strohman, R C -- New York, N.Y. -- Science. 1978 May 5;200(4341):559-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/565534" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Fusion/drug effects ; Cells, Cultured ; Chick Embryo ; Diazepam/*pharmacology ; Dose-Response Relationship, Drug ; Macromolecular Substances ; Muscles/cytology/*drug effects ; Myosins/*biosynthesis
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  • 179
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    Opiate peptide modulation of amino acid responses suggests novel form of neuronal communication (1978)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1978-03-31
    Description: Mouse spinal neurons grown in tissue culture were used to study the electrophysiological pharmacology of the opiate peptide leucine-enkephalin. Enkephalin depressed glutamate-evoked responses in a noncompetitive manner independent of any other effects on membrane properties. The results demonstrate a neuromodulatory action of opiate peptide functionally distinct from the conventional neurotransmitter class of operation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, J L -- Neale, J H -- Smith, T G Jr -- Macdonald, R L -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1451-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/204016" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Endorphins/*pharmacology ; Enkephalins/antagonists & inhibitors/*pharmacology ; Excitatory Amino Acid Antagonists ; Glutamates/*pharmacology ; Iontophoresis ; Naloxone/pharmacology ; Neurons/*drug effects ; Spinal Cord ; Synapses/*drug effects ; Synaptic Transmission/*drug effects
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  • 180
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    Loss of division potential in vitro: aging or differentiation? (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-12-15
    Description: We have examined the hypothesis that diploid cells grown in vitro age, and propose that only proliferative potential and not life-span is telescoped. We suggest that explanted or transplanted diploid cells are driven to divide by the process of subculturing in vitro or in vivo and, in response to this pressure, also complete their differentiation and become refractory to further mitotic stimulation. We conclude that differentiation rather than "mortality" distinguishes diploid from transformed cells and that the former may not age in vitro, but are lost because culture methods are selective for cycling cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, E -- Marek, L F -- Levinstone, D S -- Merrill, C -- Sher, S -- Young, I T -- Eden, M -- New York, N.Y. -- Science. 1978 Dec 15;202(4373):1158-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/725592" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; *Cell Differentiation ; *Cell Division ; *Cell Survival ; Cells, Cultured ; Fibroblasts
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  • 181
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    Neurotrophic protein regulates muscle acetylcholinesterase in culture (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-04-21
    Description: Skeletal muscles lose acetylcholinesterase in culture as a result of denervation. A protein fraction isolated from peripheral nerves maintained the level of acetylcholinesterase in cultures of aneural embryonic muscle or denervated adult chicken muscle. These results indicate that trophic regulation of muscle acetylcholinesterase might be mediated by a protein produced by nerves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, T H -- Markelonis, G J -- New York, N.Y. -- Science. 1978 Apr 21;200(4339):337-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/635593" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/biosynthesis/*metabolism ; Cells, Cultured ; Enzyme Induction/drug effects ; Muscle Denervation ; Muscles/*enzymology ; Nerve Tissue Proteins/*pharmacology ; Peripheral Nerves/*physiology
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  • 182
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    Different actions of anticonvulsant and anesthetic barbiturates revealed by use of cultured mammalian neurons (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-05-19
    Description: Barbiturate anesthetics, but not anticonvulsants, abolish the spontaneous activity of cultured spinal cord neurons; directly increase membrane conductance, an effect which is suppressed by the gamma-aminobutyric acid (GABA) antagonists picrotoxin and penicillin; and are more potent than anticonvulsants in augmenting GABA and depressing glutamate responses. Barbiturate anticonvulsants abolish picrotoxin-induced convulsive activity. These results indicate qualitative and quantitative differences between anesthetic and anticonvulsant barbiturates, which may explain their different clinical effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macdonald, R L -- Barker, J L -- New York, N.Y. -- Science. 1978 May 19;200(4343):775-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/205953" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Cells, Cultured ; Electric Conductivity ; Glutamates/pharmacology ; Membrane Potentials/drug effects ; Neurons/*drug effects ; Pentobarbital/*pharmacology ; Phenobarbital/*pharmacology ; Picrotoxin/pharmacology ; Receptors, Neurotransmitter/drug effects ; gamma-Aminobutyric Acid/pharmacology
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  • 183
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    Specific-opiate-induced depression of transmitter release from dorsal root ganglion cells in culture (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-03-31
    Description: The opiate etorphine depresses monosynaptic excitatory postsynaptic potentials (EPSP's) elicited in spinal cord cells by activation of dorsal root ganglion cells in murine neuronal cell culture. The depression is reversed by naloxone. Statistical analysis of the synaptic responses reveals that the opiate reduces EPSP quantal content at this synapse without altering quantal size. Therefore, the opiate action is presynaptic and affects transmitter release rather than postsynaptic responsiveness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macdonald, R L -- Nelson, P G -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1449-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/204015" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Depression, Chemical ; Dose-Response Relationship, Drug ; Etorphine/*pharmacology ; Ganglia, Spinal/*drug effects ; Membrane Potentials/drug effects ; Morphinans/*pharmacology ; Naloxone/pharmacology ; Nerve Endings/drug effects ; Spinal Cord/drug effects ; Synapses/drug effects ; Synaptic Transmission/*drug effects
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  • 184
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    Potent antidopaminergic activity of estradiol at the pituitary level on prolactin release (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-06-09
    Description: Prior incubation of rat anterior pituitary cells with 17beta-estradiol led to an almost complete reversal of the inhibitory effect of two dopamine agonists, dihydroergocornine and RU 24213, on both basal prolactin release and thyrotropin releasing hormone-induced prolactin release. These experiments thus demonstrate a direct interference of dopamine action by a peripheral hormone. Prolactin secretion by pituitary cells in primary culture could possibly serve as an easily accessible model of a system under dopaminergic control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raymond, V -- Beaulieu, M -- Labrie, F -- Boissier, J -- New York, N.Y. -- Science. 1978 Jun 9;200(4346):1173-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/418505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dihydroergotoxine/antagonists & inhibitors ; *Dopamine Antagonists ; Estradiol/*pharmacology ; Female ; Phenethylamines/antagonists & inhibitors ; Pituitary Gland, Anterior/*drug effects/secretion ; Prolactin/*secretion ; Rats ; Thyrotropin-Releasing Hormone/pharmacology
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  • 185
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    Nature and nurture in development of the autonomic neuron (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-03-31
    Description: Arguments are presented for the hypothesis that during an early stage of development the cells which become principal neurons of the autonomic nervous system possess information regarding the positions they will occupy within the body. A second stage of development, during which a decision is made regarding which neurotransmitter to employ, is delayed until each neuron has assumed its permanent position in the body and has sampled, presumably via its growing axons, the peripheral field which it will innervate. The development of cholinergic mechanisms takes precedence; adrenergic neurons may develop only when cholinergic sites have been occupied. An extended period during which the differentiation of transmitter mechanisms may be modulated permits the neuron to adequately sample the periphery prior to commitment to a specific transmitter economy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bunge, R -- Johnson, M -- Ross, C D -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1409-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24273" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/cytology ; Animals ; Autonomic Nervous System/*embryology/growth & development ; Cell Differentiation ; Cells, Cultured ; Chimera ; Cholinergic Fibers/cytology ; Embryonic Induction ; Ganglia, Autonomic/cytology ; Heart/innervation ; Intestines/innervation ; Nerve Endings/ultrastructure ; Neurotransmitter Agents/metabolism ; Phylogeny ; Synaptic Vesicles/ultrastructure
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  • 186
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    Metabolism of theophylline to caffeine in human fetal liver (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-12-14
    Description: Caffeine (1,3,7-trimethylxanthine) is a biotransformation product of theophylline (1,3-dimethylxanthine) in the human fetus. Liver explants, obtained from human fetuses with gestational ages of 12 to 20 weeks, were incubated with theophylline and produced caffeine and, in lesser amounts, 1,3-dimethyluric acid and 3-methylxanthine. These findings suggest that the predominant pathway in theophylline metabolism in the fetus and newborn infant is the methylation reaction producing caffeine. This may contribute to the neonate's exceedingly slower elimination of caffeine relative to theophylline. Caffeine produced from theophylline may add to the pharmacologic effects of theophylline in newborn infants with apnea.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aranda, J V -- Louridas, A T -- Vitullo, B B -- Thom, P -- Aldridge, A -- Haber, R -- New York, N.Y. -- Science. 1979 Dec 14;206(4424):1319-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/515734" target="_blank"〉PubMed〈/a〉
    Keywords: Apnea/drug therapy ; Biotransformation ; Caffeine/*biosynthesis/metabolism/therapeutic use ; Cells, Cultured ; Gestational Age ; Humans ; Infant, Newborn ; Liver/*embryology/metabolism ; Methylation ; Theophylline/*metabolism/therapeutic use
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  • 187
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    Enhanced 5-fluorouracil nucleotide formation after methotrexate administration: explanation for drug synergism (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-09-14
    Description: Exposure of L1210 leukemia cells first to 0.1 to 100 micromolar methotrexate and then to 10 micromolar 5-fluorouracil produces a synergistic effect on the number of cells killed in culture. Methotrexate dose-related increases occur in the concentrations of intracellular 5-fluorouracil ribonucleotides and 5-fluoro-2'-deoxyuridylate and in the incorporation of 5-fluorouracil into RNA. These increases are correlated with increased concentrations of intracellular phosphoribosylpyrophosphate. It is proposed that the enhanced formation of ribonucleotides of 5-fluorouracil and the subsequent incorporation of these compounds into RNA in methotrexate-treated cells may account for synergism between these agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cadman, E -- Heimer, R -- Davis, L -- New York, N.Y. -- Science. 1979 Sep 14;205(4411):1135-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/472732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Drug Administration Schedule ; Drug Synergism ; Fluorouracil/metabolism/*pharmacology ; Leukemia L1210 ; Methotrexate/*pharmacology ; Mice ; Phosphoribosyl Pyrophosphate/metabolism ; RNA, Neoplasm/metabolism ; Ribonucleotides/metabolism ; Thymidylate Synthase/metabolism
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  • 188
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    Neuronal chemotaxis: chick dorsal-root axons turn toward high concentrations of nerve growth factor (1979)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1979-11-30
    Description: Micropipettes containing 2 to 50 biological units of beta growth factor (NGF) were placed near growing axons of chick dorsal-root ganglion neurons in tissue culture. The axons turned and grew toward the NGF source within 21 minutes. This turning response to elevated concentrations of NGF appears to represent chemotactic guidance rather than a general enhancement of growth rate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gundersen, R W -- Barrett, J N -- New York, N.Y. -- Science. 1979 Nov 30;206(4422):1079-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/493992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/growth & development/*physiology ; Cells, Cultured ; *Chemotaxis/drug effects ; Chick Embryo ; Dose-Response Relationship, Drug ; Ganglia, Spinal/physiology ; Nerve Growth Factors/*pharmacology
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  • 189
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    Specific nonopiate receptors for beta-endorphin (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-09-07
    Description: Iodinated beta H-[2-D-alanine]endorphin exhibits specific binding to cultured human lymphocytes. The binding is inhibited by low concentrations of beta-endorphin and its D-alanine derivative, but is not affected by opiate agonists and antagonists, or by enkephalin analogs, beta-lipotropin, adrenocorticotrophic hormone, or alpha-melanocyte-stimulating hormone; this suggests the existence of a specific, non-opiate binding site (receptor) for beta-endorphin. The carboxy-terminal region of beta-endorphin is essential for this binding activity, since alpha-endorphin is not active. beta-Endorphin may be a circulating hormone with peripheral physiological effects that are not primarily mediated through interactions with opiate or enkephalin receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hazum, E -- Chang, K J -- Cuatrecasas, P -- New York, N.Y. -- Science. 1979 Sep 7;205(4410):1033-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/224457" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cells, Cultured ; Endorphins/blood/*metabolism ; Humans ; Lymphocyte Activation ; Lymphocytes/*metabolism ; Receptors, Drug/*metabolism ; Receptors, Opioid/metabolism ; Stress, Physiological/metabolism ; Structure-Activity Relationship
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  • 190
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    Inosine may be an endogenous ligand for benzodiazepine receptors on cultured spinal neurons (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-08-17
    Description: Mouse spinal neurons grown in tissue culture were used to study the membrane effects of the benzodiazepine flurazepam and the naturally occurring purine nucleoside inosine, which competes for benzodiazepine receptor sites in the central nervous system. Application of inosine elicited two types of transmitter-like membrane effects: a rapidly desensitizing excitatory response and a nondesensitizing inhibitory response. Flurazepam produced a similar excitatory response which showed cross-desensitization with the purine excitation. Flurazepam also blocked the inhibitory inosine response. The results provide electrophysiological evidence that an endogenous purine can activate two different conductances on spinal neurons and that flurazepam can activate one of the conductances and antagonize the other.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacDonald, J F -- Barker, J L -- Paul, S M -- Marangos, P J -- Skolnick, P -- New York, N.Y. -- Science. 1979 Aug 17;205(4407):715-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/37602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/*metabolism ; Cells, Cultured ; Electric Conductivity ; Flurazepam/antagonists & inhibitors ; Inosine/*metabolism/pharmacology ; Ligands ; Mice ; Neurotransmitter Agents/metabolism ; Receptors, Drug/*metabolism ; Receptors, Neurotransmitter/metabolism ; Spinal Cord/*metabolism
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  • 191
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    New information about the development of the autonomic nervous system (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1979 Oct 26;206(4417):434-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/41320" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Adrenergic Fibers/growth & development ; Animals ; Autonomic Nervous System/*growth & development ; Cell Communication ; Cell Differentiation ; Cells, Cultured ; Cholinergic Fibers/growth & development ; Nerve Growth Factors/physiology ; Neural Crest/cytology ; Neural Pathways/growth & development ; Neurotransmitter Agents/*metabolism ; Synaptic Transmission
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  • 192
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    DNA synthesis and mitosis in adult amphibian cardiac muscle cells in vitro (1979)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1979-09-21
    Description: High-resolution autoradiography and fine structural analysis of adult newt heart tissue in long-term culture revealed that tritiated thymidine was concentrated in the nuclei of dedifferentiated myocardial cells. Mitotic chromosomes were observed in some of these cells. This demonstrates that adult amphibian myocardial cells in vitro are capable of DNA synthesis and mitosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nag, A C -- Healy, C J -- Cheng, M -- New York, N.Y. -- Science. 1979 Sep 21;205(4412):1281-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/472744" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cells, Cultured ; DNA/*biosynthesis ; *Mitosis ; Muscle Proteins/metabolism ; Myocardial Contraction ; Myocardium/*metabolism ; Salamandridae ; Time Factors
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  • 193
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    Substance P: evidence for diverse roles in neuronal function from cultured mouse spinal neurons (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-09-28
    Description: Mouse spinal neurons grown in tissue culture were used to examine the membrane mechanisms of action of the peptide substance P. Two functionally distinct actions were observed, one being a rapidly desensitizing excitation, and the other being a dose-dependent, reversible depression of excitatory responses to the putative amino acid neurotransmitter glutamate. These effects on excitability suggest that substance P may play more than one role in intercellular communication in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vincent, J D -- Barker, J L -- New York, N.Y. -- Science. 1979 Sep 28;205(4413):1409-12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/224464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cells, Cultured ; Electric Conductivity ; Excitatory Amino Acid Antagonists ; Glutamates/pharmacology ; Membrane Potentials ; Mice ; Neural Inhibition ; Spinal Cord/cytology/*physiology ; Substance P/*physiology ; Synaptic Transmission
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  • 194
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    Deficiencies of glucosamine-6-sulfate or galactosamine-6-sulfate sulfatases are responsible for different mucopolysaccharidoses (1978)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1978-01-06
    Description: [1-3H]Galactitol-6-sulfate, N- [1-3H]acetylgalactosaminitol-6-sulfate, N-[1-3H]acetylglucosaminitol-6-sulfate, N-acetylglucosamine-6-sulfate, and 6-sulfated tetrasaccharides from chondroitin-6-sulfate have been used for the measurement of 6-sulfatase activity of extracts of normal skin fibroblasts and of fibroblasts cultured from patients with genetic mucopolysaccharidoses. With these substrates, extracts of fibroblasts derived from Morquio patients lack or have greatly reduced activities for galactitol-6-sulfate, N-acetylgalactosaminitol-6-sulfate, and 6-sulfated tetrasaccharides but have normal activity for N-acetylglucosamine-6-sulfate and its alditol; those derived from a patient with a newly discovered mucopolysaccharidosis have greatly reduced activity for N-acetylglucosamine-6-sulfate and its alditol but normal activity for galactitol-6-sulfate, N-acetylgalactosaminitol-6-sulfate, and the 6-sulfated tetrasaccharides. These findings demonstrate the existence of two different hexosamine-6-sulfate sulfatases, specific for the glucose or galactose configuration of their substrates. Their respective deficiencies, causing inability to degrade keratan sulfate and heparan sulfate in one case and keratan sulfate and chondroitin-6-sulfate in the other, are responsible for different clinical phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Ferrante, N -- Ginsberg, L C -- Donnelly, P V -- Di Ferrante, D T -- Caskey, C T -- New York, N.Y. -- Science. 1978 Jan 6;199(4324):79-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratories of Connective Tissue Research, Department of Biochemistry, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569489" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylgalactosamine/analogs & derivatives/metabolism ; Acetylglucosamine/analogs & derivatives/metabolism ; Cells, Cultured ; Child, Preschool ; Chondroitin Sulfates/metabolism ; Chondroitinsulfatases/*deficiency/metabolism ; Fibroblasts/enzymology ; Galactitol/metabolism ; Heparitin Sulfate/metabolism ; Humans ; Hydrogen-Ion Concentration ; Keratan Sulfate/metabolism ; Male ; Mucopolysaccharidoses/*enzymology ; Mucopolysaccharidosis III/enzymology ; Mucopolysaccharidosis IV/*enzymology ; Skin/cytology/enzymology ; Substrate Specificity ; Sulfatases/*deficiency/metabolism
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  • 195
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    Age affect and replicative life-span of fibroblasts of diabetic, prediabetic, and normal donors: another look at the data (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gleason, R E -- Goldstein, S -- New York, N.Y. -- Science. 1978 Dec 15;202(4373):1217-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/725599" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; *Aging ; Cell Division ; Cell Survival ; Cells, Cultured ; Diabetes Mellitus/*physiopathology ; Humans ; Middle Aged ; Prediabetic State/*physiopathology
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  • 196
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    Entry of insulin into human cultured lymphocytes: electron microscope autoradiographic analysis (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-11-17
    Description: Electron microscope autoradiographs were prepared of IM-9 human cultured lymphocytes incubated with iodine-125-labeled insulin. With the use of [125I]insulin and Ilford L-4 emulsion, the technique had a resolution half-distance of approximately 0.085 micrometer. Autoradiographs revealed a time-dependent entry of insulin into the cell interior that was maximal after 30 minutes of incubation. At this time point nearly 40 percent of the [125I]insulin was in the interior of the cell at a distance 1 micrometer or greater from the plasma membrane. Grain distribution and volume density analyses revealed that the intracellular insulin was concentrated in the endoplasmic reticulum and nuclear membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldfine, I D -- Jones, A L -- Hradek, G T -- Wong, K Y -- Mooney, J S -- New York, N.Y. -- Science. 1978 Nov 17;202(4369):760-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/715440" target="_blank"〉PubMed〈/a〉
    Keywords: Autoradiography ; Biological Transport ; Cell Nucleus/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/metabolism ; Humans ; Insulin/*metabolism ; Kinetics ; Lymphocytes/*metabolism
    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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  • 197
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    Chronologic and physiologic age affect replicative life-span of fibroblasts from diabetic, prediabetic, and normal donors (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-02-17
    Description: Cultured skin fibroblasts from subjects with clinically apparent diabetes mellitus and from subjects genetically predisposed to diabetes have a replicative lifespan that is inversely related to donor age. Fibroblasts from carefully defined normal subjects not predisposed to diabetes fail to show this correlation. The data support the idea that physiologic status of the tissue donor is a more precise determinant of fibroblast replicative lifespan than chronologic age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldstein, S -- Moerman, E J -- Soeldner, J S -- Gleason, R E -- Barnett, D M -- New York, N.Y. -- Science. 1978 Feb 17;199(4330):781-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/622567" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; *Aging ; Cell Division ; Cell Survival ; Cells, Cultured ; Diabetes Mellitus/pathology/*physiopathology ; Fibroblasts/*cytology/pathology ; Humans ; Middle Aged ; Prediabetic State/pathology/*physiopathology ; Regression Analysis ; Skin/cytology/pathology
    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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  • 198
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    Pattern formation by cultured human epidermal cells: development of curved ridges resembling dermatoglyphs (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-06-23
    Description: In cultures made from disaggregated human epidermal cells, growth to a confluent cell layer is followed by the emergence of patterns resembling those of human dermatoglyphs. These patterns reflect intrinsic properties of kertinocytes. In vivo, only the epidermis of the volar surfaces forms patterns, but in culture, patterns are formed by epidermal cells from other sites as well. Patterns develop by a process of cell movement which first produces ridges and then curves the ridges into figures of increasing complexity, ultimately whorls.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, H -- Thomas, J -- New York, N.Y. -- Science. 1978 Jun 23;200(4348):1385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/663617" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Movement ; Cells, Cultured ; *Dermatoglyphics ; Embryonic Induction ; Epidermis/*cytology ; Fibroblasts/cytology ; Humans ; Time Factors
    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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  • 199
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    Lichen myxedematosus serum stimulates human skin fibroblast proliferation (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-02-03
    Description: Serum from patients with lichen myxedematosus, when added to exponentially growing normal human skin fibroblasts, stimulates DNA synthesis and cell proliferation. The degree of response in vitro is correlated with the extent of the disease in vivo and is specific for fibroblasts. The results suggest that there is a systemic factor (or factors) which may play a role in the etiology of diseases affecting the connective tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harper, R A -- Rispler, J -- New York, N.Y. -- Science. 1978 Feb 3;199(4328):545-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/622555" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cells, Cultured ; Female ; Fibroblasts/metabolism ; Humans ; Immunoglobulin G/analysis ; Male ; Middle Aged ; Skin Diseases/*blood/immunology/pathology ; Thymidine/metabolism
    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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  • 200
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    Chemotactic antibody (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-05-05
    Description: Antibody of the immunoglobulin G class to herpes simplex virus and antibody of the immunoglobulin M class to sheep red blood cells were coupled to the synthetic peptide formylmethionylleucylphenylalanine (fMet-Leu-Phe), which is chemotactic for both mononuclear and polymorphonuclear leukocytes. The resulting molecules were chemotactic and retained their antigen-binding activity. When antibodies coupled to fMet-Leu-Phe were incubated with antigen, the resulting immune complexes were also chemotactic. Chemotactic antibody may provide a potent means of enhancing the migration of inflammatory cells to specific sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isturiz, M A -- Sandberg, A L -- Schiffmann, E -- Wahl, S M -- Notkins, A L -- New York, N.Y. -- Science. 1978 May 5;200(4341):554-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/205950" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibodies ; Antibodies, Viral ; Antigen-Antibody Complex ; Cells, Cultured ; Chemotaxis, Leukocyte/*drug effects ; Erythrocytes/immunology ; Immunoglobulin G ; Immunoglobulin M ; Inflammation/immunology ; Oligopeptides/*pharmacology ; Simplexvirus/immunology
    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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