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  • Articles  (105)
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  • American Association for the Advancement of Science (AAAS)  (105)
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  • Articles  (105)
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  • American Association for the Advancement of Science (AAAS)  (105)
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  • 1
    Publication Date: 1993-01-01
    Description: A myelin-associated protein from the central nervous system, the neurite growth inhibitor NI-35, inhibits regeneration of lesioned neuronal fiber tracts in vivo and growth of neurites in vitro. Growth cones of cultured rat dorsal root ganglion neurons arrested their growth and collapsed when exposed to liposomes containing NI-35. Before morphological changes, the concentration of free intracellular calcium ([Ca2+]i) showed a rapid and large increase in growth cones exposed to liposomes containing NI-35. Neither an increase in [Ca2+]i nor collapse of growth cones was detected in the presence of antibodies to NI-35. Dantrolene, an inhibitor of calcium release from caffeine-sensitive intracellular calcium stores, protected growth cones from collapse evoked by NI-35. Depletion of these caffeine-sensitive intracellular calcium stores prevented the increase in [Ca2+]i evoked by NI-35. The NI-35-evoked cascade of intracellular messengers that mediates collapse of growth cones includes the crucial step of calcium release from intracellular stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandtlow, C E -- Schmidt, M F -- Hassinger, T D -- Schwab, M E -- Kater, S B -- NS24683/NS/NINDS NIH HHS/ -- NS28323/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Institute, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Drug Carriers ; Fura-2 ; Ganglia, Spinal/*physiology ; Growth Inhibitors/*pharmacology ; Kinetics ; Liposomes ; Nerve Fibers/drug effects/*physiology/ultrastructure ; Neurons/drug effects/*physiology/ultrastructure ; Rats
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  • 2
    Publication Date: 1993-10-15
    Description: In cystic fibrosis (CF), absence or dysfunction of a phosphorylation-regulated chloride channel [CF transmembrane conductance regulator (CFTR)] leads to the loss or reduction of chloride secretion into the airways. Active sodium absorption is also increased in CF, and both of these ion transport changes could alter fluid transport across the airways. Under baseline conditions, cultured human airway epithelia from normal individuals absorbed fluid, and this absorption was increased in epithelia from patients with CF. In normal and CF epithelial cultures fluid absorption was inhibited by amiloride. Adenosine 3',5'-monophosphate stimulated fluid secretion in normal epithelial cultures but not in cultures from individuals with CF. In contrast, fluid secretion induced by nucleotide triphosphates (uridine triphosphate or adenosine triphosphate) was unaltered in cultures of epithelia from patients with CF, suggesting an approach to the treatment of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, C -- Finkbeiner, W E -- Widdicombe, J H -- McCray, P B Jr -- Miller, S S -- HL 42368/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211164" target="_blank"〉PubMed〈/a〉
    Keywords: Absorption ; Adenosine Triphosphate/pharmacology ; Adolescent ; Adult ; Amiloride/pharmacology ; Body Fluids/*metabolism ; Cells, Cultured ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*metabolism ; Epithelial Cells ; Epithelium/metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa/cytology/*metabolism ; Sodium/metabolism ; Sodium Channels/metabolism ; Trachea/cytology/*metabolism ; Uridine Triphosphate/pharmacology
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  • 3
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):762-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/physiology ; Caenorhabditis elegans/embryology/genetics ; Cell Death/*physiology ; Cells, Cultured ; Embryo, Nonmammalian/physiology ; Nerve Growth Factors/physiology ; Nervous System/cytology/*embryology ; Neurons/cytology/*physiology ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-07-02
    Description: Histamine is a neuromodulator in the brain, and the hippocampus is one of the regions of the brain that is innervated by histaminergic neurons. When applied to cultured hippocampal neurons, histamine selectively increased by up to tenfold the amplitude of the component of synaptic transmission that was mediated by N-methyl-D-aspartate (NMDA) receptors. Spontaneous miniature synaptic currents and the current elicited by applied NMDA also were enhanced, indicating that the histamine effect was expressed primarily postsynaptically. These results suggest that histamine may modulate processes involving NMDA receptors, such as the induction of long-term potentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekkers, J M -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, John Curtin School of Medical Research, Australian National Univresity, Canberra, ACT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Hippocampus/cytology/drug effects/*physiology ; Histamine/*pharmacology ; Ion Channel Gating/drug effects ; N-Methylaspartate/*metabolism/pharmacology ; Rats ; Receptors, Histamine/physiology ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Transmission/*drug effects ; Virulence Factors, Bordetella/pharmacology
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-07-02
    Description: The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Vila, M P -- Durum, S K -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):93-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; *DNA-Binding Proteins ; Gene Expression ; *Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, RAG-1 ; Hematopoietic Cell Growth Factors/pharmacology ; Interleukin-7/*pharmacology ; Ionomycin/pharmacology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Proteins/genetics ; Stem Cell Factor ; T-Lymphocytes/cytology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/embryology/immunology ; Tumor Cells, Cultured
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  • 7
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    American Association for the Advancement of Science (AAAS)
    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
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  • 8
    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
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  • 9
    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
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  • 10
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    American Association for the Advancement of Science (AAAS)
    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
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  • 11
    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
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  • 12
    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
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  • 13
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    American Association for the Advancement of Science (AAAS)
    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
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  • 14
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    American Association for the Advancement of Science (AAAS)
    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
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  • 15
    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
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  • 16
    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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  • 17
    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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  • 18
    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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  • 19
    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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  • 20
    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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  • 21
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    American Association for the Advancement of Science (AAAS)
    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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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉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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  • 23
    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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  • 24
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    American Association for the Advancement of Science (AAAS)
    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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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1993-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉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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  • 26
    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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  • 27
    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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  • 28
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    American Association for the Advancement of Science (AAAS)
    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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  • 29
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    American Association for the Advancement of Science (AAAS)
    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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  • 30
    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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  • 31
    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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  • 32
    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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  • 33
    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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  • 34
    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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  • 35
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    American Association for the Advancement of Science (AAAS)
    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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  • 36
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    American Association for the Advancement of Science (AAAS)
    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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  • 37
    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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  • 38
    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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  • 39
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    American Association for the Advancement of Science (AAAS)
    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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  • 40
    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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  • 41
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    American Association for the Advancement of Science (AAAS)
    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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  • 42
    Publication Date: 1987-10-23
    Description: Exposure to bacterial endotoxins has long been known to stimulate the release of anterior pituitary hormones; administration of endotoxin was at one time a common clinical test of anterior pituitary function. Endotoxin is a potent stimulus for production of the endogenous pyrogenic protein, interleukin-1 (IL-1), by macrophages and monocytes. The possibility that IL-1 has a direct effect on the secretion of hormones by rat pituitary cells in a monolayer culture was investigated. Recombinant human IL-1 beta stimulated the secretion of adrenocorticotropic hormone, luteinizing hormone, growth hormone, and thyroid-stimulating hormone. Increased hormone secretion into culture supernatants was found with IL-1 concentrations ranging from 10(-9) M to 10(-12) M. Prolactin secretion by the monolayers was inhibited by similar doses. These concentrations of IL-1 are within the range reported for IL-1 in serum, suggesting that IL-1 generated peripherally by mononuclear immune cells may act directly on anterior pituitary cells to modulate hormone secretion in vivo. Incubation of IL-1 solutions with antibody to IL-1 neutralized these actions. These pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernton, E W -- Beach, J E -- Holaday, J W -- Smallridge, R C -- Fein, H G -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):519-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropsychiatry, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821620" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Cells, Cultured ; Dinoprostone ; Female ; Growth Hormone/secretion ; Humans ; Infection/physiopathology ; Inflammation/physiopathology ; Interleukin-1/*physiology ; Luteinizing Hormone/secretion ; Pituitary Gland, Anterior/*secretion ; Pituitary Hormones, Anterior/*secretion ; Prolactin/secretion ; Prostaglandins E/secretion ; Rats ; Rats, Inbred Strains ; Recombinant Proteins/pharmacology ; Thyrotropin/secretion
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  • 43
    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
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  • 44
    Publication Date: 1987-10-09
    Description: Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, S E -- Wright, J A -- Jarolim, L -- Yanagihara, K -- Bassin, R H -- Greenberg, A H -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; *Genes ; Mice ; *Neoplasm Metastasis ; *Oncogenes ; Phenotype ; Protein Kinases/*genetics
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  • 45
    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 46
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-05-15
    Description: Neoplasms produce substances that induce blood vessel formation (angiogenesis). Fractions from ethanol extracts of the Walker 256 carcinoma were isolated by silica column chromatography and C18 reversed-phase high-performance liquid chromatography. Two of the isolated fractions induced neovascularization when tested in the rabbit corneal micropocket assay. One of the fractions was identified as nicotinamide by desorption-electron impact mass spectrometry, nuclear magnetic resonance spectroscopy, and gas chromatography-mass spectrometry. The second active fraction contained nicotinamide as part of a more complex, as yet unidentified, molecular arrangement. Microgram quantities of commercial nicotinamide induced neovascularization in the corneal micropocket assay and in the chick chorioallantoic membrane assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kull, F C Jr -- Brent, D A -- Parikh, I -- Cuatrecasas, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437656" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification/pharmacology ; Animals ; Carcinoma 256, Walker/*physiopathology ; Cells, Cultured ; Chick Embryo ; Cornea/blood supply ; Endothelium/cytology/drug effects ; Gas Chromatography-Mass Spectrometry ; Growth Substances/*isolation & purification ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Mice ; Neovascularization, Pathologic ; Niacinamide/isolation & purification/pharmacology
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  • 47
    Publication Date: 1987-10-02
    Description: Epidermal growth factor (EGF) is a potent polypeptide mitogen originally isolated from the adult male mouse submaxillary gland. It also acts as a gastrointestinal hormone. EGF-immunoreactive material has recently been identified within neuronal fibers and terminals in rodent brain. In the present study, EGF was found to enhance survival and process outgrowth of primary cultures of subneocortical telencephalic neurons of neonatal rat brain in a dose-dependent manner. This effect was observed with EGF concentrations as low as 100 picograms per milliliter (0.016 nanomolar) and was dependent on the continuous presence of EGF in the medium. Similar effects were observed with basic fibroblast growth factor, but several other growth-promoting substances, including other mitogens for glial elements, were without effect. Thus EGF, in addition to its mitogenic and hormonal activities, may act as a neurite elongation and maintenance factor for select neurons of the rodent central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, R S -- Kornblum, H I -- Leslie, F M -- Bradshaw, R A -- NS19319/NS/NINDS NIH HHS/ -- NS19964/NS/NINDS NIH HHS/ -- T32-CA0905A/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 2;238(4823):72-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, College of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/*cytology ; Cell Survival/drug effects ; Cells, Cultured ; Epidermal Growth Factor/*physiology ; Growth Substances/pharmacology ; Rats
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  • 48
    Publication Date: 1987-07-10
    Description: Inhibin is a gonadal glycoprotein hormone that regulates the production of follicle-stimulating hormone (FSH) by the anterior pituitary gland and exhibits intragonadal actions as well. The present study shows that inhibin-like immunoreactivity (inhibin-LI) is present in cells of the cytotrophoblast layer of human placenta at term and in primary cultures of human trophoblasts. Human chorionic gonadotropin (hCG) stimulated secretion of inhibin-LI from these cultured placental cells. This effect was mimicked by 8-bromo-cyclic adenosine monophosphate (8-bromo-cAMP), forskolin, and cholera toxin, suggesting that the mechanism of hCG induction of placental inhibin-LI secretion is cAMP-dependent. Incubation with an antiserum that binds the alpha-subunit of human inhibin increased the secretion of hCG and gonadotropin-releasing hormone-like immunoreactivity (GnRH-LI) from trophoblast cells in culture, suggesting a local tonic inhibitory action of endogenous inhibin on hCG and GnRH-LI release. The action of inhibin on hCG secretion may partially require the presence of placental GnRH, as suggested by evidence that a synthetic GnRH antagonist partially reverses the hCG increase induced by inhibin immunoneutralization. Results suggest paracrine roles for both inhibin and GnRH in the regulation of placental hCG production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petraglia, F -- Sawchenko, P -- Lim, A T -- Rivier, J -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- HD13527/HD/NICHD NIH HHS/ -- NS21182/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):187-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299703" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Cells, Cultured ; Cholera Toxin/pharmacology ; Chorionic Gonadotropin/pharmacology/*secretion ; Chorionic Villi/analysis ; Colforsin/pharmacology ; Feedback ; Female ; Gonadotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/secretion ; Humans ; Infant, Newborn ; Inhibins/analysis/*physiology ; Male ; Pregnancy ; Secretory Rate/drug effects ; Trophoblasts/analysis/drug effects/*secretion
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  • 49
    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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  • 50
    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
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  • 51
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-18
    Description: The traditional view that quantal release of neurotransmitter results from the fusion of transmitter-containing vesicles with the neuronal membrane has been recently challenged. Although various alternative mechanisms have been proposed, a common element among them is the release of cytoplasmic transmitter, which, in one view, could occur through large conductance channels on the presynaptic membrane. Six nerve-muscle cell pairs were examined with a whole-cell patch clamp for the presence of such channels that are associated with the production of miniature end-plate potentials. Examination of the neuronal membrane current during the occurrence of 822 miniature end-plate potentials produced no evidence of large channels. Thus it is unlikely that quantal release is mediated by such channels in the neuromuscular junction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, S H -- Chow, I -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1712-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2891190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; Cells, Cultured ; Membrane Potentials ; Motor Endplate/cytology/*physiology ; Neuromuscular Junction/*physiology ; Neurons/cytology/*physiology ; Neurotransmitter Agents/*secretion ; Xenopus
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  • 52
    Publication Date: 1987-08-21
    Description: The genome of the human immunodeficiency virus HIV-1 contains at least eight genes, of which three (sor, R, and 3' orf) have no known function. In this study, the role of the sor gene was examined by constructing a series of proviral genomes of HIV-1 that either lacked the coding sequences for sor or contained point mutations in sor. Analysis of four such mutants revealed that although each clone could generate morphologically normal virus particles upon transfection, the mutant viruses were limited in their capacity to establish stable infection. Virus derived from transfection of Cos-1 cells (OKT4-) with sor mutant proviral DNA's was resistant to transmission to OKT4+ "susceptible" cells under cell-free conditions, and was transmitted poorly by coculture. In contrast, virus derived from clones with an intact sor frame was readily propagated by either approach. Normal amounts of gag-, env-, and pol-derived proteins were produced by all four mutants and assays in both lymphoid and nonlymphoid cells indicated that their trans-activating capacity was intact and comparable with wild type. Thus the sor gene, although not absolutely required in HIV virion formation, influences virus transmission in vitro and is crucial in the efficient generation of infectious virus. The data also suggest that sor influences virus replication at a novel, post-translational stage and that its action is independent of the regulatory genes tat and trs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ensoli, B -- Ivanoff, L -- Chamberlain, M -- Petteway, S -- Ratner, L -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):888-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cells, Cultured ; Cercopithecus aethiops ; Cytopathogenic Effect, Viral ; Genes, Viral ; HIV/*genetics ; T-Lymphocytes/microbiology ; Viral Proteins/*physiology ; *Virus Replication
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  • 53
    Publication Date: 1987-01-16
    Description: Second messenger systems may modulate neuronal activity through protein phosphorylation. However, interactions between two major second messenger pathways, the cyclic AMP and phosphatidylinositol systems, are not well understood. The effects of activators of cyclic AMP-dependent protein kinase and protein kinase C on resting membrane properties, action potentials, and currents recorded from mouse dorsal root ganglion neurons and cerebral hemisphere neurons grown in primary dissociated cell culture were investigated. Neither forskolin (FOR) nor phorbol 12,13-dibutyrate (PDBu) altered resting membrane properties but both increased the duration of calcium-dependent action potentials in both central and peripheral neurons. By means of the single-electrode voltage clamp technique, FOR and PDBu were shown to decrease the same voltage-dependent potassium conductance. This suggests that two independent second messenger systems may affect the same potassium conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grega, D S -- Werz, M A -- Macdonald, R L -- NS 07231/NS/NINDS NIH HHS/ -- NS 19613/NS/NINDS NIH HHS/ -- NS 19692/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):345-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432663" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Brain/cytology ; Calcium/physiology ; Cells, Cultured ; Colforsin/*pharmacology ; Electric Conductivity ; Ganglia, Spinal/cytology ; Ion Channels/physiology ; Membrane Potentials ; Mice ; Neurons/drug effects/*physiology ; Phorbol Esters/*pharmacology ; Potassium/*physiology
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  • 54
    Publication Date: 1987-08-07
    Description: Human peripheral blood eosinophils, cells often associated with allergic and parasitic diseases, were maintained in vitro for at least 14 days when they were cocultured with bovine endothelial cells and for at least 7 days when cultured with either bovine or human endothelial cell-derived conditioned medium. The cocultured eosinophils became hypodense and generated about three times as much leukotriene C4 upon activation with calcium ionophore and killed about three times as many antibody-coated larvae of Schistosoma mansoni as freshly isolated normodense eosinophils. That these cells can be maintained in vitro by coculture with endothelial cells, and the surprising finding that the cocultured eosinophils have biochemical, cytotoxic, and density properties similar to those of eosinophils in patients with allergic and other disorders, will facilitate investigation of the regulation and role of these cells in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothenberg, M E -- Owen, W F Jr -- Silberstein, D S -- Soberman, R J -- Austen, K F -- Stevens, R L -- AI-22531/AI/NIAID NIH HHS/ -- AI-23483/AI/NIAID NIH HHS/ -- AM-01401/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):645-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3110954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Dependent Cell Cytotoxicity ; Calcimycin/pharmacology ; Cattle ; *Cell Communication ; Cell Survival ; Cells, Cultured ; Endothelium/*cytology ; Eosinophils/*cytology ; Humans ; SRS-A/biosynthesis ; Schistosoma mansoni/immunology ; Time Factors
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  • 55
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-04
    Description: The establishment of a cell culture system for the clonal development of blood cells has made it possible to identify the proteins that regulate the growth and differentiation of different blood cell lineages and to discover the molecular basis of normal and abnormal cell development in blood forming tissues. A model system with myeloid blood cells has shown that (i) normal blood cells require different proteins to induce cell multiplication (growth inducers) and cell differentiation (differentiation inducers), (ii) there is a hierarchy of growth inducers as cells become more restricted in their developmental program, and (iii) a cascade of interactions between proteins determines the correct balance between immature and mature cells in normal blood cell development. Gene cloning has shown that there is a family of different genes for these proteins. Normal protein regulators of blood cell development can control the abnormal growth of certain types of leukemic cells and suppress malignancy by inducing differentiation to mature nondividing cells. Chromosome abnormalities that give rise to malignancy in these leukemic cells can be bypassed and their effects nullified by inducing differentiation, which stops cells from multiplying. These blood cell regulatory proteins are active in culture and in the body, and they can be used clinically to correct defects in blood cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, L -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cells, Cultured ; Clone Cells/cytology ; Colony-Stimulating Factors/physiology/therapeutic use ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-3/physiology/therapeutic use ; Leukemia, Myeloid/drug therapy/physiopathology ; Mice ; Neoplastic Stem Cells/drug effects/pathology
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  • 56
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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  • 57
    Publication Date: 1987-05-22
    Description: To explore the potential use of retrovirus vectors for the transfer of genomic DNA sequences into mammalian cells, recombinant retroviral genomes were constructed that encode a functionally rearranged murine lambda 1 immunoglobulin gene. Several of these genomes could be transmitted intact to recipient cells by viral infection, although successful transmission depended both on the orientation of the lambda 1 sequences and on their specific placement within vector sequences. The lambda 1 gene transduced by viral infection was expressed in a cell lineage-specific manner, albeit at lower levels than endogenous lambda 1 gene expression in cells from the B-lymphocyte lineage. Vectors yielding integrated proviruses that lacked viral transcriptional enhancer sequences were used to show that neither viral transcription nor the viral transcriptional sequences themselves had any effect on the tissue specificity of lambda 1 gene expression or the absolute amount of lambda 1 transcription. Vector transcription did, however, dramatically decrease the amount of lambda 1 protein that could be detected in tranduced cells. These results suggest that retrovirus vectors may be useful reagents not only for the expression of complementary DNA sequences but also for studies of tissue-specific transcription in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cone, R D -- Reilly, E B -- Eisen, H N -- Mulligan, R C -- CA26712/CA/NCI NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):954-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Enhancer Elements, Genetic ; *Genes ; *Genes, Viral ; Genetic Vectors ; Immunoglobulin lambda-Chains/*genetics ; Retroviridae/*genetics ; *Transcription, Genetic
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  • 58
    Publication Date: 1987-01-23
    Description: Previous studies have shown that cytotoxic activated macrophages cause inhibition of DNA synthesis, of mitochondrial respiration, and of aconitase activity in tumor target cells. An L-arginine-dependent biochemical pathway synthesizing L-citrulline and nitrite, coupled to an effector mechanism, is now shown to cause this pattern of metabolic inhibition. Murine cytotoxic activated macrophages synthesize L-citrulline and nitrite in the presence of L-arginine but not D-arginine. L-Citrulline and nitrite biosynthesis by cytotoxic activated macrophages is inhibited by NG-monomethyl-L-arginine, which also inhibits this cytotoxic effector mechanism. This activated macrophage cytotoxic effector system is associated with L-arginine deiminase activity, and the imino nitrogen removed from the guanido group of L-arginine by the deiminase reaction subsequently undergoes oxidation to nitrite. L-Homoarginine, an alternative substrate for this deiminase, is converted to L-homocitrulline with concurrent nitrite synthesis and similar biologic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hibbs, J B Jr -- Taintor, R R -- Vavrin, Z -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432665" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonia/biosynthesis ; Animals ; Cells, Cultured ; Citrulline/biosynthesis ; Cytotoxicity, Immunologic ; Homoarginine/metabolism ; Hydrolases/metabolism ; *Macrophage Activation ; Macrophages/*physiology ; Mice ; Nitrates/metabolism ; Nitrites/metabolism
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  • 59
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-05-22
    Description: Macrophages that rapidly enter injured peripheral nerve synthesize and secrete large quantities of apolipoprotein E. This protein may be involved in the redistribution of lipid, including cholesterol released during degeneration, to the regenerating axons. To test this postulate, apolipoprotein E-associated lipid particles released from segments of injured rat sciatic nerve and apolipoprotein E-containing lipoproteins from plasma were used to determine whether sprouting neurites, specifically their growth cones, possessed lipoprotein receptors. Pheochromocytoma (PC12) cells, which can be stimulated to produce neurites in vitro, were used as a model system. Apolipoprotein E-containing lipid particles and lipoproteins, which had been labeled with fluorescent dye, were internalized by the neurites and their growth cones; the unmetabolized dye appeared to be localized to the lysosomes. The rapid rate of accumulation in the growth cones precludes the possibility of orthograde transport of the fluorescent particles from the PC12 cell bodies. Thus, receptor-mediated lipoprotein uptake is performed by the apolipoprotein B,E(LDL) (low density lipoprotein) receptors, and in the regenerating peripheral nerve apolipoprotein E may deliver lipids to the neurites and their growth cones for membrane biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ignatius, M J -- Shooter, E M -- Pitas, R E -- Mahley, R W -- MH 17047/MH/NIMH NIH HHS/ -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):959-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576212" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Gland Neoplasms ; Animals ; Apolipoproteins E/*metabolism ; Axons/ultrastructure ; Cell Line ; Cells, Cultured ; Neurons/*cytology/metabolism ; Pheochromocytoma ; Rats ; Sciatic Nerve/*cytology/metabolism
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  • 60
    Publication Date: 1987-12-11
    Description: Peptides corresponding to the amino-terminal region of the parathyroid hormone-related protein (PTHrP) of humoral hypercalcemia of malignancy were synthesized. A 34-amino acid peptide, PTHrP(1-34), was two to four times more potent than bovine or human PTH(1-34) in bioassays promoting the formation of adenosine 3',5'-monophosphate (cAMP) and plasminogen activator activity in osteogenic sarcoma cells and adenylate cyclase activity in chick kidney membranes. Like parathyroid hormone itself, in which the activity resides in the first 34 residues, PTHrP peptides of less than 30 residues from the amino terminus showed substantially reduced activity. PTHrP(1-34) had only 6% of the potency of bovine PTH(1-34) in promoting bone resorption in vitro. PTHrP(1-34) strongly promoted the excretion of cAMP and phosphorus and reduced the excretion of calcium in the isolated, perfused rat kidney consistent with the symptoms seen in malignant hypercalcemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kemp, B E -- Moseley, J M -- Rodda, C P -- Ebeling, P R -- Wettenhall, R E -- Stapleton, D -- Diefenbach-Jagger, H -- Ure, F -- Michelangeli, V P -- Simmons, H A -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1568-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Melbourne, Department of Medicine, Repatriation General Hospital, Heidelberg, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Resorption/*drug effects ; Bone and Bones/metabolism ; Calcium/metabolism ; Cattle ; Cells, Cultured ; Humans ; Hypercalcemia/etiology ; Neoplasms/*physiopathology ; Parathyroid Hormone/*pharmacology/physiology ; Peptide Fragments/*pharmacology/physiology ; Structure-Activity Relationship ; Teriparatide
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  • 61
    Publication Date: 1987-11-20
    Description: Two different assays for B cell growth factors (BCGF) and an antibody against lymphotoxin were used to show that the presence of lymphotoxin in conditioned media derived from normal activated T cells and in a partially purified BCGF accounts for a substantial portion of their B cell growth-promoting activity. A competitive binding assay confirmed the presence of significant amounts of lymphotoxin in the partially purified BCGF. Recombinant lymphotoxin enhanced the proliferation of activated B cells and augmented B cell proliferation and immunoglobulin secretion induced by interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kehrl, J H -- Alvarez-Mon, M -- Delsing, G A -- Fauci, A S -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1144-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500512" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody Formation/drug effects ; B-Lymphocytes/*cytology ; Cell Differentiation/drug effects ; Cells, Cultured ; DNA/biosynthesis ; Growth Substances/*physiology ; Humans ; In Vitro Techniques ; Interleukin-4 ; *Interleukins ; Lymphocyte Activation ; Lymphotoxin-alpha/*physiology ; Recombinant Proteins/pharmacology ; T-Lymphocytes/*physiology
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  • 62
    Publication Date: 1987-05-15
    Description: Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koyanagi, Y -- Miles, S -- Mitsuyasu, R T -- Merrill, J E -- Vinters, H V -- Chen, I S -- New York, N.Y. -- Science. 1987 May 15;236(4803):819-22.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3646751" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology/pathology ; Brain/*microbiology/pathology ; Cells, Cultured ; HIV/isolation & purification ; Humans ; Lymphocyte Activation ; Lymphocytes/immunology/microbiology ; Macrophages/microbiology ; Monocytes/microbiology ; Species Specificity ; Virus Replication
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  • 63
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-08-07
    Description: Factors that regulate synaptic specificity were investigated with Aplysia buccal and bag cell neurons in primary cell culture. In the presence of fetal calf serum electrical synapses are formed between buccal-buccal or bag-bag cell pairs, but not between buccal-bag cell pairs. Instead, buccal neurons make inhibitory chemical synapses on bag cells. However, in the presence of nanomolar concentrations of the lectin concanavalin A this pattern changes, such that more than 75 percent of buccal-bag pairs exhibit electrical synapses and the frequency of occurrence of buccal-bag chemical synapses is reduced. Such changes in synaptic specificity may be important in determining the types of synapses formed during neuronal development and neurite regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S S -- Levitan, I B -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):648-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603045" target="_blank"〉PubMed〈/a〉
    Keywords: Aplysia ; Cell Communication ; Cells, Cultured ; Concanavalin A/*pharmacology ; Microelectrodes ; Neurons/*drug effects ; Organ Specificity ; Synapses/*drug effects
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  • 64
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-10-16
    Description: Calcium influx is often an essential intermediate step for the release of neurotransmitter. However, some retinal neurons appear to release transmitter by a mechanism that does not require calcium influx. It was uncertain whether depolarization released calcium from an intracellular store or released transmitter by a mechanism that does not require calcium. The possibility that voltage, and not calcium, can regulate the release of transmitter was studied with pairs of solitary retinal neurons. Horizontal and bipolar cells were isolated from fish retinas and juxtaposed in culture. Communication between them was studied with electrophysiological methods. A horizontal cell released its neurotransmitter, gamma-aminobutyric acid, when depolarized during conditions that buffered the internal calcium concentration and prohibited calcium entry. The speed and amount of material released were sufficient for a contribution to synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, E A -- EY02440/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):350-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzofurans ; Calcium/*physiology ; Catfishes ; Cell Communication ; Cell Membrane/physiology ; Cells, Cultured ; Chlorides/metabolism ; Egtazic Acid/analogs & derivatives/pharmacology ; Electrophysiology ; Fluorescent Dyes ; Fura-2 ; Ion Channels/physiology ; Neurons/drug effects/*physiology ; Nipecotic Acids/pharmacology ; Photoreceptor Cells/physiology ; *Proline/*analogs & derivatives ; Retina/*cytology/drug effects ; Synapses/physiology ; gamma-Aminobutyric Acid/pharmacology/*secretion
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  • 65
    Publication Date: 1987-07-24
    Description: Adipsin is a serine protease homolog whose primary structure was predicted from the nucleotide sequence of a differentiation-dependent adipocyte messenger RNA. Immunoblots probed with antisera to synthetic peptides identify two forms of adipsin that are synthesized and secreted by 3T3 adipocytes. These proteins of 44 and 37 kilodaltons are converted to 25.5 kilodaltons by enzymatic deglycosylation. Although adipsin is principally synthesized in adipose tissue, it is also produced by sciatic nerve and is found in the bloodstream. Because of the apparent restriction of adipsin synthesis to tissues highly active in lipid metabolism, its presence in serum, and its modulation in altered metabolic states, this molecule may play a previously unrecognized role in systemic lipid metabolism or energy balance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, K S -- Min, H Y -- Johnson, D -- Chaplinsky, R J -- Flier, J S -- Hunt, C R -- Spiegelman, B M -- AM07230/AM/NIADDK NIH HHS/ -- AM31405/AM/NIADDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):402-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299705" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*enzymology ; Animals ; Cells, Cultured ; Complement Factor D ; Endopeptidases/blood/genetics/*secretion ; Male ; Mice ; Molecular Weight ; Organ Culture Techniques ; RNA, Messenger/genetics ; Sciatic Nerve/*enzymology ; *Serine Endopeptidases ; Transcription, Genetic
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  • 66
    Publication Date: 1987-08-28
    Description: Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, M R -- Ho, D D -- Gurney, M E -- 5P01 NS-21443/NS/NINDS NIH HHS/ -- K08-AI00685/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1047-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039662" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Brain/microbiology ; Cells, Cultured ; Ganglia, Spinal/drug effects ; Glucose-6-Phosphate Isomerase ; Growth Substances/*genetics/pharmacology ; HIV/*genetics ; HIV Envelope Protein gp120 ; Humans ; Lymphokines/*genetics/pharmacology ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/drug effects ; Retroviridae Proteins/genetics/pharmacology ; Sequence Homology, Nucleic Acid ; Viral Envelope Proteins/genetics/pharmacology
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  • 67
    Publication Date: 1987-12-04
    Description: The epidermal growth factor (EGF) receptor gene EGFR has been placed in a retrovirus vector to examine the growth properties of cells that experimentally overproduce a full-length EGF receptor. NIH 3T3 cells transfected with the viral DNA or infected with the corresponding rescued retrovirus developed a fully transformed phenotype in vitro that required both functional EGFR expression and the presence of EGF in the growth medium. Cells expressing 4 x 10(5) EGF receptors formed tumors in nude mice, while control cells did not. Therefore, the EGFR retrovirus, which had a titer on NIH 3T3 cells that was greater than 10(7) focus-forming units per milliliter, can efficiently transfer and express this gene, and increased numbers of EGF receptors can contribute to the transformed phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Velu, T J -- Beguinot, L -- Vass, W C -- Willingham, M C -- Merlino, G T -- Pastan, I -- Lowy, D R -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1408-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/chemically induced/*genetics ; Cells, Cultured ; DNA, Recombinant ; Epidermal Growth Factor/*pharmacology ; Fibroblasts/pathology ; Genetic Vectors ; Harvey murine sarcoma virus/genetics ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasms, Experimental/etiology ; *Proto-Oncogenes ; Receptor, Epidermal Growth Factor/drug effects/*genetics ; Recombinant Proteins/genetics
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  • 68
    Publication Date: 1987-04-10
    Description: The development of Wilms' tumor, a pediatric nephroblastoma, has been associated with a deletion in the p13 region of chromosome 11. The structure and function or functions of this deleted genetic material are unknown. The role of this deletion in the process of malignant transformation was investigated by introducing a normal human chromosome 11 into a Wilms' tumor cell line by means of the microcell transfer technique. These variant cells, derived by microcell hybridization, expressed similar transformed traits in culture as the parental cell line. Furthermore, expression of several proto-oncogenes by the parental cells was unaffected by the introduction of this chromosome. However, the ability of these cells to form tumors in nude mice was completely suppressed. Transfer of other chromosomes, namely X and 13, had no effect on the tumorigenicity of the Wilms' tumor cells. These studies provide support for the existence of genetic information on chromosome 11 which can control the malignant expression of Wilms' tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissman, B E -- Saxon, P J -- Pasquale, S R -- Jones, G R -- Geiser, A G -- Stanbridge, E J -- CA 19401/CA/NCI NIH HHS/ -- SO7RR05469-23/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):175-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3031816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/genetics ; Cells, Cultured ; *Chromosomes, Human, Pair 11 ; Gene Expression Regulation ; Humans ; Hybrid Cells ; Karyotyping ; Mice ; Mice, Nude ; Oncogenes ; Suppression, Genetic ; Wilms Tumor/*genetics/pathology
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  • 69
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-02-06
    Description: Calcium influx through voltage-gated membrane channels plays a crucial role in a variety of neuronal processes, including long-term potentiation and epileptogenesis in the mammalian cortex. Recent studies indicate that calcium channels in some cell types are heterogeneous. This heterogeneity has now been shown for calcium channels in mammalian cortical neurons. When dissociated embryonic hippocampal neurons from rat were grown in culture they first had only low voltage-activated, fully inactivating somatic calcium channels. These channels were metabolically stable and conducted calcium better than barium. Appearing later in conjunction with neurite outgrowth and eventually predominating in the dendrites, were high voltage-activated, slowly inactivating calcium channels. These were metabolically labile and more selective to barium than to calcium. Both types of calcium currents were reduced by classical calcium channel antagonists, but the low voltage-activated channels were more strongly blocked by the anticonvulsant drug phenytoin. These findings demonstrate the development and coexistence of two distinct types of calcium channels in mammalian cortical neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yaari, Y -- Hamon, B -- Lux, H D -- New York, N.Y. -- Science. 1987 Feb 6;235(4789):680-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barium/pharmacology ; Cadmium/pharmacology ; Calcium/*physiology ; Cell Differentiation ; Cells, Cultured ; Hippocampus/cytology/*physiology ; Ion Channels/classification/drug effects/*physiology ; Membrane Potentials ; Rats
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  • 70
    Publication Date: 1985-10-18
    Description: Developments in microscope, sensor, and image-processing technologies have led to integrated systems for the quantification of low-light-level emission signals from biological samples. Specificity is provided in the form of monoclonal antibodies and other ligands or enzyme substrates conjugated with efficient fluorophores. Fluorescent probes are also available for cellular macromolecular constituents and for free ions of biological interest such as H+ and Ca2+. The entire spectrum of photophysical phenomena can be exploited. Representative data are presented from studies of DNA conformation and architecture in polytene chromosomes and from studies of receptor-mediated endocytosis, calcium distribution, and the organization of the contractile apparatus in muscle cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arndt-Jovin, D J -- Robert-Nicoud, M -- Kaufman, S J -- Jovin, T M -- FO6 TWOO960/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):247-56.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048934" target="_blank"〉PubMed〈/a〉
    Keywords: Analog-Digital Conversion ; Animals ; Cell Cycle ; Cells/*cytology ; Cells, Cultured ; Chromosomes/ultrastructure ; Drosophila ; Fluorescent Dyes ; Kinetics ; Microscopy, Fluorescence/instrumentation/*methods ; Salivary Glands/cytology
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  • 71
    Publication Date: 1985-05-31
    Description: The carcinogenic process is extremely complex and is affected by diverse environmental and host factors. The mechanism for the gradual development of the transformed phenotype (a process termed "progression") was studied in type 5 adenovirus (Ad5)-transformed rat embryo cells. Progression was not correlated with major changes in the pattern of integration of viral DNA sequences. Instead, it was associated with an increased methylation of integrated viral sequences other than those corresponding to the E1 transforming genes of Ad5. A single exposure of progressed cells to the demethylating agent 5-azacytidine (Aza) resulted in a stable reversion to the unprogressed state of the original parental clone. A further selection of cells after growth in agar allowed the isolation of Aza-treated clones that had regained the progressed phenotype. These observations indicate that progression is a reversible process and suggest that progression may be associated with changes in the state of methylation of one or more specific genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babiss, L E -- Zimmer, S G -- Fisher, P B -- CA-33434/CA/NCI NIH HHS/ -- CA-35675/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1099-101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2581317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; Azacitidine/*pharmacology ; Cell Division ; Cell Transformation, Viral/*drug effects ; Cells, Cultured ; DNA, Neoplasm/genetics ; DNA, Viral/genetics ; Gene Expression Regulation ; Genes, Viral ; *Methylation ; Mice ; Neoplasms, Experimental/*pathology ; Rats ; Rats, Inbred Strains/embryology ; Transcription, Genetic
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  • 72
    Publication Date: 1985-06-07
    Description: Many higher plants produce economically important organic compounds such as oils, resins, tannins, natural rubber, gums, waxes, dyes, flavors and fragrances, pharmaceuticals, and pesticides. However, most species of higher plants have never been described, much less surveyed for chemical or biologically active constituents, and new sources of commercially valuable materials remain to be discovered. Advances in biotechnology, particularly methods for culturing plant cells and tissues, should provide new means for the commercial processing of even rare plants and the chemicals they produce. These new technologies will extend and enhance the usefulness of plants as renewable resources of valuable chemicals. In the future, biologically active plant-derived chemicals can be expected to play an increasingly significant role in the commercial development of new products for regulating plant growth and for insect and weed control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balandrin, M F -- Klocke, J A -- Wurtele, E S -- Bollinger, W H -- New York, N.Y. -- Science. 1985 Jun 7;228(4704):1154-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3890182" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents, Phytogenic/isolation & purification ; Cells, Cultured ; Insecticides/isolation & purification ; Plant Extracts/analysis ; Plant Growth Regulators/isolation & purification ; *Plants/analysis ; *Plants, Medicinal
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  • 73
    Publication Date: 1985-12-06
    Description: Rat atrial natriuretic factor (ANF) is translated as a 152-amino acid precursor preproANF. PreproANF is converted to the 126-amino acid proANF, the storage form of ANF in the atria. ANF isolated from the blood is approximately 25 amino acids long. It is demonstrated here that rat cardiocytes in culture store and secrete proANF. Incubation of proANF with serum produced a smaller ANF peptide. PreproANF seems to be processed to proANF in the atria, and proANF appears to be released into the blood, where it is converted by a protease to a smaller peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloch, K D -- Scott, J A -- Zisfein, J B -- Fallon, J T -- Margolies, M N -- Seidman, C E -- Matsueda, G R -- Homcy, C J -- Graham, R M -- Seidman, J G -- 1R23CA33570/CA/NCI NIH HHS/ -- HL07208/HL/NHLBI NIH HHS/ -- HL26215/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1168-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2933808" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrial Natriuretic Factor/*biosynthesis/genetics/secretion ; Autoradiography ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Heart/physiology ; Immune Sera/immunology ; Myocardium/*cytology/metabolism ; Protein Precursors/*biosynthesis/genetics/secretion ; RNA, Messenger/genetics ; Rabbits/immunology ; Rats
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  • 74
    Publication Date: 1985-06-21
    Description: Fibroblasts possess several distinct mechanisms that control cellular adhesion to extracellular matrix macromolecules. Monoclonal antibodies to a 140-kilodalton (kD) cell surface glycoprotein inhibited the adhesion of fibroblastic Chinese hamster ovary cells to fibronectin-coated substrata but did not inhibit adhesion to substrata coated with vitronectin, laminin, serum, or other adhesive macromolecules. Thus the 140-kD glycoprotein appears to be involved in the fibronectin-mediated adhesion mechanism but not in other adhesion processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, P J -- Juliano, R L -- GM26165/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1448-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Cell Adhesion ; Cell Membrane/immunology/*metabolism ; Cells, Cultured ; Cricetinae ; Cricetulus ; Fibroblasts/metabolism ; Fibronectins/*metabolism ; Glycoproteins/immunology/*metabolism ; Molecular Weight
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  • 75
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-06-28
    Description: Both elemental distribution and ion transport in cultured cells have been imaged by ion microscopy. Morphological and chemical information was obtained with a spatial resolution of approximately 0.5 micron for sodium, potassium, calcium, and magnesium in freeze-fixed, cryofractured, and freeze-dried normal rat kidney cells and Chinese hamster ovary cells. Ion transport was successfully demonstrated by imaging Na+-K+ fluxes after the inhibition of Na+- and K+ -dependent adenosine triphosphatase with ouabain. This method allows measurements of elemental (isotopic) distribution to be related to cell morphology, thereby providing the means for studying ion distribution and ion transport under different physiological, pathological, and toxicological conditions in cell culture systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandra, S -- Morrison, G H -- R01GM24314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1543-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis ; Cell Line ; Cells, Cultured ; Cricetinae ; Elements/*analysis ; Female ; Freeze Fracturing ; Kidney/*ultrastructure ; Magnesium/analysis ; Microscopy/methods ; Ouabain/pharmacology ; Ovary/*ultrastructure ; Potassium/analysis ; Rats ; Sodium/analysis ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Tissue Distribution
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  • 76
    Publication Date: 1985-03-22
    Description: Fibrinogen fragment D, which is heterogeneous, has several important biological functions. Human fibrinogen fragments D94 (molecular weight, 94,000), D78 (78,000), and E (52,000) were purified. Fragments D78 and D94 but not purified fibrinogen or fragment E specifically caused disorganization of bovine aortic endothelial cells cultured as monolayers. Within 2 hours of exposure to pathophysiological concentrations of fragment D, the confluent endothelial cells retracted from each other and projected pseudopodia. These disturbed cells subsequently became rounded and detached from the substrate. The actin present in stress fibers in stationary monolayer cells was diffusely redistributed in cells with fragment D-induced alterations in morphology. This effect was not observed in monolayers of kidney epithelial cells. The results demonstrate a specific effect of fibrinogen fragment D on the disorganization of cultured vascular endothelial cell monolayers and suggest that fragment D plays a role in the pathogenesis of syndromes with vascular endothelial damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dang, C V -- Bell, W R -- Kaiser, D -- Wong, A -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1487-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038818" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Animals ; Aorta ; Cattle ; Cell Adhesion/drug effects ; Cell Line ; Cells, Cultured ; Cytoskeleton/drug effects ; Endothelium/analysis/*cytology/drug effects/ultrastructure ; Epithelial Cells ; Fibrin Fibrinogen Degradation Products/*pharmacology ; Humans ; Kidney ; Pseudopodia/drug effects
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  • 77
    Publication Date: 1985-03-15
    Description: Human lymphocytes were exposed in vitro to ultrasound from two clinical devices, one of which was previously reported to have increased the frequency of sister chromatid exchanges. The ultrasonic exposures had no significant effect on the frequency of sister chromatid exchanges from three blood donors. Exposure to ultrasound also had no effect on cell cycle progression. A concomitant positive control (mitomycin C) resulted in a significant increase in sister chromatid exchanges.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciaravino, V -- Brulfert, A -- Miller, M W -- Jacobson-Kram, D -- Morgan, W F -- ES03000/ES/NIEHS NIH HHS/ -- ES03238/ES/NIEHS NIH HHS/ -- GM22680/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1349-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883487" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cells, Cultured ; Humans ; Lymphocytes ; *Sister Chromatid Exchange ; Ultrasonography/*adverse effects
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  • 78
    Publication Date: 1985-12-20
    Description: A retroviral expression vector (N2) containing the selectable gene, neoR, has been used to determine the optimal conditions for infecting murine hematopoietic progenitor cells at high efficiency. After infected bone marrow cells were introduced into lethally irradiated mice, the presence, stability, and expression of the vector DNA sequences were analyzed either in individual spleen foci 10 days later or in the blood, bone marrow, and spleens of mice 4 months later. When bone marrow cells were cultured in medium containing virus with titers of more than 10(6) colony-forming units per milliliter in the presence of purified murine interleukin-3, more than 85 percent of the resulting foci contained vector DNA. This proviral vector DNA was intact. Efficient expression of the neoR gene was demonstrated in most of the DNA-positive foci examined. The spleens of reconstituted animals (over a long term) contained intact "vector DNA" and the blood and bone marrow expressed the neoR gene in some animals. Thus, a retroviral vector can be used to introduce intact exogenous DNA sequences into hematopoietic stem cells with high efficiency and with substantial expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eglitis, M A -- Kantoff, P -- Gilboa, E -- Anderson, W F -- New York, N.Y. -- Science. 1985 Dec 20;230(4732):1395-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bone Marrow/microbiology ; Cells, Cultured ; DNA Transposable Elements ; DNA, Viral/genetics ; *Genes, Viral ; *Genetic Vectors ; Mice ; Moloney murine leukemia virus/*genetics ; Spleen/microbiology ; *Transcription, Genetic
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  • 79
    Publication Date: 1985-02-15
    Description: Isolated rat hepatocytes were incubated in the presence or absence of extracellular calcium and alpha-tocopherol succinate with three different toxic chemicals; namely, adriamycin in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea, ethyl methanesulfonate, and the calcium ionophore A23187. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. The addition of vitamin E to calcium-free medium, however, protected hepatocytes against toxic injury, whereas cells incubated in medium containing calcium were not protected. Hepatocyte viability during each toxic insult correlated well with the cellular alpha-tocopherol content but not with the presence or absence of extracellular calcium. These results suggest that cellular alpha-tocopherol maintains the viability of the cell during a toxic insult and that the presence or absence of vitamin E in the incubation medium probably explains the conflicting reports on the role of extracellular calcium in toxic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fariss, M W -- Pascoe, G A -- Reed, D J -- ES01978/ES/NIEHS NIH HHS/ -- ES07060/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):751-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3918345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/toxicity ; Calcium/*physiology ; Carmustine/toxicity ; Cell Survival/*drug effects ; Cells, Cultured ; Doxorubicin/toxicity ; Ethyl Methanesulfonate/toxicity ; Liver/cytology/*drug effects ; Male ; Rats ; Rats, Inbred Strains ; Vitamin E/*physiology
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  • 80
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-04-26
    Description: The interleukins, which have a regulatory role in immune function, may also mediate inflammation associated with injury to the brain. In experiments to determine the effect of these peptide hormones on glial cell proliferation in culture, interleukin-1 was a potent mitogen for astroglia but had no effect on oligodendroglia. Interleukin-2 did not alter the growth of either type of glial cell. Activity similar to that of interleukin-1 was detected in brains of adult rats 10 days after the brains had been injured. These findings suggest that interleukin-1, released by inflammatory cells, may promote the formation of scars by astroglia in the damaged mammalian brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Lachman, L B -- EY04915/EY/NEI NIH HHS/ -- R01CA38043/CA/NCI NIH HHS/ -- RR5511/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):497-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3872478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Astrocytes/*pathology ; Brain Injuries/*pathology ; Cells, Cultured ; Chromatography, High Pressure Liquid/methods ; Chromatography, Ion Exchange/methods ; Interleukin-1/isolation & purification/*physiology ; Interleukin-2/physiology ; Isoelectric Focusing ; *Mitogens ; Oligodendroglia/pathology ; Rats
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  • 81
    Publication Date: 1985-11-29
    Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Gene Expression Regulation ; *Genetic Engineering ; Genetic Vectors ; Hematopoietic Stem Cells/*physiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Mice ; Retroviridae/*genetics ; Transfection
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  • 82
    Publication Date: 1985-04-05
    Description: Formaldehyde, a common environmental pollutant, inhibits repair of O6-methylguanine and potentiates the mutagenicity of an alkylating agent, N-methyl-N-nitrosourea, in normal human fibroblasts. Because formaldehyde alone also causes mutations in human cells, the compound may cause genotoxicity by a dual mechanism of directly damaging DNA and inhibiting repair of mutagenic and carcinogenic DNA lesions caused by other chemical and physical carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grafstrom, R C -- Curren, R D -- Yang, L L -- Harris, C C -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):89-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975633" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/cytology ; Cells, Cultured ; DNA Repair/*drug effects ; Drug Synergism ; Fibroblasts/drug effects ; Formaldehyde/*adverse effects/pharmacology ; Guanine/analogs & derivatives/metabolism ; Humans ; Methylnitrosourea/pharmacology ; Mutagens/*pharmacology
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  • 83
    Publication Date: 1985-01-25
    Description: An in vitro model was developed to study the hepatic phase of Plasmodium falciparum, the only malaria parasite lethal to man. Primary cultures of human hepatocytes were inoculated with sporozoites of Brazilian and African strains of P. falciparum. On days 1 through 7 after inoculation examination of fluorescence-labeled and Giemsa-stained preparations demonstrated the presence of many intracellular parasites. In three separate sets of experiments all cultures were found to be infected with as many as 650 liver schizonts measuring up to 40 micrometers. After the addition of red blood cells, intraerythrocytic forms of P. falciparum were detected on days 12 and 13 by an immunofluorescence assay, indicating that the hepatic cycle had been completed in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazier, D -- Beaudoin, R L -- Mellouk, S -- Druilhe, P -- Texier, B -- Trosper, J -- Miltgen, F -- Landau, I -- Paul, C -- Brandicourt, O -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):440-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3880923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azure Stains ; Cells, Cultured ; Culture Media ; Erythrocytes/parasitology ; Fluorescent Antibody Technique ; Liver/*parasitology ; Plasmodium falciparum/cytology/*growth & development ; Time Factors
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  • 84
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-07-19
    Description: In addition to nerve growth factor (NGF), many proteins present in soluble tissue extracts and in the extracellular matrix influence the survival and development of cultured neurons. The structure, synthesis, and mechanism of action of NGF as a neurotrophic factor are considered along with the experiments on the new putative trophic molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thoenen, H -- Edgar, D -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):238-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2409599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Chickens ; Cyclic AMP/physiology ; DNA/genetics ; Extracellular Matrix/physiology ; Humans ; Ion Channels/physiology ; Male ; Mice ; Molecular Weight ; Myocardium/cytology ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/physiology ; Protein Precursors/genetics ; RNA, Messenger/metabolism ; Rats ; Receptors, Cell Surface/physiology ; Receptors, Nerve Growth Factor ; Sympathetic Nervous System/cytology
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  • 85
    Publication Date: 1985-03-22
    Description: An earlier finding that lymphocytes from African patients with the acquired immune deficiency syndrome (AIDS) react with rabbit antiserum to purified antigens of bovine leukemia virus (BLV) prompted a study of the possible cross-reactions between a BLV-infected ovine cell line and human lymphocytes inoculated with a strain of lymphadenopathy syndrome-associated virus (LAV). A solid-phase radioimmunoassay was used to detect antigenic markers of the retroviruses. Crude extracts from short-term cultures of lymphocytes infected with LAV bound rabbit antisera to the LAV glycoprotein gp13 (molecular weight 13,000) and the BLV proteins p24 and gp51, but did not bind antibodies to the p24 of human T-cell leukemia virus type I (HTLV-I). Antiserum to LAV gp13 reacted with an ovine cell line producing BLV but also weakly with virus-free ovine cells. Lymphocyte cultures from four African patients with AIDS expressed BLV-related antigens within 6 to 10 days of culture, at the moment when particle-bound reverse transcriptase was produced. BLV-related antigens were induced in lymphocyte cultures from healthy individuals by addition of filtered supernatant or irradiated cells of the original culture. The antisera to BLV used in this study may prove useful for the detection of AIDS-associated viruses in short-term cultures of lymphocytes from AIDS patients or their contacts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiry, L -- Sprecher-Goldberger, S -- Jacquemin, P -- Cogniaux, J -- Burny, A -- Bruck, C -- Portetelle, D -- Cran, S -- Clumeck, N -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1482-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2579433" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Animals ; Antigens, Viral/analysis/*immunology ; Cell Line ; Cells, Cultured ; Cross Reactions ; Deltaretrovirus/*immunology ; Epitopes/immunology ; Humans ; Leukemia Virus, Bovine/*immunology ; Lymph Nodes/microbiology ; Lymphocytes/immunology/*microbiology ; Radioimmunoassay ; Retroviridae/*immunology ; Sheep ; Viral Proteins/immunology
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  • 86
    Publication Date: 1985-08-23
    Description: The DNA genomes of human T-lymphotropic virus type III (HTLV-III) isolated from 18 individuals with AIDS or who were at risk for AIDS were evaluated for evidence of variation. Although all of the 18 viral DNA's hybridized throughout their entire genomes to a full-length cloned probe of the original HTLV-III isolate, each of the 18 isolates showed a different restriction enzyme pattern. The number of restriction site differences between isolates ranged from only 1 site in 23 to at least 16 sites in 31. No particular viral genotype was associated with a particular disease state and 2 of the 18 patients had evidence of concurrent infection by more than one viral genotype. Propagation of three different viral isolates in vitro for up to 9 months did not lead to detectable changes in their restriction patterns. These findings indicate that different isolates of HTLV-III comprise a spectrum of highly related but distinguishable viruses and have important implications regarding the pathogenicity of HTLV-III and attempts to develop effective diagnostic, therapeutic, and preventive measures for this virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong-Staal, F -- Shaw, G M -- Hahn, B H -- Salahuddin, S Z -- Popovic, M -- Markham, P -- Redfield, R -- Gallo, R C -- New York, N.Y. -- Science. 1985 Aug 23;229(4715):759-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2992084" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Carrier State ; Cells, Cultured ; DNA Restriction Enzymes ; Deltaretrovirus/*genetics ; Humans ; Polymorphism, Genetic
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  • 87
    Publication Date: 1985-02-01
    Description: Potomac horse fever, a disease characterized by fever, anorexia, leukopenia, and occasional diarrhea, is fatal in approximately 30 percent of affected animals. The seasonal occurrence of the disease (June to October) and evidence of antibodies to the rickettsia Ehrlichia sennetsu in the serum of convalescing horses suggested that a related rickettsia might be the causative agent. Such an agent was isolated in cultured blood monocytes from an experimentally infected pony. This intracytoplasmic organism was adapted to growth in primary cultures of canine blood monocytes. A healthy pony inoculated with these infected monocytes also developed the disease. The organism was reisolated from this animal which, at autopsy, had pathological manifestations typical of Potomac horse fever. Cross serologic reactions between the newly isolated agent and antisera to 15 rickettsiae revealed that it is related to certain members of the genus Ehrlichia, particularly to Ehrlichia sennetsu. Since the disease occurs in other parts of the United States as well as in the vicinity of the Potomac River, and since it has also been reported in Europe, the name equine monocytic ehrlichiosis is proposed as being more descriptive.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holland, C J -- Ristic, M -- Cole, A I -- Johnson, P -- Baker, G -- Goetz, T -- New York, N.Y. -- Science. 1985 Feb 1;227(4686):522-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3880925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/immunology ; Cells, Cultured ; Cross Reactions ; Ehrlichia/growth & development/immunology/*isolation & ; purification/ultrastructure ; Fluorescent Antibody Technique ; Horse Diseases/blood/*microbiology/transmission ; Horses ; Monocytes/*microbiology ; Rickettsiaceae/*isolation & purification ; Rickettsiaceae Infections/blood/microbiology/transmission/*veterinary ; Terminology as Topic ; Vacuoles/ultrastructure
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  • 88
    Publication Date: 1985-09-27
    Description: Infection of normal peripheral blood T cells by the acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV) was evaluated in long-term cultures of helper-inducer T cells (T4 cells). Cells that were inoculated with ARV and maintained in medium supplemented with interleukin-2 remained productively infected with this virus for more than 4 months in culture, although they showed no cytopathic effects characteristic of acute ARV infection. The presence of replicating virus was demonstrated by reverse transcriptase activity of culture fluids and by viral antigens and budding particles detected on cells by immunofluorescence and electron microscopy. Virus produced in these cultures remained infectious and could induce cytopathic effects and viral antigens in uninfected lymphoid cells. The finding that normal lymphocytes may be productively infected by an AIDS retrovirus in the absence of cell death suggests that a range of biologic effects may occur after infection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoxie, J A -- Haggarty, B S -- Rackowski, J L -- Pillsbury, N -- Levy, J A -- CA-34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1400-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994222" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antigens, Viral/immunology ; Cells, Cultured ; Deltaretrovirus/immunology ; Humans ; Microscopy, Fluorescence ; Retroviridae Infections/immunology/microbiology ; T-Lymphocytes/*microbiology
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  • 89
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-06-14
    Description: While a number of oncogenes are expressed in a cell cycle-dependent manner, their role in the control of cell proliferation can only be established by a direct functional assay. The c-myc protein, upon microinjection into nuclei of quiescent Swiss 3T3 cells, cooperated with platelet-poor plasma in the stimulation of cellular DNA synthesis. This suggests that c-myc protein, like platelet-derived growth factor (PDGF), may act as a competence factor in the cell cycle to promote the progression of cells to S phase. The presence in the medium of an antibody against PDGF abolished DNA synthesis induced by microinjected PDGF; however, the microinjected c-myc protein stimulated DNA synthesis even when its own antibody was present in the medium. The c-myc protein may act as an intracellular competence factor, while PDGF expresses its biological activity only from outside the cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaczmarek, L -- Hyland, J K -- Watt, R -- Rosenberg, M -- Baserga, R -- New York, N.Y. -- Science. 1985 Jun 14;228(4705):1313-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001943" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle/drug effects ; Cells, Cultured ; DNA/biosynthesis ; Mice ; *Oncogenes ; Platelet-Derived Growth Factor/pharmacology
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  • 90
    Publication Date: 1985-05-17
    Description: Endothelial cells, which line the interior walls of blood vessels, proliferate at the site of blood vessel injury. Knowledge of the factors that control the proliferation of these cells would help elucidate the role of endothelial cells in wound healing, tumor growth, and arteriosclerosis. In vitro, endothelial cells organize into viable, three-dimensional tubular structures in environments that limit cell proliferation. The process of endothelial cell organization was found to result in decreased levels of the sis messenger RNA transcript and increased levels of the messenger RNA transcript for fibronectin. This situation was reversed on transition from the organized structure to a proliferative monolayer. These results suggest a reciprocity for two biological response modifiers involved in the regulation of endothelial cell proliferation and differentiation in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaye, M -- McConathy, E -- Drohan, W -- Tong, B -- Deuel, T -- Maciag, T -- 14147/PHS HHS/ -- 310765/PHS HHS/ -- 4807/PHS HHS/ -- etc. -- New York, N.Y. -- Science. 1985 May 17;228(4701):882-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3890179" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Division ; Cells, Cultured ; Culture Media ; Endothelial Growth Factors ; Endothelium/*cytology/metabolism ; Extracellular Matrix/metabolism ; Fibronectins/biosynthesis/genetics ; *Gene Expression Regulation ; Growth Substances/pharmacology ; Humans ; Platelet-Derived Growth Factor/*genetics ; RNA, Messenger/*genetics ; *Transcription, Genetic
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  • 91
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-05-17
    Description: Primary cultures of astrocytes from neonatal rat brain were incubated with tritiated serotonin. After fixation they were stained by immunofluorescence for the astrocyte-specific marker glial fibrillary acidic protein and processed for autoradiography. Silver grain density was increased over cells positive for glial fibrillary acidic protein and was reduced to background levels when sodium was omitted from the medium or the specific inhibitors of serotonin uptake fluoxetine and chlorimipramine were present. The results indicate that mammalian astrocytes can take up serotonin by a sodium-dependent, high-affinity system previously thought to be the exclusive property of serotonergic nerve endings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimelberg, H K -- Katz, D M -- NS 19492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 May 17;228(4701):889-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3890180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/analysis/drug effects/*metabolism ; Autoradiography ; Biological Transport ; Cells, Cultured ; Clomipramine/pharmacology ; Fluorescent Antibody Technique ; Fluoxetine/pharmacology ; Glial Fibrillary Acidic Protein/analysis ; Rats ; Serotonin/*metabolism ; Sodium/pharmacology
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  • 92
    Publication Date: 1985-08-09
    Description: Microfluorometric recordings were made of changes in the concentration of cytosolic-free calcium in cultured rat vascular smooth muscle cells treated with quin 2, an intracellularly trapped dye, under several conditions. Nitroglycerin decreased calcium in both the presence and absence of extracellular calcium and strongly and progressively decreased the extent of transient increases in calcium induced by repeated applications of caffeine in the absence of extracellular calcium. Therefore nitroglycerin probably decreases cytosolic-free calcium by accelerating the extrusion of calcium through the sarcolemmal membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, S -- Kanaide, H -- Nakamura, M -- New York, N.Y. -- Science. 1985 Aug 9;229(4713):553-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3927484" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Aorta ; Caffeine/pharmacology ; Calcium/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytosol/metabolism ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Microscopy, Fluorescence ; Muscle, Smooth, Vascular/drug effects/*metabolism ; Nitroglycerin/pharmacology ; Photomicrography ; Potassium/pharmacology ; Rats
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  • 93
    Publication Date: 1985-06-07
    Description: Infection of human T cells by human T-lymphotropic virus, type I (HTLV-I), a retrovirus, is uniformly associated with the constitutive expression of large numbers of cellular receptors for interleukin-2 (IL-2). Comparison with normal T cells shows that neither IL-2 receptor gene organization nor IL-2 receptor messenger RNA processing are altered in the leukemic cells. However, mitogenic stimuli activate IL-2 receptor gene expression in normal T cells, whereas these stimuli paradoxically inhibit IL-2 receptor gene transcription in HTLV-I-infected leukemic T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kronke, M -- Leonard, W J -- Depper, J M -- Greene, W C -- New York, N.Y. -- Science. 1985 Jun 7;228(4704):1215-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2988127" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/physiology ; Cells, Cultured ; DNA/genetics ; Deltaretrovirus ; Humans ; Leukemia/*genetics ; Molecular Weight ; Poly A/genetics ; RNA, Messenger/genetics ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2 ; T-Lymphocytes/microbiology/*physiology ; Transcription, Genetic
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  • 94
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-03-08
    Description: Cholesterol accumulates within smooth muscle cells and macrophages in atherosclerotic lesions, thereby contributing to the progressive enlargement of these lesions. The mechanism of this cellular accumulation of cholesterol is not known. The possibility that platelets may have a role in the cellular cholesterol accumulation that occurs during atherogenesis was investigated. Incubation of thrombin-activated washed rat platelets (or platelet-free supernatants prepared from thrombin-activated platelets) with cultured rat aortic smooth muscle cells induced cholesteryl ester lipid droplet accumulation within the smooth muscle cells. No cholesteryl ester lipid droplets accumulated when smooth muscle cells were incubated with unactivated platelets. Smooth muscle cell lipid droplet accumulation occurred in the absence of serum lipoproteins and was not inhibited by mevinolin, a drug that blocks cholesterol synthesis. These findings suggest that activated platelets may release cholesterol, which can be accumulated by cells and stored as lipid droplets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruth, H S -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1243-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/physiopathology ; Arteriosclerosis/*physiopathology ; Blood Platelets/*physiology ; Cells, Cultured ; Cholesterol/*physiology ; Male ; Muscle, Smooth, Vascular/*cytology/physiopathology ; Platelet Aggregation ; Rats ; Rats, Inbred Strains ; Thrombin/physiology
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  • 95
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-06-21
    Description: Repeated administration of morphine in increasing doses delayed normal cell death in the ciliary ganglion of the chick embryo; the effect was completely blocked by naloxone. Survival of spinal motoneurons was not affected. Morphine also inhibited potassium-stimulated synthesis of acetylcholine in ganglion cells cultured with muscle, suggesting that morphine can influence neurotransmission. Morphine's effect on cell death may be due to an inhibition of transmission at the neuromuscular junction, but opiates may also directly affect cell death. Although it is now known whether the endogenous opiates in the ciliary ganglion influence neuronal survival during embryogenesis, exogenous opiates can affect normal cell death in the autonomic nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meriney, S D -- Gray, D B -- Pilar, G -- NS 10338/NS/NINDS NIH HHS/ -- NS 19640/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1451-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990029" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Birds ; Cell Survival/*drug effects ; Cells, Cultured ; Ganglia, Parasympathetic/*cytology/drug effects/metabolism ; Morphine/*pharmacology ; Naloxone/pharmacology ; Potassium/pharmacology ; Spinal Nerves/drug effects ; Synaptic Transmission/drug effects
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  • 96
    Publication Date: 1985-09-27
    Description: When vole cells that had been transformed by Rous sarcoma virus were treated with the tumor-promoting phorbol ester 12-O-tetradecanoyl-13-acetate (TPA), specific phosphorylation of pp60v-src was increased. Partial V8 protease mapping indicated that the increased phosphorylation occurred exclusively on serine residues located in the amino terminus of the molecule. Treatment of cells with dimethyl sulfoxide or 4 alpha-phorbol-12,13-didecanoate did not elicit this response. Two-dimensional tryptic phosphopeptide mapping of pp60v-src immunoprecipitated from untreated and TPA-treated cells indicated that a specific tryptic amino-terminal peptide was hyperphosphorylated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purchio, A F -- Shoyab, M -- Gentry, L E -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1393-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994221" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arvicolinae ; Carcinogens/*pharmacology ; Cell Transformation, Neoplastic/metabolism ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Mice ; Mice, Inbred BALB C ; Oncogene Protein pp60(v-src) ; Phorbol Esters/pharmacology ; Phosphorylation ; Protein Kinase C ; Protein Kinases/metabolism ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; Sarcoma, Avian/*genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Viral Proteins/*metabolism
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  • 97
    Publication Date: 1985-04-12
    Description: Tumor necrosis factor (TNF) is a soluble protein that causes damage to tumor cells but has no effect on normal cells. Human TNF was purified to apparent homogeneity as a 17.3-kilodalton protein from HL-60 leukemia cells and showed cytotoxic and cytostatic activities against various human tumor cell lines. The amino acid sequence was determined for the amino terminal end of the purified protein, and oligodeoxyribonucleotide probes were synthesized on the basis of this sequence. Complementary DNA (cDNA) encoding human TNF was cloned from induced HL-60 messenger RNA and was confirmed by hybrid-selection assay, direct expression in COS-7 cells, and nucleotide sequence analysis. The human TNF cDNA is 1585 base pairs in length and encodes a protein of 233 amino acids. The mature protein begins at residue 77, leaving a long leader sequence of 76 amino acids. Expression of high levels of human TNF in Escherichia coli was accomplished under control of the bacteriophage lambda PL promoter and gene N ribosome binding site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, A M -- Creasey, A A -- Ladner, M B -- Lin, L S -- Strickler, J -- Van Arsdell, J N -- Yamamoto, R -- Mark, D F -- New York, N.Y. -- Science. 1985 Apr 12;228(4696):149-54.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; *Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant/metabolism ; Glycoproteins/*genetics/isolation & purification/pharmacology ; Humans ; Leukemia, Myeloid/metabolism ; Mice ; Mice, Nude ; Neoplasms, Experimental/drug therapy ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rabbits ; Rats ; Tumor Necrosis Factor-alpha ; Xenopus
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  • 98
    Publication Date: 1985-03-22
    Description: Endothelial cell functions, such as arachidonic acid metabolism, may be modulated by membrane stresses induced by blood flow. The production of prostacyclin by primary human endothelial cell cultures subjected to pulsatile and steady flow shear stress was measured. The onset of flow led to a sudden increase in prostacyclin production, which decreased to a steady rate within several minutes. The steady-state production rate of cells subjected to pulsatile shear stress was more than twice that of cells exposed to steady shear stress and 16 times greater than that of cells in stationary culture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frangos, J A -- Eskin, S G -- McIntire, L V -- Ives, C L -- HL-17437/HL/NHLBI NIH HHS/ -- HL-18672/HL/NHLBI NIH HHS/ -- HL-23016/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1477-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883488" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood Circulation ; Cells, Cultured ; Endothelium/cytology/*metabolism ; Epoprostenol/*biosynthesis ; Humans ; Kinetics ; Models, Biological ; Stress, Mechanical
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  • 99
    Publication Date: 1985-02-15
    Description: Addition of norepinephrine to primary cultures of adult rat hepatocytes stimulates the incorporation of [3H]thymidine in a dose-dependent manner. This effect has been observed in serum-free medium containing epidermal growth factor and insulin. Stimulation of DNA synthesis by norepinephrine was strongly antagonized by the alpha 1-adrenergic antagonist prazosin but not by an alpha 2 antagonist or by a beta-adrenergic blocker. The beta agonist isoproterenol did not stimulate significant DNA synthesis. These results indicate that catecholamines interact with the alpha 1 adrenoreceptor to stimulate DNA synthesis in hepatocytes. Since alpha 1 receptors are present in most cells, this receptor may be important in cell growth regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruise, J L -- Houck, K A -- Michalopoulos, G K -- CA 35373/CA/NCI NIH HHS/ -- T32 GM07184/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):749-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2982212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA/*biosynthesis ; Epidermal Growth Factor/pharmacology ; Female ; Insulin/pharmacology ; Liver/*cytology ; Liver Regeneration ; Norepinephrine/*physiology ; Prazosin/pharmacology ; Rats ; Receptors, Adrenergic, alpha/drug effects/*physiology ; Yohimbine/pharmacology
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  • 100
    Publication Date: 1985-10-18
    Description: A scheme for partial purification of biologically active v-sis-coded protein from cells transformed with simian sarcoma virus (SSV) has made possible a functional comparison of the transforming protein with platelet-derived growth factor (PDGF). The SSV-transforming gene product is capable of specifically binding PDGF receptors, stimulating tyrosine phosphorylation of PDGF receptors, and inducing DNA synthesis in quiescent fibroblasts. Each of these activities was specifically inhibited by antibodies to different regions of the v-sis gene product. Moreover, viral infection of a variety of cell types revealed a strict correlation between those cells possessing PDGF receptors and those susceptible to transformation by SSV. These findings provide evidence that SSV-transforming activity is mediated by the interaction of a virus-coded mitogen with PDGF receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leal, F -- Williams, L T -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):327-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996133" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/metabolism ; Cattle ; Cell Line ; *Cell Transformation, Viral ; Cells, Cultured ; Fibroblasts/metabolism ; *Genes ; *Genes, Viral ; Humans ; Kinetics ; Mink ; Molecular Weight ; Muscle, Smooth/metabolism ; Muscle, Smooth, Vascular/metabolism ; Platelet-Derived Growth Factor/*metabolism ; Receptors, Cell Surface/isolation & purification/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/genetics/*metabolism
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