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  • Cells, Cultured  (28)
  • American Association for the Advancement of Science (AAAS)  (28)
  • 1985-1989  (28)
  • 1970-1974
  • 1965-1969
  • 1950-1954
  • 1987  (28)
  • 1951
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (28)
Years
  • 1985-1989  (28)
  • 1970-1974
  • 1965-1969
  • 1950-1954
Year
  • 1
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    Release of multiple hormones by a direct action of interleukin-1 on pituitary cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Oncogenes in radioresistant, noncancerous skin fibroblasts from a cancer-prone family (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Transformation by oncogenes encoding protein kinases induces the metastatic phenotype (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 5
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    Chemical identification of a tumor-derived angiogenic factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 6
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    Trophic stimulation of cultured neurons from neonatal rat brain by epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 7
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    Localization, secretion, and action of inhibin in human placenta (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 8
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 9
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    A cell-cycle constraint on the regulation of gene expression by platelet-derived growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 10
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    Quantal release of transmitter is not associated with channel opening on the neuronal membrane (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 11
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    The sor gene of HIV-1 is required for efficient virus transmission in vitro (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 12
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    Forskolin and phorbol esters reduce the same potassium conductance of mouse neurons in culture (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 13
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    Eosinophils cocultured with endothelial cells have increased survival and functional properties (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 14
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    The molecular control of blood cell development (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 15
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 16
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    Tissue-specific expression of functionally rearranged lambda 1 Ig gene through a retrovirus vector (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 17
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    Macrophage cytotoxicity: role for L-arginine deiminase and imino nitrogen oxidation to nitrite (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 18
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    Lipoprotein uptake by neuronal growth cones in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 19
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    Parathyroid hormone-related protein of malignancy: active synthetic fragments (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 20
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    Lymphotoxin is an important T cell-derived growth factor for human B cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 21
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    Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 22
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    Concanavalin A alters synaptic specificity between cultured Aplysia neurons (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 23
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    Depolarization without calcium can release gamma-aminobutyric acid from a retinal neuron (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 24
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    Adipsin: a circulating serine protease homolog secreted by adipose tissue and sciatic nerve (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 25
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    Functional interaction and partial homology between human immunodeficiency virus and neuroleukin (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 26
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    Epidermal-growth-factor-dependent transformation by a human EGF receptor proto-oncogene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 27
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    Introduction of a normal human chromosome 11 into a Wilms' tumor cell line controls its tumorigenic expression (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 28
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    Development of two types of calcium channels in cultured mammalian hippocampal neurons (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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