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  • Dose-Response Relationship, Drug
  • American Association for the Advancement of Science (AAAS)  (10)
  • Annual Reviews
  • PANGAEA
  • 1985-1989  (10)
  • 1980-1984
  • 1960-1964
  • 1986  (10)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (10)
  • Annual Reviews
  • PANGAEA
Years
  • 1985-1989  (10)
  • 1980-1984
  • 1960-1964
Year
  • 1
    Publication Date: 1986-11-07
    Description: Lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, activates B lymphocytes and macrophages. Pertussis toxin, which inactivates several members of the G protein family of signaling components, including Gi and transducin, was found to inhibit the lipopolysaccharide-induced responses of the WEHI-231 B lymphoma cell line and the P388D1 macrophage cell line. These results, combined with the demonstration that lipopolysaccharide inhibits adenylate cyclase activity in P388D1 cells, strongly argues that lipopolysaccharide activation of cells is mediated by a Gi-like receptor-effector coupling protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jakway, J P -- DeFranco, A L -- AI-20038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):743-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095921" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenylate Cyclase Toxin ; Antibodies, Anti-Idiotypic/immunology ; B-Lymphocytes/*physiology ; Cell Line ; Dose-Response Relationship, Drug ; Escherichia coli ; GTP-Binding Proteins/*physiology ; Immunoglobulin M/immunology ; Interleukin-1/metabolism ; Lipopolysaccharides/*antagonists & inhibitors/immunology ; Lymphocyte Activation/drug effects ; Macrophage Activation/drug effects ; Macrophages/*physiology ; *Pertussis Toxin ; Virulence Factors, Bordetella/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-17
    Description: Human interferon stimulates a transient two- to threefold increase in the concentration of diacylglycerol and inositol tris-phosphate within 15 to 30 seconds of cell exposure to interferon. Antibodies to interferon inhibit this effect. The stimulation was measurable in isolated cell membranes exposed to interferon. Human alpha and beta, but not gamma, interferon stimulate this increase in cells containing the appropriate interferon receptor. The effect was proportional to the number of interferon receptors. Both the diacylglycerol increase and antiviral effects induced by interferon could be correlated in terms of dose dependence. Thus, a transient diacylglycerol increase is an early event in the interferon-induced transmembrane signaling process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yap, W H -- Teo, T S -- Tan, Y H -- New York, N.Y. -- Science. 1986 Oct 17;234(4774):355-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2429366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Membrane/drug effects ; Diglycerides/analysis ; Dose-Response Relationship, Drug ; Fibroblasts/analysis/drug effects ; Humans ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/analysis ; Interferon Type I/pharmacology ; Interferon-gamma/pharmacology ; Interferons/*pharmacology/physiology ; Mice ; Receptors, Immunologic/metabolism ; Receptors, Interferon
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-01
    Description: Decanal and N-amino-N'-1-octylguanidine (AOG), combined at 28 microM each, mediated erythrocyte lysis within 80 minutes under physiological conditions. By contrast, no lysis was observed after 20 hours with either decanal (56 microM) or AOG (100 microM) alone. The pronounced synergism observed for these chemicals and similar reactive pairs of chemicals is due to the self-assembly of more cytotoxic hydrazones in situ. Decanal and AOG also exhibit synergistic activity against cultured human cells (HeLa) and bacteria (Escherichia coli J96). This synergism may be useful in the design of cytotoxins that would self-assemble selectively from nontoxic precursors within tumors, while sparing normal tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rideout, D -- 1-F32-CA07723/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):561-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523757" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehydes/*metabolism/pharmacology ; Cytotoxins/*metabolism/pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Erythrocytes/drug effects ; Escherichia coli/drug effects ; Guanidines/*metabolism/*pharmacology ; HeLa Cells/drug effects ; Humans ; Kinetics ; Neoplasms/drug therapy
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-18
    Description: Excitability is generated in developing skeletal muscle by the incorporation of sodium-selective ion channels into the surface membrane. Whole-cell and patch voltage-clamp recording from myotubes and their embryologic precursors, myoblasts, indicated that voltage-activated sodium current in myoblasts was more resistant to block by tetrodotoxin (TTX) than that in myotubes. Single-channel recording from both cell types showed two classes of sodium channels. One class had a lower single-channel conductance, activated at more hyperpolarized voltages, and was more resistant to TTX than the other. The proportion of TTX-resistant to TTX-sensitive sodium channels was higher in myoblasts than in myotubes. Thus, the difference in TTX sensitivity between myoblasts and myotubes can be explained by a difference in the proportion of the two classes of sodium channels. In addition, the lower conductance of TTX-resistant channels provides insight into the relationship between the TTX binding site and the external mouth of the sodium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, R E -- Horn, R -- NS 00703/NS/NINDS NIH HHS/ -- NS 18608/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):361-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Drug Resistance ; Electric Conductivity ; Electric Stimulation ; Ion Channels/drug effects/*physiology ; *Muscle Development ; Muscles/metabolism ; Rats ; Sodium/*metabolism ; Tetrodotoxin/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-29
    Description: Epidermal growth factor (EGF) stimulates the proliferation of various mammalian cells in culture, but its physiological role is not well defined. In mature male mice, large amounts of EGF are produced in the submandibular gland; it is present in the circulation at approximately 5 nanograms of EGF per milliliter of plasma. Sialoadenectomy (removal of the submandibular glands) decreased the amount of circulating EGF to an undetectable level but did not affect the circulating levels of testosterone or follicle-stimulating hormone. The number of mature sperm in the epididymis decreased by as much as 55 percent; the number of spermatids in the testis decreased by 40 to 50 percent; and the number of spermatocytes increased by about 20 percent. Administration of EGF to sialoadenectomized mice restored both the sperm content of the epididymis and the number of spermatids in the testis to normal. Thus, EGF may play a role in male reproductive function by stimulating the meiotic phase of spermatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsutsumi, O -- Kurachi, H -- Oka, T -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):975-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3090686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology/*physiology ; Epididymis/drug effects/physiology ; Follicle Stimulating Hormone/physiology ; Genitalia, Male/*physiology ; Luteinizing Hormone/physiology ; Male ; Mice ; Sexual Maturation ; Sperm Count/drug effects ; Spermatogenesis/drug effects ; Spermatozoa/physiology ; Submandibular Gland/physiology ; Testis/drug effects
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  • 6
    Publication Date: 1986-12-05
    Description: Patients with Werner's syndrome, an autosomal recessive disorder, undergo an accelerated aging process that leads to premature death. Fibroblasts from such patients typically grow poorly in culture. Here it is shown that fibroblasts from a patient with Werner's syndrome have a markedly attenuated mitogenic response to platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF). In contrast, they have a full mitogenic response to fetal bovine serum. Both PDGF binding and receptor numbers per cell are unaltered. The Werner's syndrome cells express high constitutive levels of collagenase in vitro. Although PDGF enhances collagenase expression through increased levels of hybridizable collagenase messenger RNA in normal skin fibroblasts, no induction of collagenase occurs in the Werner's syndrome fibroblasts. Moreover, the failure to respond to this agonist effect of PDGF is not restored by fetal bovine serum. The data suggest that failure of one or more PDGF-mediated pathways in Werner's syndrome cells may contribute to the phenotypic expression of the disorder.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, E A -- Silverman, N -- Busiek, D F -- Kronberger, A -- Deuel, T F -- AM 12129/AM/NIADDK NIH HHS/ -- AM 19537/AM/NIADDK NIH HHS/ -- TO-AM 07284/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1240-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022382" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Dose-Response Relationship, Drug ; Fibroblast Growth Factors/*pharmacology ; Fibroblasts/drug effects ; Humans ; Microbial Collagenase/biosynthesis ; Platelet-Derived Growth Factor/*pharmacology ; RNA, Messenger/biosynthesis ; Receptors, Cell Surface/metabolism ; Receptors, Platelet-Derived Growth Factor ; Werner Syndrome/*metabolism
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  • 7
    Publication Date: 1986-01-10
    Description: In rats infected with the parasite Schistosoma mansoni, the concentration of C-reactive protein in the serum increases after the lung stage of infection and is at its highest at the time of terminal worm rejection. The peak of platelet-mediated cytotoxicity induced by infected serum that has been heated (and is free of immunoglobulin E) as well as the time course for the development of platelet cytotoxic activity in infected rats was found to be correlated with the concentration of C-reactive protein. Rat and human platelets treated with homologous serum obtained during an acute phase of inflammation or with purified C-reactive protein were able to kill the immature forms of the worm in vitro. Platelets treated with C-reactive protein were furthermore capable of conferring significant protection against schistosomiasis in transfer experiments. Collectively these data indicate that a system that includes C-reactive protein and platelets participates in the natural resistance of the rat to schistosomal infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bout, D -- Joseph, M -- Pontet, M -- Vorng, H -- Deslee, D -- Capron, A -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):153-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3079916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*drug effects/immunology ; C-Reactive Protein/blood/immunology/*pharmacology ; Cytotoxicity, Immunologic/*drug effects ; Dose-Response Relationship, Drug ; Immunity, Innate/drug effects ; Rats ; Schistosomiasis mansoni/*immunology ; Turpentine/pharmacology
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-03
    Description: Cholinergic agonists rapidly and transiently induced transcription of the c-fos protooncogene and one or more actin genes in neuronally differentiated PC12 cells. Transcription was activated within minutes after stimulation of the nicotinic acetylcholine receptor and required an influx of extracellular Ca2+ ions through voltage-sensitive calcium channels. Nicotine activation proceeded by a different pathway from activation by nerve growth factor, whose stimulation of these genes is independent of extracellular Ca2+ ions. These findings suggest that neurotransmitters may rapidly activate specific gene transcription in nondividing neuronally differentiated cells. They also suggest a functional role for neurotransmitter induction of c-fos and actin expression in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenberg, M E -- Ziff, E B -- Greene, L A -- GM 30760/GM/NIGMS NIH HHS/ -- NS16036/NS/NINDS NIH HHS/ -- P30 CA 16087/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):80-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749894" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Adrenal Gland Neoplasms/metabolism ; Animals ; Calcium/metabolism ; Cell Line ; Dose-Response Relationship, Drug ; Nerve Growth Factors/pharmacology ; Nicotine/pharmacology ; Pheochromocytoma/metabolism ; Rats ; Receptors, Cholinergic/*drug effects ; Transcription, Genetic/*drug effects
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  • 9
    Publication Date: 1986-04-04
    Description: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells that has been implicated in the pathogenesis of atherosclerosis. The potential role of PDGF in the altered vasoreactivity of atherosclerotic vessels has been studied through an examination of its effects on contractility in the rat aorta. PDGF caused a concentration-dependent contraction of aortic strips and was significantly more potent on a molar basis than the classic vasoconstrictor peptide angiotensin II. Furthermore, PDGF increased the cytosolic free calcium concentration in cultured rat aortic smooth muscle cells. These observations suggest a new biological activity for PDGF that may contribute to the enhanced vasoreactivity of certain atherosclerotic vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berk, B C -- Alexander, R W -- Brock, T A -- Gimbrone, M A Jr -- Webb, R C -- HL20054/HL/NHLBI NIH HHS/ -- HL22602/HL/NHLBI NIH HHS/ -- HL35013/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):87-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3485309" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Angiotensin II/pharmacology ; Animals ; Aorta/*drug effects/metabolism/physiology ; Calcium/metabolism ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology ; Fluorescent Dyes ; Homeostasis/drug effects ; Humans ; In Vitro Techniques ; Kinetics ; Platelet-Derived Growth Factor/*pharmacology ; Rats ; Vasoconstriction/*drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1986-05-23
    Description: The virulence loci of Agrobacterium tumefaciens are a set of linked transcriptional units that play an essential role in the early stages of plant tumorigenesis. These loci are induced upon cocultivation of the bacteria with plant cells. Seven phenolic compounds that are widely distributed among the angiosperm plants--catechol, gallic acid, pyrogallic acid, p-hydroxybenzoic acid, protocatechuic acid, beta-resorcylic acid, and vanillin--are able to induce the expression of the virulence loci. These phenolics in combination induce each transcriptional locus of the vir loci. Furthermore, this induction displays similar kinetics and genetic control to that observed during cocultivation of the bacteria with plant cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolton, G W -- Nester, E W -- Gordon, M P -- R01 GM32618/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):983-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085219" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Culture Media ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects ; Genetic Engineering ; Phenols/*pharmacology ; Rhizobium/*genetics/pathogenicity ; beta-Galactosidase/genetics
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