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  • Dose-Response Relationship, Drug
  • American Association for the Advancement of Science (AAAS)  (12)
  • American Chemical Society
  • Elsevier
  • Oxford University Press
  • 1980-1984  (12)
  • 1925-1929
  • 1984  (12)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (12)
  • American Chemical Society
  • Elsevier
  • Oxford University Press
Years
  • 1980-1984  (12)
  • 1925-1929
Year
  • 1
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    Criteria for evidence of chemical carcinogenicity. Interdisciplinary Panel on Carcinogenicity (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-08-17
    Description: The Interdisciplinary Panel on Carcinogenicity reviewed and reevaluated criteria for assessing evidence of carcinogenicity of chemical substances. The panel reviewed criteria applicable to data derived from human epidemiological studies and from both in vivo and in vitro laboratory studies. A critical appraisal of all these sources of information led to the conclusion that the characterization of human risk always requires interdisciplinary evaluation of the entire array of data on a case-by-case basis. Animal studies, whenever possible, should be augmented by studies of mechanisms, metabolism, and pharmacodynamics. Such studies may assist in assessing risk to man. Recognizing the utility of such data should point the way for better assessment in the future.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1984 Aug 17;225(4663):682-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6463646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; *Carcinogens/metabolism/pharmacology ; Carcinogens, Environmental ; Cell Transformation, Neoplastic ; Dose-Response Relationship, Drug ; Environmental Exposure ; Epidemiologic Methods ; Humans ; In Vitro Techniques ; Mixed Function Oxygenases/metabolism ; Mutagenicity Tests ; Neoplasms/chemically induced ; Risk ; Time Factors ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Opioid peptides mediate the suppressive effect of stress on natural killer cell cytotoxicity (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-13
    Description: The cytotoxic activity of natural killer cells was investigated in rats subjected to one of two inescapable footshock stress paradigms, both of which induce analgesia, but only one via activation of opioid mechanisms. Splenic natural killer cell activity was suppressed by the opioid, but not the nonopioid, form of stress. This suppression was blocked by the opioid antagonist naltrexone. Similar suppression of natural killer activity was induced by high doses of morphine. These results suggest that endogenous opioid peptides mediate the suppressive effect of certain forms of stress on natural killer cell cytotoxicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shavit, Y -- Lewis, J W -- Terman, G W -- Gale, R P -- Liebeskind, J C -- MH15795/MH/NIMH NIH HHS/ -- NS07628/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):188-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691146" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cytotoxicity, Immunologic/drug effects ; Dose-Response Relationship, Drug ; Endorphins/*physiology ; Female ; Killer Cells, Natural/*immunology ; Morphine/*pharmacology ; Naltrexone/pharmacology ; Rats ; Rats, Inbred F344 ; Stress, Physiological/*immunology
    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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    Insect prothoracicotropic hormone: evidence for two molecular forms (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-15
    Description: In an insect, the tobacco hornworm Manduca sexta, the cerebral neuropeptide prothoracicotropic hormone (PTTH), the primary effector of postembryonic development, exists as two molecular forms. These two PTTH's elicit characteristic in vitro dose responses of activation of prothoracic glands from different developmental stages, an indication that during development the glands change in their sensitivity to the neurohormones. Both PTTH's are active in a specific in situ bioassay. Since they may be released in situ at stage-specific times to evoke distinctly different developmental responses, the PTTH neuroendocrine axis appears to be an effective system for determining the functions of molecular forms of a neurohormone in the regulation of growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bollenbacher, W E -- Katahira, E J -- O'Brien, M -- Gilbert, L I -- Thomas, M K -- Agui, N -- Baumhover, A H -- AM-30118/AM/NIADDK NIH HHS/ -- AM-31642/AM/NIADDK NIH HHS/ -- NS-18791/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 15;224(4654):1243-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6732895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Bombyx ; Chromatography, Gel ; Dose-Response Relationship, Drug ; Insect Hormones/pharmacology/*physiology ; Insects/drug effects/growth & development/physiology ; Isoelectric Focusing ; Larva
    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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    Potentiation of bleomycin lethality by anticalmodulin drugs: a role for calmodulin in DNA repair (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-22
    Description: Treatment of exponentially growing Chinese hamster ovary cells with bleomycin causes a dose-dependent decrease in cell survival due to DNA damage. This lethal effect can be potentiated by the addition of a nonlethal dose of the anticalmodulin drug N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide ( W13 ) but not its inactive analog N-(4-aminobutyl)-2-naphthalenesulfonamide ( W12 ). By preventing the repair of damaged DNA, W13 also inhibits recovery from potentially lethal damage induced by bleomycin. These data suggest a role for calmodulin in the DNA repair pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chafouleas, J G -- Bolton, W E -- Means, A R -- RR-05425/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 22;224(4655):1346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6203171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bleomycin/*pharmacology ; Calmodulin/*antagonists & inhibitors/*physiology ; Cell Division/drug effects ; Cell Line ; Cell Survival/drug effects ; Cricetinae ; Cricetulus ; DNA Repair/*drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Sulfonamides/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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    A potential second messenger role for unsaturated fatty acids: activation of Ca2+-dependent protein kinase (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-05-11
    Description: Arachidonate and other unsaturated long-chain fatty acids were found to activate protein kinase C from human neutrophils. Kinase activation by arachidonate required calcium and was enhanced by diolein but did not require exogenous phosphatidylserine. Submaximal levels of arachidonate also enhanced the affinity of the kinase for calcium during activation by phosphatidylserine. Thus the release of arachidonate, which is triggered in many cell types by ligand-receptor interactions, could play a second messenger role in the regulation of cellular function by activation of protein kinase C.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McPhail, L C -- Clayton, C C -- Snyderman, R -- 5PO1CA29589/CA/NCI NIH HHS/ -- 5RO-1DEO3738/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1984 May 11;224(4649):622-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6231726" target="_blank"〉PubMed〈/a〉
    Keywords: Arachidonic Acid ; Arachidonic Acids/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; Fatty Acids, Unsaturated/pharmacology/*physiology ; Humans ; Kinetics ; Neutrophils/enzymology ; Phosphatidylserines/pharmacology ; Protein Kinase C ; Protein Kinases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Kainic acid induces sprouting of retinal neurons (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-03
    Description: The neurotoxin kainic acid caused dose-dependent morphological changes in horizontal cells of the retinas of adult cats and rabbits. High concentrations of kainic acid killed the cells, but when exposed to sublethal doses they contracted their dendritic fields and sent sprouting processes into the inner retina. It appears that kainic acid can induce neuronal growth as well as degeneration and that the potential for morphological plasticity is still present in neurons of the adult mammalian retina.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peichl, L -- Bolz, J -- New York, N.Y. -- Science. 1984 Feb 3;223(4635):503-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Dendrites/ultrastructure ; Dose-Response Relationship, Drug ; Kainic Acid/*pharmacology ; Nerve Degeneration/drug effects ; Neurons/cytology/*drug effects ; Pyrrolidines/*pharmacology ; Rabbits ; Retina/cytology/*drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Potentiation of opiate analgesia and apparent reversal of morphine tolerance by proglumide (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-27
    Description: Exogenous cholecystokinin selectively antagonizes opiate analgesia, which suggests that endogenous cholecystokinin may act physiologically as an opiate antagonist and may play a role in opiate tolerance. The use of the selective cholecystokinin antagonist proglumide provided a test of these hypotheses in rats that were either inexperienced with or tolerant to opiates. Proglumide potentiated analgesia produced by morphine and endogenous opiates and seemed to reverse tolerance. These results suggest that endogenous cholecystokinin systems oppose the action of opiates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watkins, L R -- Kinscheck, I B -- Mayer, D J -- DA 00576/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):395-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6546809" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Brain/drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Drug Tolerance/drug effects ; Endorphins/physiology ; Enkephalin, Methionine/analogs & derivatives/pharmacology ; Glutamine/*analogs & derivatives ; Humans ; Injections, Spinal ; Morphine/*pharmacology ; Proglumide/administration & dosage/*pharmacology ; Rats ; Spinal Cord/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Growth hormone-releasing factor: direct effects on growth hormone, glucose, and behavior via the brain (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-26
    Description: Intracerebroventricular administration of human pancreatic growth hormone-releasing factor caused a dose-dependent inhibition of growth hormone secretion, elevated plasma glucose concentrations, and produced marked behavioral and motor effects. Immunoneutralization with antiserum to somatostatin did not reverse the suppression of growth hormone. These findings suggest that hypothalamic growth hormone-releasing factor may regulate its own neurosecretion through an "ultrashort-loop" negative feedback mechanism and may have important neurotransmitter and neuromodulatory functions in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tannenbaum, G S -- New York, N.Y. -- Science. 1984 Oct 26;226(4673):464-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6436973" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; *Blood Glucose ; Dose-Response Relationship, Drug ; Feedback ; Growth Hormone/*secretion ; Growth Hormone-Releasing Hormone/*pharmacology ; Male ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Nicotine is chemotactic for neutrophils and enhances neutrophil responsiveness to chemotactic peptides (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-13
    Description: Neutrophils contribute to chronic bronchitis and pulmonary emphysema associated with cigarette smoking. Nicotine was found to be chemotactic for human neutrophils but not monocytes, with a peak activity at approximately 31 micromolar. In lower concentrations (comparable to those in smokers' plasma), nicotine enhanced the response of neutrophils to two chemotactic peptides. In contrast to most other chemoattractants for neutrophils, however, nicotine did not affect degranulation or superoxide production. Nicotine thus may promote inflammation and consequent lung injury in smokers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Totti, N 3rd -- McCusker, K T -- Campbell, E J -- Griffin, G L -- Senior, R M -- HL16118/HL/NHLBI NIH HHS/ -- HL29594/HL/NHLBI NIH HHS/ -- HL30341/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):169-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318317" target="_blank"〉PubMed〈/a〉
    Keywords: Chemotaxis, Leukocyte/*drug effects ; Complement C5 ; Cytoplasmic Granules/metabolism ; Dose-Response Relationship, Drug ; Muramidase/blood ; N-Formylmethionine Leucyl-Phenylalanine/*pharmacology ; Neutrophils/*drug effects/metabolism ; Nicotine/*pharmacology ; Pancreatic Elastase/blood ; Peroxidase/blood ; Stimulation, Chemical ; Superoxides/blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Behavioral sensitivity to purinergic drugs parallels ethanol sensitivity in selectively bred mice (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-05-04
    Description: Behavioral responses to an adenosine receptor agonist and antagonist were examined in mice genetically selected for differential sensitivity to the soporific effects of ethanol. Both ethanol and the adenosine receptor agonist L-phenylisopropyladenosine had greater sedative and hypothermic effects in ethanol-sensitive "long-sleep" mice than in ethanol-insensitive "short-sleep" mice. Long-sleep mice were also more sensitive to the excitatory behavioral effects of theophylline, an adenosine receptor antagonist. These data suggest that adenosine may be an endogenous mediator of responses to ethanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Proctor, W R -- Dunwiddie, T V -- 07043/PHS HHS/ -- 2702/PHS HHS/ -- New York, N.Y. -- Science. 1984 May 4;224(4648):519-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6324348" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*analogs & derivatives ; Animals ; Behavior, Animal/*drug effects ; Body Temperature/drug effects ; Dose-Response Relationship, Drug ; Escape Reaction/drug effects ; Ethanol/*pharmacology ; Mice ; Phenylisopropyladenosine/*pharmacology ; Receptors, Cell Surface/physiology ; Receptors, Purinergic ; Sleep/*drug effects ; Theophylline/*pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Inhibition of human acute lymphoblastic leukemia cells by immunotoxins: potentiation by chloroquine (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: Immunotoxins containing pokeweed antiviral protein and monoclonal antibodies against human T cells or human transferrin receptor efficiently killed acute lymphoblastic leukemia cells. Chloroquine specifically enhanced the rate of protein synthesis inhibition by immunotoxin. Depending on its concentration, chloroquine (10 to 100 micromolar) reduced by up to 65-fold the amount of immunotoxin required to inhibit protein synthesis in the target cells 50 percent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramakrishnan, S -- Houston, L L -- CA 29889/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):58-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318313" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibodies, Monoclonal ; Cell Line ; Chloroquine/*pharmacology/therapeutic use ; Combined Modality Therapy ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Leukemia, Lymphoid/*metabolism/therapy ; *N-Glycosyl Hydrolases ; Neoplasm Proteins/*biosynthesis ; Plant Proteins/*pharmacology ; Receptors, Cell Surface/immunology ; Receptors, Transferrin ; Ribosome Inactivating Proteins, Type 1 ; T-Lymphocytes/immunology
    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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  • 12
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    Reversal of adriamycin resistance by verapamil in human ovarian cancer (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-01
    Description: The effectiveness of adriamycin in the treatment of ovarian cancer and other human tumors has been limited by the development of drug resistance. Verapamil, a calcium channel blocking agent, completely reversed adriamycin resistance in human ovarian cancer cells with moderate (three- to sixfold) degrees of resistance and partially reversed resistance in highly (150-fold) resistant cells. The potentiating effect of verapamil was due to inhibition of adriamycin efflux in the resistant cells. These results have led to a clinical trial of adriamycin and verapamil in refractory ovarian cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogan, A M -- Hamilton, T C -- Young, R C -- Klecker, R W Jr -- Ozols, R F -- New York, N.Y. -- Science. 1984 Jun 1;224(4652):994-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6372095" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Doxorubicin/*therapeutic use ; Drug Resistance ; Female ; Humans ; Ovarian Neoplasms/*drug therapy ; Verapamil/*therapeutic use
    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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