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  • 1
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    Nicotine activation of alpha4* receptors: sufficient for reward, tolerance, and sensitization (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-11-06
    Beschreibung: The identity of nicotinic receptor subtypes sufficient to elicit both the acute and chronic effects of nicotine dependence is unknown. We engineered mutant mice with a4 nicotinic subunits containing a single point mutation, Leu9' --〉 Ala9' in the pore-forming M2 domain, rendering a4* receptors hypersensitive to nicotine. Selective activation of a4* nicotinic acetylcholine receptors with low doses of agonist recapitulates nicotine effects thought to be important in dependence, including reinforcement in response to acute nicotine administration, as well as tolerance and sensitization elicited by chronic nicotine administration. These data indicate that activation of a4* receptors is sufficient for nicotine-induced reward, tolerance, and sensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapper, Andrew R -- McKinney, Sheri L -- Nashmi, Raad -- Schwarz, Johannes -- Deshpande, Purnima -- Labarca, Cesar -- Whiteaker, Paul -- Marks, Michael J -- Collins, Allan C -- Lester, Henry A -- DA-15663/DA/NIDA NIH HHS/ -- DA-3194/DA/NIDA NIH HHS/ -- MH-49716/MH/NIMH NIH HHS/ -- NS-11756/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1029-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528443" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alkaloids/metabolism ; Animals ; Azocines/metabolism ; Bicyclo Compounds, Heterocyclic/metabolism ; Brain/drug effects/metabolism ; Calcium/metabolism ; Cells, Cultured ; *Drug Tolerance ; Leucine ; Mice ; Mice, Inbred C57BL ; Motor Activity/drug effects ; Neurons/metabolism ; Nicotine/*pharmacology ; Point Mutation ; Pyridines/metabolism ; Quinolizines/metabolism ; Receptors, Nicotinic/genetics/*physiology ; *Reward ; Serine ; Tobacco Use Disorder/*metabolism ; Up-Regulation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1984-02-17
    Beschreibung: The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B J -- Robin, E D -- Tapper, D P -- Wong, R J -- Clayton, D A -- 5 R01 HL23701-14/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):707-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320368" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aerobiosis ; Anaerobiosis ; Animals ; Anoxia/physiopathology ; Citrate (si)-Synthase/genetics/*metabolism ; DNA, Mitochondrial/*genetics ; Electron Transport Complex IV/genetics/*metabolism ; Macrophages/*enzymology ; Mice ; Mitochondria/*enzymology ; Mitochondria, Muscle/*enzymology ; Oxidoreductases/genetics/*metabolism ; Oxo-Acid-Lyases/*metabolism ; Rats
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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    AKTUELLE ARTIKEL
  • 3
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    An enzymatic system for removing heparin in extracorporeal therapy (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1982-07-16
    Beschreibung: The need to fully heparinize patients undergoing extracorporeal therapy often leads to hemorrhagic complications. To enable heparinization of only the extracorporeal circuit, a blood filter containing immobilized heparinase was developed. This filter degraded 99 percent of heparin's anticoagulant activity within minutes in both canine and human blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langer, R -- Linhardt, R J -- Hoffberg, S -- Larsen, A K -- Cooney, C L -- Tapper, D -- Klein, M -- GM 25810/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1982 Jul 16;217(4556):261-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7089564" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Extracorporeal Circulation ; Flavobacterium/enzymology ; Hemorrhage/prevention & control ; Heparin/*blood ; Heparin Lyase ; Humans ; Polysaccharide-Lyases ; *Renal Dialysis/adverse effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
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