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  • 1
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    Lithium reduces the number of acetylcholine receptors in skeletal muscle (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-10-17
    Description: Extended treatment of rats with lithium inhibits the increase in the number of extrajunctional acetylcholine receptors that occurs in their denervated skeletal muscle. In normal muscle, lithium reduces the number of acetylcholine receptors at neuromuscular junctions. These changes appear to be a relatively specific effect of lithium on the turnover of receptors. Skeletal muscle provides an accessible system for analyzing the role of lithium (and other cations) in the regulation of cell surface receptors. This regulation may play a role in the mechanism by which lithium prevents recurrent manic-depressive episodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pestronk, A -- Drachman, D B -- 5P01-NS10920/NS/NINDS NIH HHS/ -- 5R01-HD04817/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1980 Oct 17;210(4467):342-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7423198" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Female ; Lithium/*pharmacology ; Muscle Denervation ; Muscles/*drug effects/metabolism ; Neuromuscular Junction/drug effects ; Rats ; Receptors, Cholinergic/*metabolism
    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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    Susceptibility of skeletal muscle to Coxsackie A2 virus infection: effects of botulinum toxin and denervation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: Coxsackie A viruses can infect denervated but not innervated mature skeletal muscles. The role of synaptic transmission in preventing susceptibility to Coxsackievirus infection was studied by surgically denervating leg muscles of mice or injecting the muscles with botulinum toxin to block quantal release of acetylcholine. Control muscles were injected with heat-inactivated toxin. Subsequent injection of Coxsackie A2 virus resulted in extensive virus replication and tissue destruction in the denervated and botulinum toxin-treated muscles, while the control muscles showed only minimal changes. This suggests that the susceptibility of skeletal muscle to Coxsackievirus infection is regulated by synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andrew, C G -- Drachman, D B -- Pestronk, A -- Narayan, O -- 5 K07 NS 00531-02/NS/NINDS NIH HHS/ -- 5R01 HD04817/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):714-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Botulinum Toxins/*pharmacology ; Coxsackievirus Infections/*microbiology ; Enterovirus/*pathogenicity ; Mice ; *Muscle Denervation ; Muscles/drug effects/microbiology ; Muscular Diseases/*microbiology ; Sciatic Nerve/physiology
    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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  • 3
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    Rapid degradation of "new" acetylcholine receptors at neuromuscular junctions (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-10-07
    Description: Acetylcholine receptors at innervated neuromuscular junctions are very stable, with half-lives reported to be 6 to 13 days. Their turnover is described as a first-order process, implying a single population of receptors. In this study, two subpopulations of acetylcholine receptors at normally innervated junctions have been identified. One has a rapid turnover rate with a half-life of 18.7 hours, similar to that of extrajunctional receptors, and the other has a slow turnover rate with a half-life of 12.4 days. The rapidly turned over subpopulation represents approximately 20 percent of the total junctional receptors. This finding may account for the discrepancies in previous reports of turnover rates and may explain the rapid reversibility in vivo of agents that "irreversibly" block acetylcholine receptors. This finding also implies that the synthesis rate of junctional acetylcholine receptors may be higher than previous estimates. The rapidly turned-over subpopulation may represent receptors that were newly inserted into the neuromuscular junction and that were not yet stabilized by an influence of the motor nerve.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stanley, E F -- Drachman, D B -- 5 P01 NS10920/NS/NINDS NIH HHS/ -- 5 R01 HD04817/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1983 Oct 7;222(4619):67-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6623057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bungarotoxins ; Diaphragm ; Kinetics ; Mice ; Neuromuscular Junction/*metabolism ; Receptors, Cholinergic/biosynthesis/classification/*metabolism ; Synaptic Membranes/metabolism
    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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  • 4
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    Motor nerve sprouting and acetylcholine receptors (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-03-17
    Description: Sprouting of motor nerve terminals was evoked by functional denervation of skeletal muscles brought about by presynaptic blockade or disuse. The amount of sprouting, determined by morphometric measurement, was correlated with the level of extrajunctional acetylcholine receptors. Sprouting was inhibited by blockade of acetylcholine receptors with alpha-bungarotoxin. Extrajunctional acetylcholine receptors may play an important role in eliciting motor nerve terminal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pestronk, A -- Drachman, D B -- New York, N.Y. -- Science. 1978 Mar 17;199(4334):1223-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/204007" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Botulinum Toxins/pharmacology ; Bungarotoxins/*pharmacology ; Female ; Motor Neurons/*physiology ; *Muscle Denervation ; Nerve Endings/physiology/ultrastructure ; Neural Conduction/drug effects ; Neuromuscular Junction/*physiology ; Rats ; Receptors, Cholinergic/drug effects/*physiology ; Synaptic Transmission/drug effects ; Tetrodotoxin/pharmacology
    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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  • 5
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    Effect of myasthenic immunoglobulin on acetylcholine receptors of intact mammalian neuromuscular junctions (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-06-16
    Description: Degradation of acetylcholine receptors of intact mouse neuromuscular junctions was determined in vivo and in vitro by the release of radioactivity from mouse diaphragms labeled with 125I-alpha-bungarotoxin. Treatment of mice with immunoglobulin from myasthenic patients accelerated the degradation rate to approximately three times normal, in both intact animals and organ cultures. The released radioactivity was in the form of [125I]tyrosine, confirming the nature of the degradative process. Accelerated degradation of acetylcholine receptors at neuromuscular junctions may represent an important antibody-mediated mechanisms in myasthenia gravis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stanley, E F -- Drachman, D B -- New York, N.Y. -- Science. 1978 Jun 16;200(4347):1285-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/663610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Reactions ; *Autoantibodies ; Bungarotoxins/metabolism ; Diaphragm ; Humans ; Mice ; Myasthenia Gravis/*immunology/metabolism ; Neuromuscular Junction/*metabolism ; Receptors, Cholinergic/*metabolism
    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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  • 6
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    Alcoholic rhabdomyolysis: an experimental model in the rat (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-04-25
    Description: The main features of alcoholic rhabdomyolysis-skeletal muscle necrosis, marked elevation of serum creatine phosphokinase, and myoglobinuria-were produced in rats by a combination of relatively prolonged (2 to 4 weeks) exposure to ethanol and a brief period of food deprivation. This observation suggests that fasting may similarly trigger muscle injury during binge drinking in man. The effect of fasting is in part related to an increase in blood alcohol due to reduced alcohol clearance and in part caused by a fasting-induced potentiation of the toxic effects of high concentrations of alcohol of skeletal muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haller, R G -- Drachman, D B -- New York, N.Y. -- Science. 1980 Apr 25;208(4442):412-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7189294" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/*complications ; Animals ; Creatine Kinase/blood ; *Disease Models, Animal ; Female ; *Food Deprivation ; Humans ; Muscular Diseases/blood/complications/*etiology/pathology ; Myoglobinuria/etiology ; Phosphates/blood ; Potassium/blood ; Rats ; Sodium/blood
    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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  • 7
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    Induction of suppressor cells specific for AChR in experimental autoimmune myasthenia gravis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-18
    Description: Suppressor cells specific for acetylcholine receptor (AChR) were induced in a population of lymphocytes previously sensitized to AChR, obtained from rats with experimental autoimmune myasthenia gravis (EAMG). The lymphocytes were cultured with the immunosuppressive drug cyclosporin A plus purified AChR for 7 days. These cells, when mixed with lymphocytes from rats with EAMG in vitro, strongly suppressed the antibody response to AChR. They did not inhibit antibody responses to an unrelated antigen, an indication that suppression was specific for AChR. This approach should be a useful way to induce specific suppressor cells from sensitized populations of lymphocytes and may be applicable in the treatment of autoimmune diseases such as myasthenia gravis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McIntosh, K R -- Drachman, D B -- 5RO1 HD04817-16/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):401-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclosporins/pharmacology ; Female ; Lymph Nodes/cytology ; Lymphocytes/drug effects ; Myasthenia Gravis/*immunology ; Rats ; Rats, Inbred Lew ; Receptors, Cholinergic/*immunology ; Spleen/cytology ; T-Lymphocytes, Regulatory/*immunology
    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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  • 8
    Electronic Resource
    Electronic Resource
    The Biology of Myasthenia Gravis (1981)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Neuroscience 4 (1981), S. 195-225 
    Details
    ISSN: 0147-006X
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.ne.04.030181.001211
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    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    GENERAL DISCUSSION (1974)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 228 (1974), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1974.tb20515.x
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    Paper (German National Licenses)
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  • 10
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    Inhibition of methyltransferase reduces the turnover of acetylcholine receptors. (1988)
    National Academy of Sciences
    Details
    Publication Date: 1988-06-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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