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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
1992-9-23
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pubmed:abstractText |
Using a single skinned muscle fiber, the function of the contractile system and the sarcoplasmic reticulum (SR) were analyzed in the skeletal muscle of the mdx mouse. Activation of the contractile system by calcium ion and the maximum force generation was normal. Ca2+ uptake of the SR was normal as well as regulation of the Ca-induced Ca release (CICR) by Ca2+. However, contracture by caffeine was more prominent in mdx than in control mice. Ca2+ leaked more from the SR of mdx in the presence of EGTA and ATP or its analogue. These abnormalities are probably interrelated; increased leakage of Ca2+ might cause the enhanced response to caffeine, since Ca2+ itself facilitates Ca release by caffeine. The abnormal leakage of Ca2+ might also activate the Ca pump of SR in the resting state, which consume extra ATP and disturb energy metabolism.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-510X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
110
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pubmed:geneSymbol |
mdx
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
160-4
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1506855-Animals,
pubmed-meshheading:1506855-Caffeine,
pubmed-meshheading:1506855-Calcium,
pubmed-meshheading:1506855-Egtazic Acid,
pubmed-meshheading:1506855-Mice,
pubmed-meshheading:1506855-Mice, Inbred C57BL,
pubmed-meshheading:1506855-Mice, Neurologic Mutants,
pubmed-meshheading:1506855-Muscle Contraction,
pubmed-meshheading:1506855-Muscles,
pubmed-meshheading:1506855-Muscular Dystrophy, Animal,
pubmed-meshheading:1506855-Reference Values,
pubmed-meshheading:1506855-Sarcoplasmic Reticulum
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pubmed:year |
1992
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pubmed:articleTitle |
Increased leakage of calcium ion from the sarcoplasmic reticulum of the mdx mouse.
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pubmed:affiliation |
Department of Neurology, Toranomon Hospital, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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