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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1991-12-11
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pubmed:abstractText |
The long-term administration of germanium dioxide (GeO2) to rats produced Ge myopathy characterized by the formation of ragged-red fibers. The earliest pathological changes in experimental Ge myopathy were a decrease in cytochrome c oxidase activity and accumulation of high electron-dense materials in mitochondria. These findings suggest that a mitochondrial dysfunction may be most important in the genesis of experimental Ge myopathy, which could be a useful animal model for the investigation of and therapeutic trials for human mitochondrial myopathies.
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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:issn |
0001-6322
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
82
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
55-9
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pubmed:dateRevised |
2007-11-9
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pubmed:meshHeading |
pubmed-meshheading:1950478-Animals,
pubmed-meshheading:1950478-Germanium,
pubmed-meshheading:1950478-Male,
pubmed-meshheading:1950478-Microscopy, Electron,
pubmed-meshheading:1950478-Muscles,
pubmed-meshheading:1950478-Muscular Diseases,
pubmed-meshheading:1950478-Rats,
pubmed-meshheading:1950478-Rats, Inbred Strains,
pubmed-meshheading:1950478-Time Factors,
pubmed-meshheading:1950478-Vacuoles
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pubmed:year |
1991
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pubmed:articleTitle |
Experimental germanium myopathy.
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pubmed:affiliation |
Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
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pubmed:publicationType |
Journal Article
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