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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
1981-6-25
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pubmed:abstractText |
Recurrent demyelination was produced in mice by Cuprizone administration. During the second course of Cuprizone, the animals showed greater resistance to the toxin and demyelination occurred slowly and was complete only after prolonged periods. The earliest changes in oligodendrocytes occurred in the most distal processes, the inner cytoplasmic tongues, which showed degenerative changes 3 to 4 weeks before degeneration of the oligodendrocyte cell bodies or demyelination occurred. The results show for the first time that in demyelinating disease, a "dying-back" process similar to that described in axonal disease can affect the oligodendrocyte.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
0364-5134
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
9
|
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
301-5
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7224593-Animals,
pubmed-meshheading:7224593-Axons,
pubmed-meshheading:7224593-Cerebellum,
pubmed-meshheading:7224593-Demyelinating Diseases,
pubmed-meshheading:7224593-Male,
pubmed-meshheading:7224593-Mice,
pubmed-meshheading:7224593-Neuroglia,
pubmed-meshheading:7224593-Oligodendroglia
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pubmed:year |
1981
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pubmed:articleTitle |
Evidence for a "dying-back" gliopathy in demyelinating disease.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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