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The histopathological hallmark of the cuprizone model as standardized by Hiremath is oligodendrocyte death and subsequent demyelination in the corpus callosum, superior cerebellar peduncles, hippocampus [42, 46,47,48,49,50,51,52,53,54] and several other areas of the mouse brain (reviewed in [20])
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By all of these features, CRP is assumed to increase ischemic myocard damage by participating aterosclerotic pathogenesis
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