作者: R. J. PENNINGTON
DOI: 10.1038/192884A0
关键词:
摘要: THE discovery1, in 1955, of a hereditary myopathy strain mice has provided useful subject for the investigation muscular dystrophy. Although ultimate cause mouse disease may not be identical with any human dystrophies, it is reasonable assumption that many secondary changes will similar. A number workers have reported quantitative enzyme dystrophic muscle. Some activities, example, cathepsins2 and glucose-6-phosphate dehydrogenase3, show an increase; others, lactic dehydrogenase4 phosphorylase5, are decreased.