Research Abstract |
We demonstrated that the early pathology of muscular dystrophy (MD) in dyldymice wasa defective growth of muscles, and proposed a bone-muscle-growth-imbalance hypothesis: With age, growing bones will stretch to damage growth-arrested muscles. Further we showed that centronucleation, one of the major pathological changes proceeded with growth in MD and even normal muscles, and presented a working hypothesis that it would be a growth-promotive good alteration. The injury-repair process of myofibers is not well known. Recently we observed that, in experimentally-injured rat muscles, some degenerating myofibers appeared to be filled with mononucleated cells, and postulated a myonucleus-reversion-to-myoblast hypothesis: Injured myofibers would be repaired if their myonuclei succeeded in reversion to the myoblast state to survive, otherwise they would degenerate. Dystrophic muscles seem to suffer from over-inflammation because of frequent injury-repair cycles. Now, steroids are the only medical drugs widely accepted for MD. Along the bqne-muscle-growth-imbalance hypothesis, we assumed that the sex difference in the incidence of MD might be caused by that in the relative growth of height and body weight. Actually, by analyzing the data from the School Health Statistics Research by the Ministry of Education, Culture and Sports of Japan, we found notable sex differences in the relative growth.
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