By studying mice in late adolescence, Johns Hopkins University researchers have discovered that the rapid bone growth associated with puberty is slowed not only by fewer cartilage cell divisions but also by the "aging" of bone cell precursor cells. After investigating the signaling molecules that promote this transition, the scientists conclude that some weak and brittle bone conditions in both children and adults may be due to the cells' premature "retirement" caused by glucocorticoid treatments given during puberty to treat chronic inflammation resulting from rheumatoid disorders and other diseases.
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