Is doxorubicin-induced mitochondrial dysfunction secondary to nuclear p53 activation in H9c2 cardiomyoblasts?
Mitochondrial dysfunction in H9c2 myoblasts treated with DOX is a consequence of nuclear p53 activation rather than a direct effect of the drug on mitochondria.
Morbidity in terms of permanent RLN palsy and hypocalcaemia was less frequent among patients operated on by endocrine-dedicated surgeons. Differences in surgical volume and specialized training in neck endocrine surgery may explain these variations in morbidity.