Does cardiac myocyte-specific expression of inducible nitric oxide synthase protect against ischemia/reperfusion injury by preventing mitochondrial permeability transition?
Cardiomyocyte-restricted expression of iNOS provides sustained cardioprotection. This cardioprotection is associated with a decrease in reperfusion-induced oxygen radicals and inhibition of mitochondrial swelling and permeability transition.
Men with complete spinal cord injury have markedly deteriorated trabecular bone microarchitecture in the knee, which may contribute to their increased fracture incidence.