Dystrophin proteolysis: a potential target for MMP-2 and its prevention by ischemic preconditioning.

Dystrophin is responsible for the mechanical stabilization of the sarcolemma, and it has been shown that it is one of the most sensitive proteins to ischemic injury. However, the enzyme responsible for this proteolysis is still unknown. Isolated rabbit hearts were subjected to 30 min of global ischemia with and without reperfusion (180 min) to determine whether dystrophin is cleaved by matrix metalloproteinase (MMP)-2 during acute ischemia and whether ischemic preconditioning (PC) prevents dystrophin breakdown through MMP-2 inhibition.

Ischemic postconditioning reduces infarct size through the α1-adrenergic receptor pathway.

The α1-adrenergic receptors (α1-ARs) are involved in preconditioning. Given that certain intracellular pathways seem to be shared by preconditioning and postconditioning, it is possible that postconditioning could also be mediated by α1-ARs. The objective was to evaluate, by analyzing infarct size, if α1-ARs activation could trigger postconditioning and also determine Akt and glycogen synthase kinase 3β (GSK-3β) phosphorylation.

[CAP59 gene amplification in Cryptococcus neoformans and Cryptococcus gattii directly from a yeast suspension].

Cryptococcus is an encapsulated yeast of class Basidiomycetes, etiologic agent of cryptococcosis. Cryptococcosis is one of the most common opportunistic infections in immunosuppressed patients, although it can affect immunocompetent individuals. In recent years, the identification of medically important fungal species has been achieved through the amplification of specific regions or genes of fungal DNA by polymerase chain reaction (PCR).