Transcriptional silencing of the death gene BNIP3 by cooperative action of NF-kappaB and histone deacetylase 1 in ventricular myocytes.

Earlier we identified a survival role for NF-kappaB in ventricular myocytes, however, the underlying mechanism was undefined. In this report we provide new mechanistic evidence that the hypoxia-inducible death factor BNIP3 is transcriptionally silenced by NF-kappaB through a mechanism that involves the cooperative actions of HDAC1. Activation of the NF-kappaB signaling pathway in ventricular myocytes suppressed basal and hypoxia-inducible BNIP3 gene activity.

Therapeutic opportunities for cell cycle re-entry and cardiac regeneration.

Over the last two decades, considerable effort has been made to better understand putative regulators and molecular switches that govern the cell cycle in attempts to reactivate cell cycle progression of cardiac muscle. Rapid advancements on the field of stem cycle biology including evidence of cardiac progenitors within the adult myocardium itself and reports of cardiomyocyte DNA synthesis, which each suggest that the adult myocardium may in fact have the capacity for de novo myocyte regeneration. Augmenting cardiomyocyte number by targeting specific cell cycle regulatory genes or by stimulating cardiac progenitor cells to differentiate into cardiac muscle may be of therapeutic value in repopulating the adult myocardium with functionally active cells in patients with end-stage heart failure.

A review of clinical failures associated with macrolide-resistant Streptococcus pneumoniae.

The emerging reports of clinical failures using macrolides and their associations with macrolide-resistant Streptococcus pneumoniae prompted us to review the literature describing these cases. Thirty-three cases reporting macrolide treatment failure during treatment of pneumococcal infections were available for review. The most prevalent diagnosis (24/27 or 88.