“
“Objectives: Propofol is a widely used intravenous anesthetic agent with antioxidant properties. However, the effect of propofol on reactive oxygen species-induced injury in vascular smooth muscle cells is still unknown. In this study, the authors determined the effect of propofol on hydrogen peroxide-induced injury in vascular smooth muscle cells and the potential molecular mechanisms involved.\n\nDesign: Prospective cell and animal study.\n\nSetting: University research laboratory.\n\nSubjects: Sprague-Dawley rats.\n\nInterventions: For the in vitro study, rat vascular smooth muscle cells

pretreated with vehicle or hydrogen peroxide (200 mu M) were exposed to vehicle or increasing concentrations Wnt activation of propofol (10-50 mu M). For the in vivo study, propofol selleck chemicals llc (12 mg kg (-1)/hr(-1), intravenous) or vehicle was administrated into rats after carotid artery angioplasty.\n\nMeasurements and Main Results: The cell survival and cell death were measured by MTT and trypan blue exclusion. Cell

apoptosis was evaluated by terminal deoxynucleotide transferase dUTP nick end labeling staining and cleaved caspase-3 expression. To further elucidate the molecular mechanisms in propofol-mediated cellular effect, the expression of programmed cell death 4 and microRNA-21 were measured. Unexpectedly, propofol exacerbated hydrogen peroxide-induced injury responses in vascular smooth muscle cells as demonstrated by a decrease in cell viability and an increase in trypan blue-stained cells, cell apoptosis, and cleaved caspase-3 expression. In addition, propofol inhibited hydrogen peroxide-induced up-regulation of microRNA-21 Selleckchem MK-2206 and increased its target gene programmed cell death 4. Propofol-mediated injury was attenuated by restoration of microRNA-21 expression. Finally, the pro-injury effect of propofol on vascular cells with increased reactive oxygen species was illustrated in vivo in rat carotid arteries after angioplasty.\n\nConclusions: The results revealed

that propofol exacerbates cell injury in vascular smooth muscle cells with increased reactive oxygen species, at least in part, through microRNA-21 and its target gene, programmed cell death 4. Because increased reactive oxygen species is a common pathologic component in many vascular diseases, the novel findings in the current study suggest that propofol might have some application limitations. (Crit Care Med 2011; 39:738-745)”
“Enigmatochromis lucanusi, a new cichlid genus and species, is described from Guinea (West Africa). It is a member of the chromidotilapiine cichlid clade, and differs from other genera within the group in a combination of morphological characters and coloration patterns; e. g.