We examine the sex-specific issues related to myocardial ischemia in women in terms of prevalence and prognosis, traditional and novel risk factors, diagnostic testing, as well as therapeutic management strategies for IHD. (c) 2012 Wiley Periodicals, Inc.”
“Gamboge is a dry resin secreted from Garcinia hanburryi, and gambogenic acid (GNA) is one of the main active compounds of gamboge. We have previously demonstrated the anticancer activity of GNA in A549 cells selleck compound and pointed out its potential effects in anticancer therapies. Previous studies reported that GNA induced apoptosis in many cancer cell lines and inhibited A549 tumor

growth in xenograft of nude mice in vivo. However, the anticancer mechanism of GNA has still not been well studied. In this paper, we have investigated whether GNA-induced apoptosis is critically mediated by the p38 mitogen-activated protein kinase (MAPK) pathway. Our findings revealed that GNA could induce apoptosis, inhibit proliferation, down-regulate the expression of p38 and MAPK, increase the activations of caspase-9, caspase-3, and cytochrome c release. Furthermore, using SB203580, an adenosine triphosphate-competitive inhibitor RG-7388 of p38 MAPK, inhibit the expression of p-p38 and the experimental results show that it may promote the occurrence of

apoptosis induced by GNA. Taken together, these results suggested that up-regulation of the p38 MAPK cascade may account for the activation of GNA-induced apoptosis.”
“Background: Ischemic/hypoxic myocardial damage

and functional impairment of the myocardium occurs immediately after major burns. This experimental study investigated whether GSK923295 mw the prompt cardiac dysfunction initiates hepatic, renal, and intestinal injuries soon after a severe burn.

Methods: Wistar rats were randomized to a sham burn group, a burn group (subjected to 30% total body surface area third-degree burn) that was subdivided into two groups: a simple burn group, observed at 0.5 hour, 1 hour, 3 hours, 6 hours, 12 hours, 24 hours postburn and a group medicated with propranolol (a cardiac inhibitor), cedilanid (a cardiotonic agent), enalaprilat (an angiotensin converting enzyme inhibitor), and cedilanid plus enalaprilat injected at 0.5 hour postburn and observed at 6 hours later. Serum cardiac troponin I, total bile acid, beta2-microglobulin concentrations, and diamine oxidase activity were measured to reflect the severity of cardiac, hepatic, renal, and intestinal injuries that were confirmed by histopathologic observations. Cardiac function and organs’ blood flow were also recorded.

Results: Histopathologic changes and serum cardiac troponin I increase occurred significantly earlier than the other organs, and the organ damage developments followed a similar pattern.