Although opacification grade in the intrahepatic left portal vein

was not statistically significant between CO2-based and ICM-based images (P = 0.1515), check details weak opacification was significantly frequent on CO2-based images (weak 10, sufficient 10) compared to ICM-based images (weak 0, sufficient 20; P = 0.0003) in the intrahepatic right portal vein. Inter-reviewer agreement was excellent between the two reviewers for CO2-based images (kappa = 0.913) and ICM-based images (kappa = 0.924). Conclusions:  Carbon dioxide may be a first-line contrast material for evaluating portal vein images by PTP. “
“Serum testosterone is reduced in up to 90% of men with cirrhosis, with levels falling as liver disease advances. Testosterone is an important anabolic hormone, with effects on muscle, bone, and haematopoiesis. Many of the features of advanced liver disease are similar to those seen in hypogonadal

men, including sarcopenia, osteoporosis, gynecomastia and low libido. However the relative contribution of testosterone deficiency to the symptomatology of advanced liver disease has not been well established. More recently it has been demonstrated that low testosterone in men with cirrhosis is associated with increased mortality, independent of the classically recognised prognostic factors such as MELD score. Only several small clinical trials have examined the role of testosterone therapy in men with cirrhosis, PS-341 none of which have resolved the issue of whether or not testosterone is beneficial. However, in men with organic hypogonadism due to structural

hypothalamic-pituitary-testicular axis disease, testosterone therapy has been shown to improve muscle mass, bone mineral density, increase haemoglobin and reduce insulin resistance. Despite initial concerns linking testosterone with hepatocellular carcinoma, more recent data suggests that this risk has been overstated. MCE公司 There is therefore now a strong rationale to assess the efficacy and safety of testosterone therapy in cirrhosis in well-designed randomised controlled trials. “
“miR-17-5p is overexpressed in hepatocellular carcinoma (HCC), but the specific regulatory mechanisms of miR-17-5p in HCC remain unknown. We investigated the molecular basis of miR-17-5p as an oncogene in human HCC cell lines. Our in vivo and in vitro data indicate that miR-17-5p up-regulates the migration and proliferation of HCC cells. Interestingly, proteomic and western blotting assays revealed that miR-17-5p significantly activates the p38 mitogen-activated protein kinase MAPK pathway and increases the phosphorylation of heat shock protein 27 (HSP27). Our results also suggest that E2F1-dependent down-regulation of Wip1 regulates miR-17-5p-p38-HSP27 signaling.