pylori, particularly in patients with previous eradication failure.

Our results suggest that testing for susceptibility of H. pylori to quinolones is useful for determining the optimal rescue eradication regimen. “
“Background and Aim: DOC-2/DAB2 interactive protein gene (DAB2IP) is a novel member of the Ras GTPase-activating protein family and plays a tumor suppressive role in cancer progression, but its function in hepatocellular carcinoma (HCC) remains unclear. This aims of this study were to analyze the clinicopathological features of DAB2IP expression in HCC, and to determine the effect of DAB2IP on HCC cell behaviors in vitro. Methods:  The expression of DAB2IP was detected in hepatocyte cell line and HCC cell lines by real-time reverse transcription-polymerase HDAC inhibitor chain reaction and western blot. DAB2IP expression was then examined in 120 cases of clinical paraffin-embedded HCC tissue by immunohistochemistry (IHC). 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) method and in vitro invasive assay were finally performed to evaluate the effect of DAB2IP depletion on cell proliferation or invasion of HCC cells. Results: DAB2IP expression was lower in

HCC cell Nutlin-3 concentration lines or tissues than in hepatocyte cell lines, adjacent cirrhotic livers or normal livers (P < 0.05). Its expression was positively correlated with tumor size (P = 0.01). Patients with lower DAB2IP expression had shorter overall survival time (P = 0.013). DAB2IP suppresses proliferation and invasion of HCC cells in vitro. Conclusion:  DAB2IP is a valuable marker for progression of HCC patients. Downregulation of DAB2IP is associated with poor prognosis in HCC patients. DAB2IP silence alone is sufficient to promote HCC cell proliferation

and invasion in vitro. “
“Direct measurement of portal learn more pressure (PP) is too invasive to be of clinical use. The most accurate, clinically acceptable measure of PP is by catheterization of the hepatic vein and determination of the intrahepatic wedge pressure gradient, which represents, under certain simple assumptions, the pressure in the portal vein (PV). In this issue, Lisotti et al. propose a pharmacologic approach for measurement of PP. Indocyanine green (ICG) is taken up into hepatocytes and excreted into the bile. They measured ICG blood levels 5, 10, and 15 minutes after injection of a specified amount. They hypothesized that in the case of portal hypertension (PH) and the presence of collaterals, retention of ICG will be higher. They prospectively enrolled 96 consecutive patients with Child A cirrhosis and reported an excellent correlation between the hepatic venous pressure gradient and ICG retention at 15 minutes. Moreover, they identified values for this parameter that are predictive for the presence and absence of esophageal varices.