After liver transplantation (LT), serum cholesterol levels are probably not determinant because metabolic syndrome and liver steatosis are frequently present after LT.3 In fact, the observed diminished response has been hypothesized to be due to decreased interferon bioavailability in overweight patients and the presence of hepatic steatosis,

which itself is a predictor of a poor response to antiviral treatment.4-6 After LT, metabolic syndrome and liver steatosis could lead to altered viral clearance and a decrease in SVR independently of cholesterol levels. Gianni Testino M.D.*, Paolo Borro M.D.*, * Department of Specialistic Medicine, San Martino Hospital, Genoa, Italy. “
“Based on the cellular and molecular mechanisms underlying see more hepatic fibrogenesis, several kinds of approaches have been proposed to treat liver fibrosis. Among a number of growth factors

and cytokines that regulate collagen metabolism, transforming growth factor (TGF)-β is the most potent factor to accelerate liver fibrosis by activating hepatic PD0325901 stellate cells, stimulating collagen gene transcription, and suppressing matrix metalloproteinases expression. Thus, TGF-β as well as its intracellular mediators, Smad proteins, can be potential therapeutic targets for liver fibrosis. Constitutive phosphorylation and nuclear accumulation of Smad3 is the common feature of activated stellate cells. We have synthesized a novel small compound that inhibits Smad3-dependent collagen gene transcription by promoting nuclear import of a transcriptional repressor, YB-1. Another insight into anti-fibrotic strategies is the contribution of bone marrow-derived cells to the regression of liver fibrosis. Administration of granulocyte-colony stimulating factor enhanced the migration of bone marrow-derived cells into fibrotic liver tissue and accelerated the regression of experimental liver fibrosis. We have recently identified novel unknown factors expressed by bone marrow-derived cells that not only ameliorate liver fibrosis but also accelerate regeneration of fibrotic liver. “
“The purpose of this study was to perform a meta-analysis of all available

studies of the diagnostic performance of diffusion-weighted imaging (DWI) in the detection of hepatocellular carcinoma (HCC) in patients with chronic liver disease. Databases including MEDLINE and EMBASE were searched Rho for relevant original articles published from January 2000 to April 2012. Pooled estimation and subgroup analysis data were obtained by statistical analysis. Across the nine studies (476 patients), DWI sensitivity was 81% (95%CI: 67%–90%), and specificity was 89% (95% CI: 76%–95%). Overall, positive likelihood ratio was 7.11 (95%CI: 3.50, 14.48), negative likelihood ratio was 0.21 (95%CI: 0.12–0.37), and the diagnostic odds ratio (DOR) was 33.48 (95%CI: 16.67–67.25). The area under the curve of the summary receiver operator characteristic (ROC) was 0.92 (95% CI:0.89–0.94).