Treatment with Optifast reduces hepatic steatosis and increases candidacy rates for living donor liver transplantation

Adam Doyle, Oyedele Adeyi, Korosh Khalili, Sandra Fischer, Martin Dib, Nicolas Goldaracena, Jayne Dillon, David Grant, Mark Cattral, Ian McGilvray, Paul Greig, Anand Ghanekar, Leslie Lilly, Eberhard Renner, Gary Levy, Nazia Selzner – 17 June 2016

Shared genetic effects between hepatic steatosis and fibrosis: A prospective twin study

Jeffrey Cui, Chi‐Hua Chen, Min‐Tzu Lo, Nicholas Schork, Ricki Bettencourt, Monica P. Gonzalez, Archana Bhatt, Jonathan Hooker, Katherine Shaffer, Karen E. Nelson, Michelle T. Long, David A. Brenner, Claude B. Sirlin, Rohit Loomba, for the Genetics of NAFLD in Twins Consortium – 17 June 2016 – Nonalcoholic fatty liver disease is associated with metabolic risk factors including hypertension and dyslipidemia and may progress to liver fibrosis. Studies have shown that hepatic steatosis and fibrosis are heritable, but whether they have a significant shared gene effect is unknown.

Liver transplant outcomes using ideal donation after circulatory death livers are superior to using older donation after brain death donor livers

Joseph R. Scalea, Robert R. Redfield, David P. Foley – 17 June 2016 – Multiple reports have demonstrated that liver transplantation following donation after circulatory death (DCD) is associated with poorer outcomes when compared with liver transplantation from donation after brain death (DBD) donors. We hypothesized that carefully selected, underutilized DCD livers recovered from younger donors have excellent outcomes.

SIRT1‐mediated transcriptional regulation of SOX2 is important for self‐renewal of liver cancer stem cells

Limei Liu, Chungang Liu, Qianzhen Zhang, Junjie Shen, Heng Zhang, Juanjuan Shan, Guangjie Duan, Deyu Guo, Xuejiao Chen, Jiamin Cheng, Yanmin Xu, Zhi Yang, Chao Yao, Maode Lai, Cheng Qian – 16 June 2016 – Hepatocellular carcinoma (HCC) is a highly aggressive liver tumor containing cancer stem cells (CSCs), which participate in tumor invasion, therapeutic resistance, and tumor relapse leading to poor outcome and limited therapeutic options. Histone deacetylatase sirtuin 1 (SIRT1) has been shown to be up‐regulated in human cancers; however, its role in liver CSCs is unknown.

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