Sofosbuvir with peginterferon‐ribavirin for 12 weeks in previously treated patients with hepatitis C genotype 2 or 3 and cirrhosis

Eric Lawitz, Fred Poordad, Diana M. Brainard, Robert H. Hyland, Di An, Hadas Dvory‐Sobol, William T. Symonds, John G. McHutchison, Fernando E. Membreno – 16 October 2014 – Sofosbuvir (SOF) in combination with ribavirin (RBV) for 12 or 24 weeks is the current standard of care for patients infected with hepatitis C virus (HCV) genotypes 2 and 3, respectively. However, in clinical trials treatment‐experienced patients, particularly those with cirrhosis, had suboptimal sustained virological response (SVR) rates.

Sofosbuvir with peginterferon‐ribavirin for 12 weeks in previously treated patients with hepatitis C genotype 2 or 3 and cirrhosis

Eric Lawitz, Fred Poordad, Diana M. Brainard, Robert H. Hyland, Di An, Hadas Dvory‐Sobol, William T. Symonds, John G. McHutchison, Fernando E. Membreno – 16 October 2014 – Sofosbuvir (SOF) in combination with ribavirin (RBV) for 12 or 24 weeks is the current standard of care for patients infected with hepatitis C virus (HCV) genotypes 2 and 3, respectively. However, in clinical trials treatment‐experienced patients, particularly those with cirrhosis, had suboptimal sustained virological response (SVR) rates.

Concordance of sustained virological response 4, 12, and 24 weeks post‐treatment with sofosbuvir‐containing regimens for hepatitis C virus

Eric M. Yoshida, Mark S. Sulkowski, Edward J. Gane, Robert W. Herring, Vlad Ratziu, Xiao Ding, Jing Wang, Shu‐Min Chuang, Julie Ma, John McNally, Luisa M. Stamm, Diana M. Brainard, William T. Symonds, John G. McHutchison, Kimberly L. Beavers, Ira M. Jacobson, K.

Concordance of sustained virological response 4, 12, and 24 weeks post‐treatment with sofosbuvir‐containing regimens for hepatitis C virus

Eric M. Yoshida, Mark S. Sulkowski, Edward J. Gane, Robert W. Herring, Vlad Ratziu, Xiao Ding, Jing Wang, Shu‐Min Chuang, Julie Ma, John McNally, Luisa M. Stamm, Diana M. Brainard, William T. Symonds, John G. McHutchison, Kimberly L. Beavers, Ira M. Jacobson, K.

Performance of modified‐release tacrolimus after conversion in liver transplant patients indicates potentially favorable outcomes in selected cohorts

Aisling Considine, J. Michael Tredger, Michael Heneghan, Kosh Agarwal, Marianne Samyn, Nigel D. Heaton, John G. O'Grady, Varuna R. Aluvihare – 13 October 2014 – Clinical outcomes, dose changes, and dose‐equalized tacrolimus concentrations were examined sequentially in 129 liver transplantation (LT) recipients after successful conversion to once daily modified‐release tacrolimus either early (within 1 month) or late (>1 month) after LT. The data were compared with data for a group of 60 patients maintained on twice daily conventional‐release tacrolimus.

Differential effects of targeting Notch receptors in a mouse model of liver cancer

Erik G. Huntzicker, Kathy Hötzel, Lisa Choy, Li Che, Jed Ross, Gregoire Pau, Neeraj Sharma, Christian W. Siebel, Xin Chen, Dorothy M. French – 13 October 2014 – Primary liver cancer encompasses both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA). The Notch signaling pathway, known to be important for the proper development of liver architecture, is also a potential driver of primary liver cancer. However, with four known Notch receptors and several Notch ligands, it is not clear which Notch pathway members play the predominant role in liver cancer.

Knockdown of ezrin causes intrahepatic cholestasis by the dysregulation of bile fluidity in the bile duct epithelium in mice

Ryo Hatano, Kaori Akiyama, Atsushi Tamura, Shigekuni Hosogi, Yoshinori Marunaka, Michael J. Caplan, Yoshiyuki Ueno, Sachiko Tsukita, Shinji Asano – 13 October 2014 – Cholangiopathies share common features, including bile duct proliferation, periportal fibrosis, and intrahepatic cholestasis. Damage of biliary epithelium by autoimunne disorder, virus infection, toxic compounds, and developmental abnormalities causes severe progressive hepatic disorders responsible for high mortality.

Mitochondrial dysfunction in steatotic rat livers occurs because a defect in complex i makes the liver susceptible to prolonged cold ischemia

Michael J. J. Chu, Anthony J. R. Hickey, Yannan Jiang, Amorita Petzer, Adam S. J. R. Bartlett, Anthony R. J. Phillips – 13 October 2014 – Steatotic livers are susceptible to cold ischemia, which is thought to be secondary to mitochondrial dysfunction. Ischemic preconditioning (IPC) has been reported to improve liver function in the setting of warm ischemia/reperfusion injury, but the effect of IPC on steatotic liver mitochondrial function (MF) with cold ischemia has not been previously evaluated.

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