Shunji Nagai, Atsushi Yoshida, Marcelo Facciuto, Dilip Moonka, Marwan S. Abouljoud, Myron E. Schwartz, Sander S. Florman – 7 August 2014 – Although experimental evidence has indicated that ischemia‐reperfusion (I/R) injury of the liver stimulates growth of micrometastases and adhesion of tumor cells, the clinical impact of I/R injury on recurrence of hepatocellular carcinoma (HCC) after liver transplantation (LT) has not been fully investigated.

Charlotte Hedskog, Brian Doehle, Krishna Chodavarapu, Viktoria Gontcharova, Javier Crespo Garcia, Robert De Knegt, Joost P.H Drenth, John G. McHutchison, Diana Brainard, Luisa M. Stamm, Michael D. Miller, Evguenia Svarovskaia, Hongmei Mo – 7 August 2014 – To date, intergenotypic recombinant hepatitis C viruses (HCVs) and their treatment outcomes have not been well characterized. This study characterized 12 novel HCV recombinant strains and their response to sofosbuvir in combination with ribavirin (SOF/RBV) treatment.

Betty L. Slagle, Ourania M. Andrisani, Michael J. Bouchard, Caroline G.L. Lee, J.‐H. James Ou, Aleem Siddiqui – 7 August 2014 – Chronic infection with hepatitis B virus (HBV) is a risk factor for developing hepatocellular carcinoma (HCC). The life cycle of HBV is complex and has been difficult to study because HBV does not infect cultured cells. The HBV regulatory X protein (HBx) controls the level of HBV replication and possesses an HCC cofactor role.

Charlotte Hedskog, Brian Doehle, Krishna Chodavarapu, Viktoria Gontcharova, Javier Crespo Garcia, Robert De Knegt, Joost P.H Drenth, John G. McHutchison, Diana Brainard, Luisa M. Stamm, Michael D. Miller, Evguenia Svarovskaia, Hongmei Mo – 7 August 2014 – To date, intergenotypic recombinant hepatitis C viruses (HCVs) and their treatment outcomes have not been well characterized. This study characterized 12 novel HCV recombinant strains and their response to sofosbuvir in combination with ribavirin (SOF/RBV) treatment.

Jeremie Guedj, Yaron Rotman, Scott J. Cotler, Christopher Koh, Peter Schmid, Jeff Albrecht, Vanessa Haynes‐Williams, T. Jake Liang, Jay H. Hoofnagle, Theo Heller, Harel Dahari – 7 August 2014 – There is little information on the early kinetics of hepatitis delta virus (HDV) and hepatitis B surface antigen (HBsAg) during interferon‐α therapy. Here a mathematical model was developed and fitted to frequent HDV and HBsAg kinetic data from 10 patients during the first 28 weeks of pegylated‐interferon‐α2a (peg‐IFN) therapy.

Hélène Dubois‐Pot‐Schneider, Karim Fekir, Cédric Coulouarn, Denise Glaise, Caroline Aninat, Kathleen Jarnouen, Rémy Le Guével, Takashi Kubo, Seiichi Ishida, Fabrice Morel, Anne Corlu – 6 August 2014 – Human hepatocellular carcinoma (HCC) heterogeneity promotes recurrence and resistance to therapies. Recent studies have reported that HCC may be derived not only from adult hepatocytes and hepatoblasts but also hepatic stem/progenitors.

Christoph Schramm, Inka Wahl, Ansgar W. Lohse – 6 August 2014

Giovanni Battista Levi Sandri – 6 August 2014

Mercedes Fernandez – 5 August 2014 – Over the past two decades the advances in molecular cell biology have led to significant discoveries about the pathophysiology of portal hypertension (PHT). In particular, great progress has been made in the study of the molecular and cellular mechanisms that regulate the increased intrahepatic vascular resistance (IHVR) in cirrhosis. We now know that the increased IHVR is not irreversible, but that both the structural component caused by fibrosis and the active component caused by hepatic sinusoidal constriction can be, at least partially, reversed.

Mercedes Fernandez – 5 August 2014 – Over the past two decades the advances in molecular cell biology have led to significant discoveries about the pathophysiology of portal hypertension (PHT). In particular, great progress has been made in the study of the molecular and cellular mechanisms that regulate the increased intrahepatic vascular resistance (IHVR) in cirrhosis. We now know that the increased IHVR is not irreversible, but that both the structural component caused by fibrosis and the active component caused by hepatic sinusoidal constriction can be, at least partially, reversed.