Jeremie Guedj, Alan S. Perelson – 7 March 2011 – Hepatitis C virus (HCV) RNA decay during antiviral therapy is characterized by a rapid first phase, followed by a slower second phase. The current understanding of viral kinetics attributes the magnitude of the first phase of decay to treatment effectiveness, whereas the second phase of decay is attributed to the progressive loss of infected cells. Here, we analyzed data from 44 patients treated with telaprevir, a potent HCV protease inhibitor.

Claus U. Niemann, David J. Kramer – 7 March 2011

Yong‐Han Paik, Keiko Iwaisako, Ekihiro Seki, Sayaka Inokuchi, Bernd Schnabl, Christoph H. Österreicher, Tatiana Kisseleva, David A. Brenner – 7 March 2011 – Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multicomponent enzyme that mediates electron transfer from nicotinamide adenine dinucleotide phosphate to molecular oxygen, which leads to the production of superoxide. NOX2/gp91phox is a catalytic subunit of NOX expressed in phagocytic cells. Several homologues of NOX2, including NOX1, have been identified in nonphagocytic cells.

Cristina R. Bosoi, Christian Parent‐Robitaille, Keith Anderson, Mélanie Tremblay, Christopher F. Rose – 7 March 2011 – The pathogenesis of hepatic encephalopathy is multifactorial, involving gut‐derived toxins such as ammonia, which has been demonstrated to induce oxidative stress. Therefore, a primary hepatic encephalopathy treatment target is reducing ammonia production in the gastrointestinal tract. AST‐120, an oral adsorbent of engineered activated carbon microspheres with surface areas exceeding 1600 m2/g, acts as a sink for neurotoxins and hepatotoxins present in the gut.

Lily Dara, Cheng Ji, Neil Kaplowitz – 7 March 2011 – The unfolded protein response (UPR) is an evolutionarily conserved cell signaling pathway that is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed from increased client protein load or the accumulation of unfolded or malfolded proteins. Once activated, this signaling pathway can either result in the recovery of homeostasis or can activate a cascade of events that ultimately result in cell death.

Syed‐Mohammed Jafri, Amit G. Singal, Daniel Kaul, Robert John Fontana – 7 March 2011 – The optimal means for detecting and managing liver transplantation (LT) patients with latent tuberculosis (TB) are not well defined. Our study aims were to (1) determine the frequency and risk factors of latent TB in a large cohort of consecutive adult LT candidates and (2) determine the safety and efficacy of isoniazid treatment in LT recipients with latent TB.

Françoise Degos, Louis Lebrun, Paul Perez, Isabelle Durand‐Zaleski – 7 March 2011

Faouzi Saliba, Sébastien Dharancy, Richard Lorho, Filoména Conti, Sylvie Radenne, Martine Neau‐Cransac, Monika Hurtova, Jean Hardwigsen, Yvon Calmus, Jérome Dumortier – 7 March 2011 – Data on the conversion of patients to everolimus after liver transplantation are sparse. A multicenter, retrospective study followed 240 maintenance liver transplant patients to analyze the current indications for everolimus conversion, the employed regimens and exposure levels, and the impact on efficacy and safety. The mean time from transplantation to the introduction of everolimus was 4.9 ± 5.2 years.

Benjamin L. Shneider, Jerry Vockley, George V. Mazariegos – 7 March 2011

Mauricio Sainz‐Barriga, Luigia Scudeller, Maria Gabriella Costa, Bernard de Hemptinne, Roberto Ivan Troisi – 7 March 2011 – The portal vein flow (PVF), portal vein pressure (PVP), and hepatic venous pressure gradient (HVPG) were prospectively assessed to explore their relationships and to better define hyperflow and portal hypertension (PHT) during liver transplantation (LT). Eighty‐one LT procedures were analyzed. No correlation between PVF and PVP was observed. Increases in the central venous pressure (CVP) were transmitted to the PVP (58%, range = 25%‐91%, P = 0.001).