Nicole Appel, Ralf Bartenschlager – 22 February 2006 – MicroRNAs are small RNA molecules that regulate messenger RNA (mRNA) expression. MicroRNA 122 (miR‐122) is specifically expressed and highly abundant in the human liver. We show that the sequestration of miR‐122 in liver cells results in marked loss of autonomously replicating hepatitis C viral RNAs. A genetic interaction between miR‐122 and the 5′ noncoding region of the viral genome was revealed by mutational analyses of the predicted microRNA binding site and ectopic expression of miR‐122 molecules containing compensatory mutations.

Manuel Hernández‐Guerra, Juan C. García‐Pagán, Juan Turnes, Pablo Bellot, Ramón Deulofeu, Juan G. Abraldes, Jaime Bosch – 22 February 2006 – Patients with cirrhosis show intrahepatic endothelial dysfunction, characterized by an impaired flow‐dependent vasorelaxation. This alteration is responsible for the marked postprandial increase in portal pressure and is attributed to an insufficient release of nitric oxide (NO).

Gary A. Levy, Gord Adamson, M. James Phillips, Louise A. Scrocchi, Laisum Fung, Pieter Biessels, Nancy F. Ng, Anand Ghanekar, Andrea Rowe, Max Xuezhong Ma, Adam Levy, Cheryl Koscik, William He, Reginald Gorczynski, Steve Brookes, Caroline Woods, Ian D. McGilvray, David Bell – 22 February 2006 – Side effects of interferon–ribavirin combination therapy limit the sustained viral response achievable in hepatitis C virus (HCV) patients. Coupling ribavirin to macromolecular carriers that target the drug to the liver would reduce systemic complications.

Jérôme Dumortier, Sophie Bernard, Yves Bouffard, Olivier Boillot – 22 February 2006 – Adverse effects associated with calcineurin inhibitors may impact their clinical utility in some patients. This study characterizes the clinical outcomes of liver transplanted (LT) patients who experienced diabetes mellitus (DM) on tacrolimus‐based regimen and were converted to cyclosporine‐based therapy. Since January 2002, all patients with DM on a tacrolimus‐based regimen were recruited and converted to cyclosporine‐based therapy, after a 6‐month minimal follow‐up after LT.

Adrian Reuben – 22 February 2006

Peter A Bonis, Marshall Kaplan – 22 February 2006

Claudia Zwingmann, Marc Bilodeau – 22 February 2006 – The hepatoprotective mechanisms of N‐acetylcysteine (NAC) in non–acetaminophen‐induced liver injury have not been studied in detail. We investigated the possibility that NAC could affect key pathways of hepatocellular metabolism with or without changes in glutathione (GSH) synthesis. Hepatocellular metabolites and high‐energy phosphates were quantified from mouse liver extracts by 1H‐ and 31P‐NMR (nuclear magnetic resonance) spectroscopy.

Chihiro Morishima, Denise M. Paschal, Chia C. Wang, Christina S. Yoshihara, Brent L. Wood, Anthony E. T. Yeo, Scott S. Emerson, Margaret C. Shuhart, David R. Gretch – 22 February 2006 – Prior studies have suggested that natural killer (NK) cell function might be impaired in chronic hepatitis C virus (HCV) infection. Circulating NK cell frequency and cytolytic activity were examined freshly ex vivo in HCV‐infected and uninfected subjects. Surprisingly, the intrinsic cytolytic activity of peripheral blood NK‐enriched cells was similar between HCV‐infected and uninfected groups (P = .91).

M. Salud García‐Ayllón, M. Ximena Silveyra, Asunción Candela, Antonio Compañ, Joan Clària, Rodrigo Jover, Miguel Pérez‐Mateo, Vicente Felipo, Salvador Martínez, Joan Galcerán, Javier Sáez‐Valero – 22 February 2006 – Classical studies of cholinesterase activity during liver dysfunction have focused on butyrylcholinesterase (BuChE), whereas acetylcholinesterase (AChE) has not received much attention. In the current study, liver and plasma AChE levels were investigated in rats with cirrhosis induced after 3 weeks of bile duct ligation (BDL).

Anita Pathil, Sorin Armeanu, Sascha Venturelli, Paolo Mascagni, Thomas S. Weiss, Michael Gregor, Ulrich M. Lauer, Michael Bitzer – 22 February 2006 – Hepatocellular carcinoma (HCC) displays a striking resistance to chemotherapeutic drugs or innovative tumor cell apoptosis–inducing agents such as tumor necrosis factor–related apoptosis‐inducing ligand (TRAIL). Recently, we found 2 histone deacetylase inhibitors (HDAC‐I), valproic acid and ITF2357, exhibiting inherent therapeutic activity against HCC.