Thomas F. Imperiale, Robert W. Klein, Naga Chalasani – 28 March 2007 – Although both β‐blockade (BB) and endoscopic variceal ligation (EVL) are used for primary prevention of variceal bleeding (VB) in patients with cirrhosis with moderate to large esophageal varices (EVs), the more cost‐effective option is uncertain. We created a Markov decision model to compare BB and EVL in such patients, examining both cost‐effectiveness (cost per life year [LY]) and cost‐utility (cost per quality‐adjusted life year [QALY]).

Ashraf Mohammad El‐Badry, Wolfgang Moritz, Claudio Contaldo, Yinghua Tian, Rolf Graf, Pierre‐Alain Clavien – 28 March 2007 – Macrovesicular hepatic steatosis has a lower tolerance to reperfusion injury than microvesicular steatosis with an abnormally high ratio of omega‐6 (n‐6): omega‐3 (n‐3) polyunsaturated fatty acids (PUFAs). We investigated the influence of PUFAs on microcirculation in steatotic livers and the potential to minimize reperfusion injury in the macrosteatotic liver by normalization of PUFAs.

Víctor Cortés, Attilio Rigotti – 28 March 2007

Joseph Torresi, Owen M. Stock, Alexandra E. Fischer, Lara Grollo, Heidi Drummer, Irene Boo, Weiguang Zeng, Linda Earnest‐Silveira, David C. Jackson – 28 March 2007 – We describe a peptide‐based strategy for HCV vaccine design that addresses the problem of variability in hypervariable region 1 (HVR1). Peptides representing antibody epitopes of HVR1 from genotype 1a were synthesized and incorporated into multideterminant immunogens that also included lipid moieties and helper T (Th) cell epitopes. Mice inoculated with these polyepitopes generated strong antibody responses.

Jacqueline G. O'Leary, Jessica L. Chan, Cory M. McMahon, Raymond T. Chung – 28 March 2007 – Cholesterol biosynthesis is an integral part of HCV RNA replication. Not only does HCV RNA replicate on lipid rafts, but it also requires cholesterol intermediates to replicate. In addition, it has been shown in vitro that several HMG‐CoA reductase inhibitors can decrease HCV RNA replication by ≥ 1 log. Therefore, we designed a clinical trial to evaluate the effect of atorvastatin on HCV RNA levels.

Masaya Sugiyama, Yasuhito Tanaka, Tomoyuki Sakamoto, Isao Maruyama, Takashi Shimada, Satoru Takahashi, Tomoyuki Shirai, Hideaki Kato, Masataka Nagao, Yuzo Miyakawa, Masashi Mizokami – 28 March 2007 – Of the 8 genotypes of HBV (genotypes A‐H), genotype G is unique in that it has an insertion in the core gene and two stop codons in the precore region preventing the synthesis of hepatitis B e antigen. Most individuals with genotype G are coinfected with other genotypes, typically genotype A.

Zachary D. Goodman, Robert L. Becker, Paul J. Pockros, Nezam H. Afdhal – 28 March 2007 – Fibrosis progression in chronic liver disease has usually been evaluated by liver biopsy using insensitive semiquantitative numerical scores. An alternative to this is to measure fibrous tissue quantitatively using morphometric image analysis. The aim of this study was to quantify fibrosis progression in a cohort of patients with treatment‐refractory chronic hepatitis C enrolled in a placebo‐controlled clinical trial of interferon gamma‐1b (IFN‐γ 1b) for the treatment of advanced hepatic fibrosis.

Ho Jung Shin, Naohiko Anzai, Atsushi Enomoto, Xin He, Do Kyung Kim, Hitoshi Endou, Yoshikatsu Kanai – 28 March 2007 – The liver plays an important role in the elimination of endogenous and exogenous lipophilic organic compounds from the body, which is mediated by various carrier proteins that differ in substrate specificity and kinetic properties. Here, we have characterized a novel member of the organic anion transporter family (SLC22) isolated from human liver.

Frank Tacke, Christian Trautwein – 28 March 2007

Sandra Franco, Mariona Parera, Ester Aparicio, Bonaventura Clotet, Miguel Angel Martinez – 28 March 2007 – The HCV nonstructural protein (NS)3/4A serine protease is not only involved in viral polyprotein processing but also efficiently blocks the retinoic‐acid–inducible gen I and Toll‐like receptor 3 signaling pathways and contributes to virus persistence by enabling HCV to escape the interferon antiviral response. Therefore, the NS3/4A protease has emerged as an ideal target for the control of the disease and the development of new anti‐HCV agents.