Do we need to MEND the MELD?
Robert G. Gish – 29 March 2007
Robert G. Gish – 29 March 2007
Manuel Romero‐Gómez, Juan Córdoba, Rodrigo Jover, Juan A. del Olmo, Marta Ramírez, Ramón Rey, Enrique de Madaria, Carmina Montoliu, David Nuñez, Montse Flavia, Luis Compañy, José M. Rodrigo, Vicente Felipo – 28 March 2007 – Minimal hepatic encephalopathy (MHE) is mainly diagnosed using psychometric tests such as the psychometric hepatic encephalopathy score (PHES). Despite the clinical and social relevance of MHE, psychometric testing is not widespread in routine clinical care.
Vasiliki Gkretsi, Wendy M. Mars, William C. Bowen, Lindsay Barua, Yu Yang, Lida Guo, René St.‐Arnaud, Shoukat Dedhar, Chuanyue Wu, George K. Michalopoulos – 28 March 2007 – Extracellular matrix (ECM) is fundamental for the survival of cells within a tissue. Loss of contact with the surrounding ECM often causes altered cell differentiation or cell death. Hepatocytes cultured without matrix lose patterns of hepatocyte‐specific gene expression and characteristic cellular micro‐architecture.
Helen Robertson, John A. Kirby, William W. Yip, David E.J. Jones, Alastair D. Burt – 28 March 2007 – Primary biliary cirrhosis (PBC) recurs in the allograft after liver transplantation. Study of early tissue changes in the time‐course of disease recurrence provides a unique insight into the initial stages of the disease process, which, in nontransplant patients, occurs long before clinical presentation. We describe a patient who developed classical clinical, biochemical, immunological, and histological features of PBC within 9 months after transplantation.
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.
Frank Tacke, Christian Trautwein – 28 March 2007
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.
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.
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.
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.