Winston Dunn, Ronghui Xu, Jeffrey B. Schwimmer – 21 February 2008 – People at risk for coronary heart disease are often at risk for nonalcoholic fatty liver disease (NAFLD). The association of modest wine consumption with NAFLD has not been studied and the recommendation of wine for patients at risk for both diseases is controversial. The aim is to test the hypothesis that modest wine consumption is associated with decreased prevalence of NAFLD.

Ainhoa Iglesias Ara, Meng Xia, Komal Ramani, José M. Mato, Shelly C. Lu – 21 February 2008 – We previously showed that S‐adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)‐induced tumor necrosis factor α (TNFα) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor κ B nuclear binding. However, the exact molecular mechanism or mechanisms of the inhibitory effect were unclear. While SAMe is a methyl donor, MTA is an inhibitor of methylation.

Cédric Coulouarn, Valentina M. Factor, Snorri S. Thorgeirsson – 19 February 2008 – Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The clinical heterogeneity of HCC, and the lack of good diagnostic markers and treatment strategies, has rendered the disease a major challenge. Patients with HCC have a highly variable clinical course, indicating that HCC comprises several biologically distinctive subgroups reflecting a molecular heterogeneity of the tumors.

Ghazaleh Aram, James J. Potter, Xiaopu Liu, Michael S. Torbenson, Esteban Mezey – 19 February 2008 – The role of nitric oxide (NO) in liver injury and fibrosis is unclear. The purpose of this study was to determine whether inducible NO synthase deficiency (iNOS−/−) affects liver injury and fibrosis produced in mice by chronic carbon tetrachloride (CCl4) administration. Wild‐type (WT) or iNOS−/− mice were subjected to biweekly CCl4 injections over 8 weeks, whereas controls were given isovolumetric injections of olive oil.

Joanne B. Krasnoff, Patricia L. Painter, Janet P. Wallace, Nathan M. Bass, Raphael B. Merriman – 11 February 2008 – Nonalcoholic fatty liver disease (NAFLD) has been referred to as the hepatic manifestation of the metabolic syndrome. There is a lower prevalence of metabolic syndrome in individuals with higher health‐related fitness (HRF) and physical activity (PA) participation. The relationship between NAFLD severity and HRF or PA is unknown. Our aim was to compare measures of HRF and PA in patients with a histological spectrum of NAFLD severity.

Igor Dvorchik, Myron Schwartz, M. Isabel Fiel, Sydney D. Finkelstein, J. Wallis Marsh – 11 February 2008 – Liver transplantation (LT) in the presence of hepatocellular carcinoma (HCC) remains a controversial issue because the current staging systems are not sufficiently predictive of outcomes. Paraffin blocks from 183 patients that underwent LT in the presence of HCC were collected. Molecular analysis was carried out blindly on the native liver specimens in all cases with respect to recurrence outcomes.

Beate Katharina Straub, Pamela Stoeffel, Hans Heid, Ralf Zimbelmann, Peter Schirmacher – 7 February 2008 – Fatty change (steatosis) is the most frequent liver pathology in western countries and is caused by a broad range of disorders such as alcohol abuse and metabolic syndrome. The surface layer of lipid droplets (LDs) contains members of a protein family that share homologous sequences and domains, the so‐called PAT proteins, named after their constituents, perilipin, adipophilin, and TIP47.

Muhammad Y. Sheikh, Jinah Choi, Ishtiaq Qadri, Jacob E. Friedman, Arun J. Sanyal – 7 February 2008 – Chronic infection with hepatitis C virus (HCV) can induce insulin resistance (IR) in a genotype‐dependent fashion, thus contributing to steatosis, progression of fibrosis and resistance to interferon therapy. The molecular mechanisms in genotype 1 patients that lead to metabolic syndrome are still ambiguous. Based on our current understanding, HCV proteins associate with mitochondria and endoplasmic reticulum and promote oxidative stress.

Guadalupe Garcia‐Tsao, Jaime Bosch, Roberto J. Groszmann – 7 February 2008

Craig Lammert, Stefan Einarsson, Chandan Saha, Anna Niklasson, Einar Bjornsson, Naga Chalasani – 7 February 2008 – Idiosyncratic drug‐induced liver injury (DILI) is traditionally thought not to be dose‐related. However, it has been pointed out that most medicines that were withdrawn from marketing or received a black‐box warning because of hepatotoxicity were prescribed at daily doses greater than 50 mg/day. To examine the relationship between daily dose of medications and idiosyncratic DILI, we conducted a study with two aims.