Alleluiah Rutebemberwa, Hugo R. Rosen – 27 October 2011

Georgios N. Kalambokis, Epameinondas V. Tsianos – 26 October 2011

Brigitte Grosse, Doris Cassio, Nadya Yousef, Céline Bernardo, Emmanuel Jacquemin, Emmanuel Gonzales – 26 October 2011 – Neonatal ichthyosis and sclerosing cholangitis (NISCH) syndrome is a liver disease caused by mutations of CLDN1 encoding Claudin‐1, a tight‐junction (TJ) protein. In this syndrome, it is speculated that cholestasis is caused by Claudin‐1 absence, leading to increased paracellular permeability and liver injuries secondary to paracellular bile regurgitation. We studied the role of claudin‐1 in hepatic paracellular permeability.

Ricky Harminder Bhogal, Barnaby Thomas Francis Stephenson, Simon Charles Afford – 26 October 2011

Gregory T. Everson, Mitchell L. Shiffman, John C. Hoefs, Timothy R. Morgan, Richard K. Sterling, David A. Wagner, Shannon Lauriski, Teresa M. Curto, Anne Stoddard, Elizabeth C. Wright, the HALT‐C Trial Group – 26 October 2011 – Risk for future clinical outcomes is proportional to the severity of liver disease in patients with chronic hepatitis C virus (HCV). We measured disease severity by quantitative liver function tests (QLFTs) to determine cutoffs for QLFTs that identified patients who were at low and high risk for a clinical outcome.

Toru Takahashi, Tomofumi Miura, Junichiro Nakamura, Satoshi Yamada, Tsutomu Miura, Masahiko Yanagi, Yasunobu Matsuda, Hiroyuki Usuda, Iwao Emura, Koichi Tsuneyama, Xiao‐Song He, M. Eric Gershwin – 26 October 2011 – There has been increased interest in the role of B cells in the pathogenesis of primary biliary cirrhosis (PBC). Although the vast majority of patients with this disease have anti‐mitochondrial antibodies, there is no correlation of anti‐mitochondrial antibody titer and/or presence with disease severity.

Lucia Russo, Jorge Gracia‐Sancho, Héctor García‐Calderó, Giusi Marrone, Juan Carlos García‐Pagán, Guillermo García‐Cardeña, Jaime Bosch – 26 October 2011 – Pathophysiological alterations in the endothelial phenotype result in endothelial dysfunction. Flow cessation, occurring during organ procurement for transplantation, triggers the endothelial dysfunction characteristic of ischemia/reperfusion injury, partly due to a reduction in the expression of the vasoprotective transcription factor Kruppel‐like Factor 2 (KLF2).

Felix Heymann, Linda Hammerich, Dunja Storch, Matthias Bartneck, Sebastian Huss, Vanessa Rüsseler, Nikolaus Gassler, Sergio A. Lira, Tom Luedde, Christian Trautwein, Frank Tacke – 26 October 2011 – Chemokines critically control the infiltration of immune cells upon liver injury, thereby promoting hepatic inflammation and fibrosis. The chemokine receptor CCR8 can affect trafficking of monocytes/macrophages, monocyte‐derived dendritic cells (DCs) and T‐helper cell (Th) subsets, but its role in liver diseases is currently unknown.

Nozomu Sakai, Heather L. Van Sweringen, Rebecca Schuster, John Blanchard, Justin M. Burns, Amit D. Tevar, Michael J. Edwards, Alex B. Lentsch – 26 October 2011 – The transcription factor nuclear factor kappaB (NF‐κB) plays diverse roles in the acute injury response to hepatic ischemia/reperfusion (I/R). Activation of NF‐κB in Kupffer cells promotes inflammation through cytokine expression, whereas activation in hepatocytes may be cell protective.

C. Bart Rountree, Lopa Mishra, Holger Willenbring – 26 October 2011 – Stem cells have potential for therapy of liver diseases, but may also be involved in the formation of liver cancer. Recently, the American Association for the Study of Liver Diseases Henry M. and Lillian Stratton Basic Research Single Topic Conference “Stem Cells in Liver Diseases and Cancer: Discovery and Promise” brought together a diverse group of investigators to define the status of research on stem cells and cancer stem cells in the liver and identify problems and solutions on the path to clinical translation.