Evie H. Carchman, Jayashree Rao, Patricia A. Loughran, Matthew R. Rosengart, Brian S. Zuckerbraun – 24 March 2011 – Adaptive responses to sepsis are necessary to prevent organ failure and death. Cellular signaling responses that limit cell death and structural damage allow a cell to withstand insult from sepsis to prevent irreversible organ dysfunction. One such protective pathway to reduce hepatocellular injury is the up‐regulation of heme oxygenase‐1 (HO‐1) signaling.

James A. Thomas, Caroline Pope, Davina Wojtacha, Andrew J. Robson, Timothy T. Gordon‐Walker, Stephen Hartland, Prakash Ramachandran, Marielle Van Deemter, David A. Hume, John P. Iredale, Stuart J. Forbes – 23 March 2011 – Clinical studies of bone marrow (BM) cell therapy for liver cirrhosis are under way but the mechanisms of benefit remain undefined. Cells of the monocyte‐macrophage lineage have key roles in the development and resolution of liver fibrosis. Therefore, we tested the therapeutic effects of these cells on murine liver fibrosis.

Amir A. Ghaffari, Edward K. Chow, Shankar S. Iyer, Jane C. Deng, Genhong Cheng – 23 March 2011 – Viral infections are often linked to altered drug metabolism in patients; however, the underlying molecular mechanisms remain unclear. Here we describe a mechanism by which activation of antiviral responses by the synthetic double‐stranded RNA ligand, polyinosinic‐polycytidylic acid (polyI:C), leads to decreased acetaminophen (APAP) metabolism and hepatotoxicity.

Harel Dahari, Jeremie Guedj, Alan S. Perelson – 23 March 2011

Tatiana Kisseleva, David A. Brenner – 23 March 2011

Kaori Kuramitsu, David Gallo, Myunghee Yoon, Beek Y. Chin, Eva Csizmadia, Douglas W. Hanto, Leo E. Otterbein – 23 March 2011 – Hepatocyte proliferation early after liver resection is critical in restoring liver mass and preserving function as the liver regenerates. Carbon monoxide (CO) generated by heme oxygenase‐1 (HO‐1) strongly influences cellular proliferation and both HO‐1 and CO are accepted hepatoprotective molecules. Mice lacking functional HO‐1 were unable to mount an appropriate regenerative response following partial hepatectomy (PHTx) compared to wildtype controls.

Lisa Fredriksson, Bram Herpers, Giulia Benedetti, Quraisha Matadin, Jordi C. Puigvert, Hans de Bont, Sanja Dragovic, Nico P.E. Vermeulen, Jan N.M. Commandeur, Erik Danen, Marjo de Graauw, Bob van de Water – 23 March 2011 – Drug‐induced liver injury (DILI) is an important clinical problem. It involves crosstalk between drug toxicity and the immune system, but the exact mechanism at the cellular hepatocyte level is not well understood. Here we studied the mechanism of crosstalk in hepatocyte apoptosis caused by diclofenac and the proinflammatory cytokine tumor necrosis factor α (TNF‐α).

Kai Breuhahn, Gregory Gores, Peter Schirmacher – 23 March 2011 – Over the last decade, numerous small and high‐dimensional profiling analyses have been performed in human hepatocellular carcinoma (HCC), which address different levels of regulation and modulation. Because comprehensive analyses are lacking, the following review summarizes some of the general results and compares them with insights from other tumor entities. Particular attention is given to the impact of these results on future diagnostic and therapeutic approaches. (HEPATOLOGY 2011;)

Maria S. Rosselli, Adriana L. Burgueño, Carlos J. Pirola, Silvia Sookoian – 23 March 2011

Federico Castillo‐Suescun, Gabriel C. Oniscu, Ernest Hidalgo – 21 March 2011 – The presence of large spontaneous splenorenal shunts (SSRSs) is a risk factor for poor portal vein flow and liver dysfunction. The disconnection of splenorenal shunts by left renal vein (LRV) ligation has been suggested as a potential solution for improving portal flow. We reviewed the hemodynamic consequences of splenorenal shunts in deceased donor liver transplantation and investigated the role of LRV ligation.