Carbon monoxide enhances early liver regeneration in mice after hepatectomy

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.

Polyinosinic‐polycytidylic acid suppresses acetaminophen‐induced hepatotoxicity independent of type I interferons and toll‐like receptor 3

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.

Macrophage therapy for murine liver fibrosis recruits host effector cells improving fibrosis, regeneration, and function

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.

Three ulcerative colitis susceptibility loci are associated with primary sclerosing cholangitis and indicate a role for IL2, REL, and CARD9

Marcel Janse, Laetitia E. Lamberts, Lude Franke, Soumya Raychaudhuri, Eva Ellinghaus, Kirsten Muri Boberg, Espen Melum, Trine Folseraas, Erik Schrumpf, Annika Bergquist, Einar Björnsson, Jingyuan Fu, Harm Jan Westra, Harry J.M. Groen, Rudolf S.N. Fehrmann, Joanna Smolonska, Leonard H. van den Berg, Roel A. Ophoff, Robert J. Porte, Tobias J. Weismüller, Jochen Wedemeyer, Christoph Schramm, Martina Sterneck, Rainer Günther, Felix Braun, Severine Vermeire, Liesbet Henckaerts, Cisca Wijmenga, Cyriel Y. Ponsioen, Stefan Schreiber, Tom H. Karlsen, Andre Franke, Rinse K.

Complement component 4d immunostaining in liver allografts of patients with de novo immune hepatitis

Isabel Aguilera, José Manuel Sousa, Francisco Gavilan, Lourdes Gomez, Antonia Álvarez‐Márquez, Antonio Núñez‐Roldán – 21 March 2011 – De novo immune hepatitis (DNIH) is a form of late graft dysfunction after liver transplantation. The fine mechanisms leading to the development of DNIH are not known, and whether this hepatitis is a form of rejection or a result of an auto/alloimmune injury has not been established.

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