Bo Gao, Zhijian Duan, Wei Xu, Sidong Xiong – 29 July 2009 – Members of the tripartite motif (TRIM) family are a part of the innate immune system to counter intracellular pathogens. TRIM22 has been reported to possess antiretroviral activity. Here we report that TRIM22 is involved in antiviral immunity against hepatitis B virus (HBV). Our results showed that TRIM22, being a strongly induced gene by interferons in human hepatoma HepG2 cells, could inhibit HBV gene expression and replication in a cell culture system as well as in a mouse model system.

Jon Cardinal, Pinhua Pan, Rajeev Dhupar, Mark Ross, Atsunori Nakao, Michael Lotze, Timothy Billiar, David Geller, Allan Tsung – 29 July 2009 – The nuclear protein high mobility group box 1 (HMGB1) is an important inflammatory mediator involved in the pathogenesis of liver ischemia/reperfusion (I/R) injury. Strategies aimed at preventing its release from stressed or damaged cells may be beneficial in preventing inflammation after I/R.

Maïté Lewin, Valérie Vilgrain, Violaine Ozenne, Maud Lemoine, Dominique Wendum, Valérie Paradis, Marianne Ziol, Lionel Arrivé, Michel Beaugrand, Raoul Poupon, Dominique Valla, Olivier Chazouillères, Christophe Corpechot – 29 July 2009 – The development of sclerosing cholangitis (SC) is observed in up to 50% of children followed up for autoimmune hepatitis (AIH). In adults, the prevalence is less known, although a recent study found evidence of SC in 10% of AIH patients using magnetic resonance cholangiopancreatography (MRCP).

Bingning Dong, Mohammed Qatanani, David D. Moore – 29 July 2009 – Untreated type 1 diabetes increases hepatic drug metabolism in both human patients and rodent models. We used knockout mice to test the role of the nuclear xenobiotic receptors constitutive androstane receptor (CAR) and pregnane and xenobiotic receptor (PXR) in this process. Streptozotocin‐induced diabetes resulted in increased expression of drug metabolizing cytochrome P450s and also increased the clearance of the cytochrome P450 substrate zoxazolamine.

Chiun Hsu, Shu‐Chen Wei, Ann‐Lii Cheng, Pei‐Jer Chen – 29 July 2009

Pierre Emmanuel Stoebner, Cécile Fabre, Nelly EL Kabbaj, Michael Bismuth, Georges Philippe Pageaux, Laurent Meunier – 29 July 2009

Lian‐Li Ma, Xiudan Gao, Liping Liu, Zhidan Xiang, Timothy S. Blackwell, Philip Williams, Ravi S. Chari, Deng‐Ping Yin – 29 July 2009 – Liver allografts are spontaneously accepted in the liver transplantation mouse model; however, the basis for this tolerance and the conditions that abrogate spontaneous tolerance to liver allografts are incompletely understood. We examined the role of CpG oligodeoxynucleotide (ODN) in triggering the liver inflammatory reaction and allograft rejection.

Chethan Ashokkumar, Qing Sun, Ankit Gupta, Brandon W. Higgs, Tamara Fazzolare, Lisa Remaley, George Mazariegos, Kyle Soltys, Geoffrey Bond, Rakesh Sindhi – 29 July 2009 – Donor‐induced and third‐party–induced proliferation of T‐helper and T‐cytotoxic (Tc) cells and their naïve and memory subsets was evaluated simultaneously in single blood samples from 77 children who received steroid‐free liver transplantation (LTx) after induction with rabbit anti‐human thymocyte globulin.

Ilona T. A. Pereboom, Jelle Adelmeijer, Yvonne van Leeuwen, Herman G. D. Hendriks, Robert J. Porte, Ton Lisman – 29 July 2009 – Platelet function is thought to deteriorate during liver transplantation as a result of platelet activation and proteolysis of platelet receptors by plasmin following reperfusion. However, this hypothesis has never been formally tested. Twenty patients undergoing a first or second liver transplant were included in the study. Blood samples were taken at standardized time points during transplantation and up to 10 days after transplantation.

Inmaculada Fernández, Esperanza Ulloa, Francisco Colina, Manuel Abradelo, Carlos Jiménez, Alberto Gimeno, Juan Carlos Meneu, Carlos Lumbreras, José Antonio Solís‐Herruzo, Enrique Moreno – 29 July 2009 – Antiviral therapy for recurrent hepatitis C in liver transplantation has been associated with the development of chronic rejection. The aim of this study was to assess the incidence, evolution, and risk factors associated with the development of chronic rejection during posttransplant hepatitis C virus antiviral therapy.