Dong‐Sik Kim, Sung‐Gyu Lee, Gyu‐Bo Sung, Gi‐Young Ko, Kwang‐Min Park, Ki‐Hun Kim, Chul‐Soo Ahn, Deok‐Bog Moon, Tae‐Yong Ha, Gi‐Won Song – 23 June 2006 – Subcapsular hematoma of the graft is a serious complication of liver transplantation (LT), and there has been no discussion in the literature about optimal management except in sporadic case reports. The aim of this work is to review our experience of subcapsular hematoma in living donor liver transplantation (LDLT) and to introduce our management strategy.

Anna Wieckowska, Nizar N. Zein, Lisa M. Yerian, A. Rocio Lopez, Arthur J. McCullough, Ariel E. Feldstein – 23 June 2006 – In patients with nonalcoholic fatty liver disease (NAFLD), a liver biopsy remains the only reliable way to differentiate simple steatosis from nonalcoholic steatohepatitis (NASH). Noninvasive methods are urgently needed. Increasing evidence suggests hepatocyte apoptosis is a key mediator of liver injury in NAFLD. The aim of this study was to quantify hepatocyte apoptosis in plasma from patients with NAFLD and correlate it with histological severity.

Edwina S. Baskin‐Bey, Wendong Huang, Norihisa Ishimura, Hajime Isomoto, Steven F. Bronk, Karen Braley, Ruth W. Craig, David D. Moore, Gregory J. Gores – 23 June 2006 – The constitutive androstane receptor (CAR) modulates xeno‐ and endobiotic hepatotoxicity by regulating detoxification pathways. Whether activation of CAR may also protect against liver injury by directly blocking apoptosis is unknown.

Fouad Lafdil, Marie Noële Chobert, Dominique Couchie, Arthur Brouillet, Elie Serge Zafrani, Philippe Mavier, Yannick Laperche – 23 June 2006 – The protein product of the growth arrest–specific gene 6 (Gas6) is a secreted ligand for tyrosine kinase receptors, among which Axl is the most widely distributed and displays the highest affinity for Gas6. The Gas6/Axl signaling pathway has been increasingly implicated in growth and survival processes occurring during development and tissue repair.

Gisa Tiegs – 23 June 2006 – Fulminant liver failure (FLF) consists of a cascade of events beginning with a presumed uncontrolled systemic activation of the immune system. The etiology of FLF remains undefined. In this study, we demonstrate that CCR5 deficiency promotes the development of acute FLF in mice following Con A administration by preventing activated hepatic CD1d‐restricted NKT cells (but not conventional T cells) from dying from activation‐induced apoptosis.

Maria Varela, William Sanchez, Jordi Bruix, Gregory J. Gores – 23 June 2006

Luis Servin‐Abad, Andreas Tzakis, Eugene R. Schiff, Arie Regev – 23 June 2006 – Acquired (non‐Wilsonian) hepatocerebral degeneration (AHD) is a chronic brain disorder caused by liver dysfunction and long‐standing portal‐systemic shunting. It typically presents with dysathria, ataxia, tremor, involuntary movements and altered mental status, and often does not respond to conventional medical therapy for hepatic encephalopathy. There is scarce and conflicting information regarding the clinical course of AHD after liver transplantation (OLT).

Feng Liu, Xiaoben Pan, Guodong Chen, Dong Jiang, Xu Cong, Ran Fei, Lai Wei – 23 June 2006 – On the basis of the recently recognized potential of hematopoietic stem cells (HSCs) to give rise to hepatocytes, we investigated whether HSCs mobilized by granulocyte colony‐stimulating factor (G‐CSF) or G‐CSF per se could contribute to faster recovery and promote tissue reparation after rats' (cross‐sex) partial orthotopic liver transplantation (PLTx). Sex‐mismatched (female to male) syngeneic rat PLTx was established.

Martin Loss, Wa S. Ng, Rooshdiya Z. Karim, Simone I. Strasser, David J. Koorey, Peter J. Gallagher, Deborah J. Verran, Geoffrey W. McCaughan – 23 June 2006 – Hepatic rupture is a rare condition, and treatment options are very limited. We report a case of hepatic rupture secondary to hereditary lysozyme amyloidosis that was successfully treated by liver transplantation. The mother of this patient had presented in an identical fashion 15 years earlier in the pretransplant era and died very rapidly. Liver Transpl 12:1152–1155, 2006. © 2006 AASLD.

Yongke Lu, Arthur I. Cederbaum – 23 June 2006 – The mechanisms by which alcohol causes liver injury are still not certain. Either LPS or CYP2E1 are considered independent risk factors involved in alcoholic liver disease, but mutual relationships or interactions between them are unknown. In the present study, the possible synergistic action of CYP2E1 and LPS in liver injury was investigated by evaluating the effects of pyrazole (inducer of CYP2E1), Chlormethiazole (CMZ), an inhibitor of CYP2E1, and CYP2E1‐knockout mice.