Hereditary lysozyme amyloidosis: Spontaneous hepatic rupture (15 years apart) in mother and daughter. role of emergency liver transplantation

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.

Hematopoietic stem cells mobilized by granulocyte colony‐stimulating factor partly contribute to liver graft regeneration after partial orthotopic liver transplantation

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.

Acquired hepatocerebral degeneration in a patient with HCV cirrhosis: Complete resolution with subsequent recurrence after liver transplantation

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).

Lack of chemokine receptor CCR5 promotes murine fulminant liver failure

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.

Induction of Gas6 protein in CCl4‐induced rat liver injury and anti‐apoptotic effect on hepatic stellate cells

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.

Constitutive androstane receptor (CAR) ligand, TCPOBOP, attenuates Fas‐induced murine liver injury by altering Bcl‐2 proteins

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.

In vivo assessment of liver cell apoptosis as a novel biomarker of disease severity in nonalcoholic fatty liver disease

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.

Management of subcapsular hematoma of the graft after living donor liver transplantation

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.

Extrahepatic replication of HCV: Insights into clinical manifestations and biological consequences

Jason T. Blackard, Nyingi Kemmer, Kenneth E. Sherman – 23 June 2006 – An estimated 170 million persons are infected with the hepatitis C virus (HCV) worldwide. While hepatocytes are the major site of infection, a broad clinical spectrum of extrahepatic complications and diseases are associated with chronic HCV infection, highlighting the involvement of HCV in a variety of non‐hepatic pathogenic processes. There is a growing body of evidence to suggest that HCV can replicate efficiently in extrahepatic tissues and cell types, including peripheral blood mononuclear cells.

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