Low viscosity histidine‐tryptophan‐ketoglutarate graft flush improves subsequent extended cold storage in University of Wisconsin solution in an extracorporeal rat liver perfusion and rat liver transplantation model

Gero Puhl, Peter Olschewski, Wenzel Schöning, Gerhard Hunold, Hans‐Georg Liesaus, Robert Winkler, Ulf P. Neumann, Thomas E.O. Schubert, Volker Schmitz, Peter Neuhaus – 9 October 2006 – Adequate flushing for liver donation requires large fluid volumes delivered at a high flow. This can be achieved more effectively with crystalloid solutions than with colloid‐based solutions. This study examined the combination of initial histidine‐tryptophan‐ketoglutarate solution (HTK) graft flush and subsequent storage in University of Wisconsin solution (UW) to that of the single use of each solution.

Impact of adult‐to‐adult living donor liver transplantation on access to transplantation and patients' survival: An 8‐year single‐center experience

Jérôme Dumortier, Mustapha Adham, Charles Ber, Catherine Boucaud, Yves Bouffard, Bertrand Delafosse, Pierre Sagnard, Olivier Boillot – 9 October 2006 – While the number of candidates for liver transplantation has increased in the recent years, the pool of cadaveric donor organs has remained constant and the waiting time progressively increases. These facts led us to start a program of adult‐to‐adult living‐donor liver transplantation in 1998. The aim of this study was to compare the outcome of all patients put on the waiting list since 1998.

Detection of HCV antigens in liver graft: Relevance to the management of recurrent post‐liver transplant hepatitis C

Alberto Grassi, Chiara Quarneti, Matteo Ravaioli, Francesco Bianchini, Micaela Susca, Antonia D'Errico, Fabio Piscaglia, Maria Rosa Tamè, Pietro Andreone, GianLuca Grazi, Silvia Galli, Daniela Zauli, Antonio D. Pinna, Francesco B. Bianchi, Giorgio Ballardini – 9 October 2006 – The aim of this study was to evaluate how the immunohistochemical detection of liver hepatitis C virus (HCV) antigens (HCV‐Ag) could support the histologic diagnosis and influence the clinical management of post‐liver transplantation (LT) liver disease.

De novo nonalcoholic fatty liver disease after liver transplantation

Suk Seo, Kalyani Maganti, Manjit Khehra, Rajendra Ramsamooj, Alexander Tsodikov, Christopher Bowlus, John McVicar, Mark Zern, Natalie Torok – 6 October 2006 – Hepatic steatosis is a recognized problem in patients after orthotopic liver transplant (OLT). However, de novo development of nonalcoholic fatty liver disease (NAFLD) has not been well described. The aim of this study was to determine the prevalence and predictors of de novo NAFLD after OLT. A retrospective analysis was performed on 68 OLT patients with donor liver biopsies and posttransplantation liver biopsies.

Transthyretin‐derived amyloid deposition on the gastric mucosa in domino recipients of familial amyloid polyneuropathy liver

Yo‐ichi Takei, Takahisa Gono, Masahide Yazaki, Shu‐ichi Ikeda, Toshihiko Ikegami, Yasuhiko Hashikura, Shin‐ichi Miyagawa, Yoshinobu Hoshii – 6 October 2006 – Familial amyloid polyneuropathy (FAP) is a form of hereditary generalized amyloidosis. Liver tissue explanted from FAP patients has normal structure and function, except for the production of amyloidogenic variant transthyretin (TTR), and domino liver transplantation (DLT) using grafts from FAP patients was first performed in 1995.

Tensin2 variant 3 is associated with aggressive tumor behavior in human hepatocellular carcinoma

Judy Wai Ping Yam, Frankie Chi Fat Ko, Chung‐Yiu Chan, Tai‐On Yau, Edmund Kwok Kwan Tung, Thomas Ho‐Yin Leung, Dong‐Yan Jin, Irene Oi‐Lin Ng – 27 September 2006 – Tensins are a new family of proteins that act as an important link among extracellular matrix, actin cytoskeleton, and signal transduction and have been implicated in human cancers. Tensin2 was initially identified in a search for new tensin family members that share extensive sequence homology with tensin1. Tensin2 was highly expressed in liver tissues.

Leptin‐mediated neovascularization is a prerequisite for progression of nonalcoholic steatohepatitis in rats

Mitsuteru Kitade, Hitoshi Yoshiji, Hideyuki Kojima, Yasuhide Ikenaka, Ryuichi Noguchi, Kosuke Kaji, Junichi Yoshii, Koji Yanase, Tadashi Namisaki, Kiyoshi Asada, Masaharu Yamazaki, Tatsuhiro Tsujimoto, Takemi Akahane, Masahito Uemura, Hiroshi Fukui – 27 September 2006 – Nonalcoholic steatohepatitis (NASH) may cause fibrosis, cirrhosis, and hepatocellular carcinoma (HCC); however, the exact mechanism of disease progression is not fully understood. Angiogenesis has been shown to play an important role in the progression of chronic liver disease.

An autoimmune biliary disease mouse model for primary biliary cirrhosis: Something for everyone

Andrew L. Mason – 27 September 2006 – Primary biliary cirrhosis (PBC) is an autoimmune disease with a strong genetic component characterized by biliary ductular inflammation with eventual liver cirrhosis. The serologic hallmark of PBC is antimitochondrial antibodies that react with the pyruvate dehydrogenase complex, targeting the inner lipoyl domain of the E2 subunit (anti‐PDC‐E2). Herein we demonstrate that NOD.c3c4 mice congenically derived from the non‐obese diabetic strain develop an autoimmune biliary disease (ABD) that models human PBC.

Significance of circulating endothelial progenitor cells in hepatocellular carcinoma

Joanna W. Y. Ho, Roberta W. C. Pang, Cecilia Lau, Chris K. Sun, Wan Ching Yu, Sheung Tat Fan, Ronnie T. P. Poon – 27 September 2006 – This study evaluated the significance of circulating bone marrow‐derived endothelial progenitor cells (EPCs) in patients with hepatocellular carcinoma (HCC), a solid tumor with rich neovasculature. Eighty patients with HCC were recruited for the study, and 16 patients with liver cirrhosis and 14 healthy subjects were also included for comparison. Blood samples were taken before treatment.

Impaired 11β‐hydroxysteroid dehydrogenase contributes to renal sodium avidity in cirrhosis: Hypothesis or fact?

Felix J. Frey – 27 September 2006 – Exaggerated renal sodium retention with concomitant potassium loss is a hallmark of cirrhosis and contributes to the accumulation of fluid as ascites, pleural effusion, or edema. This apparent mineralocorticoid effect is only partially explained by increased aldosterone concentrations. I present evidence supporting the hypothesis that cortisol confers mineralocorticoid action in cirrhosis.

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