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.

Hepatobiliary transporters and drug‐induced cholestasis

Christiane Pauli‐Magnus, Peter J. Meier – 27 September 2006 – Drug‐induced liver injury is an important clinical problem with significant morbidity and mortality. Whereas for most hepatocellular forms of drug‐induced hepatic injury the underlying pathophysiological mechanism is poorly understood, there is increasing evidence that cholestatic forms of drug‐induced liver damage result from a drug‐ or metabolite‐mediated inhibition of hepatobiliary transporter systems.

Correlation of paired liver biopsies in morbidly obese patients with suspected nonalcoholic fatty liver disease

Raphael B. Merriman, Linda D. Ferrell, Marco G. Patti, Shiobhan R. Weston, Mark S. Pabst, Bradley E. Aouizerat, Nathan M. Bass – 27 September 2006 – In the absence of surrogate markers, the evaluation of suspected nonalcoholic fatty liver disease (NAFLD) is highly dependent on histological examination. The extent of sampling variability affecting the reliability of a single liver biopsy in patients with suspected NAFLD is poorly characterized.

STAT1 contributes to dsRNA inhibition of liver regeneration after partial hepatectomy in mice

Rui Sun, Ogyi Park, Norio Horiguchi, Shailin Kulkarni, Won‐Il Jeong, Hao‐Yu Sun, Svetlana Radaeva, Bin Gao – 27 September 2006 – Increasing evidence suggests that liver regeneration is suppressed in patients with chronic HCV infection; however, the underlying mechanisms remain unclear. Previously, we demonstrated that injection of the synthetic double‐stranded RNA (dsRNA) poly I:C to mimic viral infection suppresses liver regeneration in the partial hepatectomy (PHx) model, whereby IFN‐γ contributes to the inhibition.

Subscribe to