Nonalcoholic fatty liver disease after liver transplantation for cryptogenic cirrhosis or nonalcoholic fatty liver disease

Kanthi Yalamanchili, Sherif Saadeh, Göran B. Klintmalm, Linda W. Jennings, Gary L. Davis – 16 December 2009 – Nonalcoholic steatohepatitis (NASH) may account for many cases of cryptogenic cirrhosis. If so, then steatosis might recur after liver transplantation. Two thousand fifty‐two patients underwent primary liver transplantation for chronic liver disease between 1986 and 2004. Serial liver biopsy samples were assessed for steatosis and fibrosis. Two hundred fifty‐seven patients (12%) had a pretransplant diagnosis of cryptogenic cirrhosis (239) or NASH (18).

Modified pediatric end‐stage liver disease scoring system and pediatric liver transplantation in Brazil

Joao Seda Neto, Eduardo Carone, Renata P. S. Pugliese, Eduardo A. Fonseca, Gilda Porta, Irene Miura, Vera B. Danesi, Teresa C. Guimaraes, Andre L. Godoy, Adriana Porta, Rodrigo Vincenzi, Francisco Carnevale Filho, Mario Kondo, Paulo Chapchap – 15 December 2009 – The Pediatric End‐Stage Liver Disease (PELD) scoring system is a formula developed to provide a continuous numerical assessment of the risk of death in order to allocate livers to children in need of transplantation. The PELD scoring system was introduced in Brazil in July 2006.

Lactoferrin protects against acetaminophen‐induced liver injury in mice

Hao Yin, Linling Cheng, Michael Holt, Numsen Hail, Robert MacLaren, Cynthia Ju – 30 November 2009 – Acetaminophen‐induced liver injury (AILI) is a significant health problem and represents the most frequent cause of drug‐induced liver failure in the United States. The development and implementation of successful therapeutic intervention strategies have been demanding, due to significant limitations associated with the current treatment for AILI. Lactoferrin (Lac), a glycoprotein present in milk, has been demonstrated to possess a multitude of biological functions.

MicroRNA‐30d promotes tumor invasion and metastasis by targeting Galphai2 in hepatocellular carcinoma

Jian Yao, Linhui Liang, Shenglin Huang, Jie Ding, Ning Tan, Yingjun Zhao, Mingxia Yan, Chao Ge, Zhenfeng Zhang, Taoyang Chen, Dafang Wan, Ming Yao, Jinjun Li, Jianren Gu, Xianghuo He – 30 November 2009 – The pathological relevance and significance of microRNAs (miRNAs) in hepatocarcinogenesis have attracted much attention in recent years; however, little is known about the underlying molecular mechanisms through which miRNAs are involved in the development and progression of hepatocellular carcinoma (HCC).

Oncogenic and tumor suppressive roles of polo‐like kinases in human hepatocellular carcinoma

Rossella Pellegrino, Diego F. Calvisi, Sara Ladu, Volker Ehemann, Tommaso Staniscia, Matthias Evert, Frank Dombrowski, Peter Schirmacher, Thomas Longerich – 30 November 2009 – Polo‐like kinase (PLK) proteins play critical roles in the control of cell cycle progression, either favoring or inhibiting cell proliferation, and in DNA damage response. Although either overexpression or down‐regulation of PLK proteins occurs frequently in various cancer types, no comprehensive analysis on their function in human hepatocellular carcinoma (HCC) has been performed to date.

Expression of pituitary tumor–transforming gene 1 (PTTG1)/securin in hepatitis B virus (HBV)‐associated liver diseases: Evidence for an HBV X protein–mediated inhibition of PTTG1 ubiquitination and degradation

Francisca Molina‐Jiménez, Ignacio Benedicto, Miki Murata, Samuel Martín‐Vílchez, Toshihito Seki, José Antonio Pintor‐Toro, María Tortolero, Ricardo Moreno‐Otero, Kazuichi Okazaki, Kazuhiko Koike, José Luchi Barbero, Koichi Matsuzaki, Pedro L. Majano, Manuel López‐Cabrera – 30 November 2009 – Chronic infection with hepatitis B virus (HBV) is strongly associated with hepatocellular carcinoma (HCC), and the viral HBx protein plays a crucial role in the pathogenesis of liver tumors.

5‐lipoxygenase deficiency reduces hepatic inflammation and tumor necrosis factor α–induced hepatocyte damage in hyperlipidemia‐prone ApoE‐null mice

Marcos Martínez‐Clemente, Natàlia Ferré, Ana González‐Périz, Marta López‐Parra, Raquel Horrillo, Esther Titos, Eva Morán‐Salvador, Rosa Miquel, Vicente Arroyo, Colin D. Funk, Joan Clària – 30 November 2009 – The actual risk factors that drive hepatic inflammation during the transition from steatosis to steatohepatitis are unknown. We recently demonstrated that hyperlipidemia‐prone apolipoprotein E–deficient (ApoE−/−) mice exhibit hepatic steatosis and increased susceptibility to hepatic inflammation and advanced fibrosis.

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