Deletion of interleukin‐6 in mice with the dominant negative form of transforming growth factor β receptor II improves colitis but exacerbates autoimmune cholangitis

Weici Zhang, Masanobu Tsuda, Guo‐Xiang Yang, Koichi Tsuneyama, Guanghua Rong, William M. Ridgway, Aftab A. Ansari, Richard A. Flavell, Ross L. Coppel, Zhe‐Xiong Lian, M. Eric Gershwin – 23 June 2010 – The role of interleukin‐6 (IL‐6) in autoimmunity attracts attention because of the clinical usage of monoclonal antibodies to IL‐6 receptor (IL‐6R), designed to block IL‐6 pathways.

Use of surveillance for hepatocellular carcinoma among patients with cirrhosis in the United States

Jessica A. Davila, Robert O. Morgan, Peter A. Richardson, Xianglin L. Du, Katherine A. McGlynn, Hashem B. El‐Serag – 23 June 2010 – Surveillance for hepatocellular carcinoma (HCC) in patients with cirrhosis is recommended but may not be performed. The extent and determinants of HCC surveillance are unknown. We conducted a population‐based United States cohort study of patients over 65 years of age to examine use and determinants of prediagnosis surveillance in patients with HCC who were previously diagnosed with cirrhosis.

Overexpression of aspartyl‐(asparaginyl)‐β‐hydroxylase in hepatocellular carcinoma is associated with worse surgical outcome

Kui Wang, Jian Liu, Zhen‐Lin Yan, Jun Li, Le‐Hua Shi, Wen‐Ming Cong, Yong Xia, Qi‐Fei Zou, Tao Xi, Feng Shen, Hong‐Yang Wang, Meng‐Chao Wu – 23 June 2010 – The association between the overexpression of aspartyl‐(asparaginyl)‐β‐hydroxylase (AAH) and the invasiveness of hepatocellular carcinoma (HCC) in vitro has been reported. However, the prognostic value of AAH expression in HCC remains unclear. The purpose of this study was to investigate the relationship between AAH expression, tumor recurrence, and patient survival.

A meta‐analysis of randomized trials for the treatment of nonalcoholic fatty liver disease

Giovanni Musso, Roberto Gambino, Maurizio Cassader, Gianfranco Pagano – 23 June 2010 – Nonalcoholic fatty liver disease (NAFLD) encompasses a histological spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH). NAFLD carries a higher risk of cardio‐metabolic and liver‐related complications, the latter being confined to NASH and demanding specific treatment. We assessed the efficacy of proposed treatments for NAFLD/NASH by reviewing reports of randomized controlled trials (RCTs) on online databases and national and international meeting abstracts through January 2010.

Fitness versus fatness: Moving beyond weight loss in nonalcoholic fatty liver disease

Nathan A. Johnson, Jacob George – 23 June 2010 – The rapid emergence of nonalcoholic fatty liver disease (NAFLD) as a cause of both liver‐related morbidity and mortality and cardiometabolic risk has led to the search for effective lifestyle strategies to reduce liver fat. Lifestyle intervention comprising dietary restriction in conjunction with increased physical activity has shown clear hepatic benefits when weight loss approximating 3%‐10% of body weight is achieved.

Macroautophagy and chaperone‐mediated autophagy are required for hepatocyte resistance to oxidant stress

Yongjun Wang, Rajat Singh, Youqing Xiang, Mark J. Czaja – 23 June 2010 – The function of the lysosomal degradative pathway of autophagy in cellular injury is unclear, because findings in nonhepatic cells have implicated autophagy as both a mediator of cell death and as a survival response. Autophagic function is impaired in steatotic and aged hepatocytes, suggesting that in these settings hepatocellular injury may be altered by the decrease in autophagy.

Activation of Rac1 promotes hedgehog‐mediated acquisition of the myofibroblastic phenotype in rat and human hepatic stellate cells

Steve S. Choi, Rafal P. Witek, Liu Yang, Alessia Omenetti, Wing‐Kin Syn, Cynthia A. Moylan, Youngmi Jung, Gamze F. Karaca, Vanessa S. Teaberry, Thiago A. Pereira, Jiangbo Wang, Xiu‐Rong Ren, Anna Mae Diehl – 23 June 2010 – Hepatic accumulation of myofibroblastic hepatic stellate cells (MF‐HSCs) is pivotal in the pathogenesis of cirrhosis. Two events are necessary for MF‐HSCs to accumulate in damaged livers: transition of resident, quiescent hepatic stellate cells (Q‐HSCs) to MF‐HSCs and expansion of MF‐HSC numbers through increased proliferation and/or reduced apoptosis.

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