Elizabeth K. Speliotes, Joseph M. Massaro, Udo Hoffmann, Ramachandran S. Vasan, James B. Meigs, Dushyant V. Sahani, Joel N. Hirschhorn, Christopher J. O'Donnell, Caroline S. Fox – 23 May 2010 – Obesity is not uniformly associated with the development of metabolic sequelae. Specific patterns of body fat distribution, in particular fatty liver, may preferentially predispose at‐risk individuals to disease. In this study, we characterize the metabolic correlates of fat in the liver in a large community‐based sample with and without respect to visceral fat.

John F. Reinus, Allan W. Wolkoff – 23 May 2010

Stuart F. W. Kendrick, Graeme O'Boyle, Jelena Mann, Mujdat Zeybel, Jeremy Palmer, David E. J. Jones, Chris P. Day – 23 May 2010 – Acute alcoholic hepatitis is characterized by disproportionate macrophage inflammatory cytokine responses to bacterial lipopolysaccharide. Lack of knowledge of the underlying mechanism has limited progress toward effective therapy. We postulated a novel mechanism by which ethanol increases histone acetylation, increasing proinflammatory gene transcription and cytokine synthesis.

Barbara A. Wetmore, Dominique J. Brees, Reetu Singh, Paul B. Watkins, Melvin E. Andersen, James Loy, Russell S. Thomas – 23 May 2010 – Serum aminotransferases have been the clinical standard for evaluating liver injury for the past 50‐60 years. These tissue enzymes lack specificity, also tracking injury to other tissues. New technologies assessing tissue‐specific messenger RNA (mRNA) release into blood should provide greater specificity and permit indirect assessment of gene expression status of injured tissue.

Wing‐Kin Syn, Ye Htun Oo, Thiago A. Pereira, Gamze F. Karaca, Youngmi Jung, Alessia Omenetti, Rafal P. Witek, Steve S. Choi, Cynthia D. Guy, Caitlin M. Fearing, Vanessa Teaberry, Fausto E.L. Pereira, David H. Adams, Anna Mae Diehl – 23 May 2010 – Liver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, suggesting that immune responses contribute to nonalcoholic fatty liver disease (NAFLD) progression. Livers normally contain many natural killer T (NKT) cells that produce factors that modulate inflammatory and fibrogenic responses.

Peter V. E. van den Berghe, Roderick H. J. Houwen, Leo W. J. Klomp – 23 May 2010

Tugrul Purnak, Cumali Efe, Yavuz Beyazit, Ersan Ozaslan – 23 May 2010

Ming Bai, Guohong Han, Xingshun Qi, Zhanxin Yin, Daiming Fan – 23 May 2010

Adriana L. Burgueño, Julieta Carabelli, Silvia Sookoian, Carlos J. Pirola – 23 May 2010

Don C. Rockey, Leonard B. Seeff, James Rochon, James Freston, Naga Chalasani, Maurizio Bonacini, Robert J. Fontana, Paul H. Hayashi, for the US Drug‐Induced Liver Injury Network – 23 May 2010 – Drug‐induced liver injury (DILI) is largely a diagnosis of exclusion and is therefore challenging. The US Drug‐Induced Liver Injury Network (DILIN) prospective study used two methods to assess DILI causality: a structured expert opinion process and the Roussel‐Uclaf Causality Assessment Method (RUCAM).