Claudio J. Villanueva, Mara Monetti, Michelle Shih, Ping Zhou, Steve M. Watkins, Sanjay Bhanot, Robert V. Farese – 29 July 2009 – Nonalcoholic fatty liver disease, characterized by the accumulation of triacylglycerols (TGs) and other lipids in the liver, often accompanies obesity and is a risk factor for nonalcoholic steatohepatitis and fibrosis. To treat or prevent fatty liver, a thorough understanding of hepatic fatty acid and TG metabolism is crucial.

Sumeet K. Asrani, W. Ray Kim, Julie K. Heimbach – 29 July 2009

Elizabeth Kenny‐Walsh – 29 July 2009

Mladen I. Yovchev, Jialin Zhang, David S. Neufeld, Petar N. Grozdanov, Mariana D. Dabeva – 29 July 2009 – Thymus cell antigen‐1 (Thy‐1)‐expressing cells proliferate in the liver during oval cell (OC)‐mediated liver regeneration. We characterized these cells in normal liver, in carbon tetrachloride‐injured liver, and in several models of OC activation.

Vincente Arroyo – 29 July 2009

Adeel A. Butt, Xiaoqiang Wang, Charity G. Moore – 29 July 2009 – The effect of hepatitis C virus (HCV) and its treatment on survival is not well defined. We undertook this study to determine the effect of HCV and its treatment on survival in a national cohort of HCV‐infected veterans and uninfected controls. We used a national sample of HCV‐infected persons and HCV‐uninfected controls from the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) to compare survival between the two groups.

Mark E. Mailliard, Mary E. Capadano, Matthew J. Hrnicek, Richard K. Gilroy, James M. Gulizia – 29 July 2009 – Between March 2000 and July 2001, at least 99 persons acquired a hepatitis C virus genotype 3a (HCV‐3a) infection in an oncology clinic. This nosocomial HCV outbreak provided an opportunity to examine the subsequent clinical course in a well‐defined cohort. This was a retrospective/prospective observational study of the short‐term significant health outcomes of a large, single‐source, patient‐to‐patient HCV‐3a outbreak.

Shelly C. Lu, Komal Ramani, Xiaopeng Ou, Mark Lin, Victor Yu, Kwangsuk Ko, Ryan Park, Teodoro Bottiglieri, Hidekazu Tsukamoto, Gary Kanel, Samuel W. French, José M. Mato, Rex Moats, Edward Grant – 29 July 2009 – Hepatocellular carcinoma (HCC) remains a common cancer worldwide that lacks effective chemoprevention or treatment. Chronic liver disease often leads to impaired hepatic S‐adenosylmethionine (SAMe) biosynthesis, and mice with SAMe deficiency develop HCC spontaneously. SAMe is antiapoptotic in normal hepatocytes but proapoptotic in cancerous hepatocytes.

Alessia Omenetti, Wing‐Kin Syn, Youngmi Jung, Heather Francis, Alessandro Porrello, Rafal P. Witek, Steve S. Choi, Liu Yang, Marlyn J. Mayo, M. Eric Gershwin, Gianfranco Alpini, Anna Mae Diehl – 29 July 2009 – The mechanisms mediating hepatic accumulation of inflammatory cells in cholestatic liver disease remain enigmatic. Our thesis is that Hedgehog (Hh) pathway activation promotes hepatic accumulation of immune cells that interact with cholangiocytes.

Laura Elisa Buitrago‐Molina, Deepika Pothiraju, Jutta Lamlé, Silke Marhenke, Uta Kossatz, Kai Breuhahn, Michael P. Manns, Nisar Malek, Arndt Vogel – 29 July 2009 – In this study, everolimus (RAD001) was used to determine the role of mammalian target of rapamycin (mTOR) in hepatocarcinogenesis. We show that RAD001 effectively inhibits proliferation of hepatocytes during chronic liver injury. Remarkably, the ability of RAD001 to impair cell cycle progression requires activation of the DNA damage response; loss of p53 significantly attenuates the antiproliferative effects of mTOR inhibition.