Lysine acetylation induced by chronic ethanol consumption impairs dynamin‐mediated clathrin‐coated vesicle release

Blythe D. Shepard, Dean J. Tuma, Pamela L. Tuma – 16 November 2011 – The liver is the major site of ethanol metabolism and thus sustains the most injury from chronic alcohol consumption. Ethanol metabolism by the hepatocyte leads to the generation of reactive metabolites and oxygen radicals that can readily adduct DNA, lipids, and proteins. More recently, it has become apparent that ethanol consumption also leads to increased post‐translational modifications of the natural repertoire, including lysine hyperacetylation.

Albumin infusion in patients undergoing large‐volume paracentesis: A meta‐analysis of randomized trials

Mauro Bernardi, Paolo Caraceni, Roberta J. Navickis, Mahlon M. Wilkes – 16 November 2011 – Albumin infusion reduces the incidence of postparacentesis circulatory dysfunction among patients with cirrhosis and tense ascites, as compared with no treatment. Treatment alternatives to albumin, such as artificial colloids and vasoconstrictors, have been widely investigated. The aim of this meta‐analysis was to determine whether morbidity and mortality differ between patients receiving albumin versus alternative treatments.

Endoplasmic reticulum‐tethered transcription factor cAMP responsive element‐binding protein, hepatocyte specific, regulates hepatic lipogenesis, fatty acid oxidation, and lipolysis upon metabolic stress in mice

Chunbin Zhang, Guohui Wang, Ze Zheng, Krishna Rao Maddipati, Xuebao Zhang, Gregory Dyson, Paul Williams, Stephen A. Duncan, Randal J. Kaufman, Kezhong Zhang – 16 November 2011 – cAMP responsive element‐binding protein, hepatocyte specific (CREBH), is a liver‐specific transcription factor localized in the endoplasmic reticulum (ER) membrane. Our previous work demonstrated that CREBH is activated by ER stress or inflammatory stimuli to induce an acute‐phase hepatic inflammation.

Hepatic ratio of phosphatidylcholine to phosphatidylethanolamine predicts survival after partial hepatectomy in mice

Ji Ling, Todd Chaba, Lin‐Fu Zhu, René L. Jacobs, Dennis E. Vance – 16 November 2011 – A major predictor of failed liver resection and transplantation is nonalcoholic fatty liver disease (NAFLD). NAFLD is linked to a wide spectrum of diseases including obesity and diabetes that are increasingly prevalent in Western populations. Thus, it is important to develop therapies aimed at improving posthepatectomy outcomes in patients with NAFLD, as well as to improve the evaluation of patients slated for hepatic surgery.

Family history of liver cancer and hepatocellular carcinoma

Federica Turati, Valeria Edefonti, Renato Talamini, Monica Ferraroni, Matteo Malvezzi, Francesca Bravi, Silvia Franceschi, Maurizio Montella, Jerry Polesel, Antonella Zucchetto, Carlo La Vecchia, Eva Negri, Adriano Decarli – 16 November 2011 – Familial clustering of hepatocellular carcinoma (HCC) has been frequently reported in eastern Asiatic countries, where hepatitis B infection is common. Little is known about the relationship between family history of liver cancer and HCC in Western populations.

Homozygosity mapping identifies a bile acid biosynthetic defect in an adult with cirrhosis of unknown etiology

Vered Molho‐Pessach, Jonathan J. Rios, Chao Xing, Kenneth D.R. Setchell, Jonathan C. Cohen, Helen H. Hobbs – 16 November 2011 – The most common inborn error of bile acid metabolism is 3β‐hydroxy‐Δ5‐C27‐steroid oxidoreductase (3β‐HSD) deficiency, a disorder that usually presents in early childhood with hepatic dysfunction. Timely diagnosis of this disorder is crucial because it can be effectively treated with primary bile acid replacement. Here we describe a 24‐year‐old woman from Iran with cirrhosis of unknown etiology.

Protease‐activated receptor 2 promotes experimental liver fibrosis in mice and activates human hepatic stellate cells

Virginia Knight, Jorge Tchongue, Dinushka Lourensz, Peter Tipping, William Sievert – 16 November 2011 – Protease‐activated receptor (PAR) 2 is a G‐protein–coupled receptor that is activated after proteolytic cleavage by serine proteases, including mast cell tryptase and activated coagulation factors. PAR‐2 activation augments inflammatory and profibrotic pathways through the induction of genes encoding proinflammatory cytokines and extracellular matrix proteins. Thus, PAR‐2 represents an important interface linking coagulation and inflammation.

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