Karolina Bojkowska, Fabio Aloisio, Marco Cassano, Adamandia Kapopoulou, Francesca Santoni de Sio, Nadine Zangger, Sandra Offner, Cristina Cartoni, Charles Thomas, Simon Quenneville, Kai Johnsson, Didier Trono – 8 June 2012 – The liver is characterized by sexually dimorphic gene expression translating into sex‐specific differences in lipid, drug, steroid hormone, and xenobiotic metabolism, with distinct responses of males and females to environmental challenges.

Giovanni Musso, Maurizio Cassader, Franco De Michieli, Floriano Rosina, Fabio Orlandi, Roberto Gambino – 8 June 2012 – Nonalcoholic fatty liver disease (NAFLD) ranges from simple steatosis (SS) to nonalcoholic steatohepatitis (NASH). Though liver‐related risk seems confined to NASH, it is currently unclear whether NASH has a higher risk of cardiovascular disease (CVD) and diabetes than SS as a result of the coexistence of obesity and other cardiometabolic confounders. Adipose tissue is an emerging modulator of liver disease in NAFLD and of cardiometabolic disease in the general population.

Toru Ikegami, Ken Shirabe, Rumi Matono, Tomoharu Yoshizumi, Yuji Soejima, Hideaki Uchiyama, Hiroto Kayashima, Kazutoyo Morita, Yoshihiko Maehara – 4 June 2012 – The prevalence and clinical characteristics of bacterial pneumonia after living donor liver transplantation (LDLT) have not yet been elucidated. We performed a retrospective analysis of 346 LDLT recipients. Fifty patients (14.5%) experienced bacterial pneumonia after LDLT, and they had a higher short‐term mortality rate (42.0%) than patients with other types of bacterial infections after LDLT.

Jasmohan S. Bajaj, Leroy R. Thacker, Douglas M. Heuman, Richard K. Sterling, R. Todd Stravitz, Arun J. Sanyal, Velimir Luketic, Michael Fuchs, Ho Chong S. Gilles, James B. Wade – 4 June 2012 – Psychiatric disorders and medications may affect the cognitive performance of patients with cirrhosis and complicate the diagnosis and prediction of hepatic encephalopathy (HE).

Zeenat Safdar, Sonja Bartolome, Norman Sussman – 4 June 2012 – Portopulmonary hypertension (POPH) is a serious complication of cirrhosis that is associated with mortality beyond that predicted by the Model for End‐Stage Liver Disease (MELD) score. Increased pulmonary vascular resistance (PVR) may be initiated by pulmonary vasoconstriction, altered levels of circulating mediators, or shear stress, and can eventually lead to the classic vascular remodeling (plexiform lesion) that characterizes POPH.

Max A. Cayo, Jun Cai, Ann DeLaForest, Fallon K. Noto, Masato Nagaoka, Brian S. Clark, Ross F. Collery, Karim Si‐Tayeb, Stephen A. Duncan – 31 May 2012 – Elevated levels of low‐density lipoprotein cholesterol (LDL‐C) in plasma are a major contributor to cardiovascular disease, which is the leading cause of death worldwide. Genome‐wide association studies (GWAS) have identified 95 loci that associate with control of lipid/cholesterol metabolism.

Carlo Spirli, Carola M. Morell, Luigi Locatelli, Stefano Okolicsanyi, Cecilia Ferrero, Amy K. Kim, Luca Fabris, Romina Fiorotto, Mario Strazzabosco – 31 May 2012 – Mutations in polycystins are a cause of polycystic liver disease. In polycystin‐2 (PC2)‐defective mice, cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)‐dependent activation of the Rat Sarcoma (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen signal‐regulated kinase–extracellular signal‐regulated kinase (ERK) 1/2 pathway stimulates the growth of liver cysts.

Kurt Zatloukal – 29 May 2012

Kymberly D. Watt, Ross Dierkhising, Julie K. Heimbach, Michael R. Charlton – 29 May 2012 – By analyzing 26,414 patients [12,589 with hepatitis C virus (HCV)] in the Scientific Registry of Transplant Recipients database, we sought to determine comparative risk factors (including primary immunosuppression) predictive of death and graft loss among patients with HCV and patients without HCV.

Emily Rothbaum Perito, Audrey Lau, Sue Rhee, John P. Roberts, Philip Rosenthal – 29 May 2012 – During long‐term follow‐up, 18% to 67% of pediatric liver transplant recipients are overweight or obese, with rates varying by age and pretransplant weight status. A similar prevalence of posttransplant obesity has been seen in adults. Adults also develop posttransplant metabolic syndrome and, consequently, cardiovascular disease at rates that exceed the rates in age‐ and sex‐matched populations.