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Hongli Hu, Daming Gao – 12 August 2017
Hongli Hu, Daming Gao – 12 August 2017
Yang‐Hsiang Lin, Meng‐Han Wu, Ya‐Hui Huang, Chau‐Ting Yeh, Mei‐Ling Cheng, Hsiang‐Cheng Chi, Chung‐Ying Tsai, I‐Hsiao Chung, Ching‐Ying Chen, Kwang‐Huei Lin – 12 August 2017 – Cancer cells display altered glucose metabolism characterized by a preference for aerobic glycolysis. The aerobic glycolytic phenotype of hepatocellular carcinoma (HCC) is often correlated with tumor progression and poorer clinical outcomes. However, the issue of whether glycolytic metabolism influences metastasis in HCC remains unclear.
Boris Halgand, Christophe Desterke, Lise Rivière, Guillaume Fallot, Mylène Sebagh, Julien Calderaro, Paulette Bioulac‐Sage, Christine Neuveut, Marie‐Annick Buendia, Didier Samuel, Cyrille Féray – 12 August 2017 – Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). However, very little is known about the replication of HBV in HCC tissues. We analyzed viral and cellular parameters in HCC (T) and nontumor liver (NT) samples from 99 hepatitis B surface antigen (HBsAg)‐positive, virologically suppressed patients treated by tumor resection or liver transplantation.
Chris Estes, Homie Razavi, Rohit Loomba, Zobair Younossi, Arun J. Sanyal – 12 August 2017 – Nonalcoholic fatty liver disease (NAFLD) and resulting nonalcoholic steatohepatitis (NASH) are highly prevalent in the United States, where they are a growing cause of cirrhosis and hepatocellular carcinoma (HCC) and increasingly an indicator for liver transplantation. A Markov model was used to forecast NAFLD disease progression. Incidence of NAFLD was based on historical and projected changes in adult prevalence of obesity and type 2 diabetes mellitus (DM).
Melania Gaggini, Fabrizia Carli, Chiara Rosso, Emma Buzzigoli, Milena Marietti, Veronica Della Latta, Demetrio Ciociaro, Maria Lorena Abate, Roberto Gambino, Maurizio Cassader, Elisabetta Bugianesi, Amalia Gastaldelli – 12 August 2017 – Plasma concentrations of amino acids (AAs), in particular, branched chain AAs (BCAAs), are often found increased in nonalcoholic fatty liver disease (NAFLD); however, if this is due to increased muscular protein catabolism, obesity, and/or increased insulin resistance (IR) or impaired tissue metabolism is unknown.
Anja Moncsek, Mohammed S. Al‐Suraih, Christy E. Trussoni, Steven P. O'Hara, Patrick L. Splinter, Camille Zuber, Eleonora Patsenker, Piero V. Valli, Christian D. Fingas, Achim Weber, Yi Zhu, Tamar Tchkonia, James L. Kirkland, Gregory J. Gores, Beat Müllhaupt, Nicholas F. LaRusso, Joachim C. Mertens – 12 August 2017 – Cholangiocyte senescence has been linked to primary sclerosing cholangitis (PSC). Persistent secretion of growth factors by senescent cholangiocytes leads to the activation of stromal fibroblasts (ASFs), which are drivers of fibrosis.
Meng Wang, S. Courtney Frasch, Guiying Li, Dechun Feng, Bin Gao, Liangguo Xu, Diana Ir, Daniel N. Frank, Donna L. Bratton, Cynthia Ju – 11 August 2017 – Hepatic macrophages (MΦs) are important in the development and progression of alcoholic liver disease (ALD). This study investigates the role of gp91phox (nicotinamide adenine dinucleotide phosphate oxidase 2) in the severity of ALD and specifically in regulating hepatic MΦ efferocytic capability and the subsequent reprogramming associated with resolution of inflammation.
Ryoichi Fujiwara, Ryo Mitsugi, Asuka Uemura, Tomoo Itoh, Robert H. Tukey – 10 August 2017 – Neurotoxic bilirubin is solely conjugated by UDP‐glucuronosyltransferase (UGT) 1A1. Due to an inadequate function of UGT1A1, human neonates develop mild to severe physiological hyperbilirubinemia. Accumulation of bilirubin in the brain leads to the onset of irreversible brain damage called kernicterus. Breastfeeding is one of the most significant factors that increase the risk of developing kernicterus in infants.
Katrin Hochrath, Bernd Schnabl – 6 August 2017
Michitaka Matsuda, Shinya Tsurusaki, Naoko Miyata, Eiko Saijou, Hitoshi Okochi, Atsushi Miyajima, Minoru Tanaka – 5 August 2017 – Fibrosis is an important wound‐healing process in injured tissues, but excessive fibrosis is often observed in patients with chronic inflammation. Although oncostatin M (OSM) has been reported to play crucial roles for recovery from acute liver injury by inducing tissue inhibitor of metalloproteinase 1 (Timp1) expression, the role of OSM in chronic liver injury (CLI) is yet to be elucidated.