Hepcidin in hemochromatosis: The message or the messenger?
Paul C. Adams – 31 August 2013
Relationship between sarcopenia and nonalcoholic fatty liver disease: The Korean Sarcopenic Obesity Study
Ho Cheol Hong, Soon Young Hwang, Hae Yoon Choi, Hye Jin Yoo, Ji A Seo, Sin Gon Kim, Nan Hee Kim, Sei Hyun Baik, Dong Seop Choi, Kyung Mook Choi – 31 August 2013 – Previous studies have shown that nonalcoholic fatty liver disease (NAFLD) and sarcopenia may share pathophysiological mechanisms, such as insulin resistance, inflammation, vitamin D deficiency, and decreased physical activity. However, their direct relationship has not been investigated.
Center differences in model for end‐stage liver disease exceptions: Fairness, local culture, and norms of practice
Michael L. Volk – 31 August 2013
Transforming growth factor beta signaling in hepatocytes participates in steatohepatitis through regulation of cell death and lipid metabolism in mice
Ling Yang, Yoon Seok Roh, Jingyi Song, Bi Zhang, Cheng Liu, Rohit Loomba, Ekihiro Seki – 30 August 2013 – Transforming growth factor beta (TGF‐β) signaling activates Smad‐ and TGF‐β‐activated kinase 1 (TAK1)‐dependent signaling to regulate cell survival, proliferation, fibrosis, and tumorigenesis. The effects of TGF‐β signaling on metabolic syndrome, including nonalcoholic fatty liver disease, remain elusive. Wild‐type (WT) and hepatocyte‐specific TGF‐β receptor type II‐deficient (Tgfbr2ΔHEP) mice were fed a choline‐deficient amino acid (CDAA)‐defined diet for 22 weeks to induce NASH.
Transforming growth factor beta signaling in hepatocytes participates in steatohepatitis through regulation of cell death and lipid metabolism in mice
Ling Yang, Yoon Seok Roh, Jingyi Song, Bi Zhang, Cheng Liu, Rohit Loomba, Ekihiro Seki – 30 August 2013 – Transforming growth factor beta (TGF‐β) signaling activates Smad‐ and TGF‐β‐activated kinase 1 (TAK1)‐dependent signaling to regulate cell survival, proliferation, fibrosis, and tumorigenesis. The effects of TGF‐β signaling on metabolic syndrome, including nonalcoholic fatty liver disease, remain elusive. Wild‐type (WT) and hepatocyte‐specific TGF‐β receptor type II‐deficient (Tgfbr2ΔHEP) mice were fed a choline‐deficient amino acid (CDAA)‐defined diet for 22 weeks to induce NASH.
Isoniazid hepatotoxicity: Progress in understanding the immunologic component
Laura James, Dean Roberts – 28 August 2013
Relapse of chronic hepatitis B after discontinuation of nucleos(t)ide analogs: Is the glass half full or half empty?
Jurriën G.P. Reijnders, Harry L.A. Janssen – 28 August 2013
Hepatic histological findings in suspected drug‐induced liver injury: Systematic evaluation and clinical associations
David E. Kleiner, Naga P. Chalasani, William M. Lee, Robert J. Fontana, Herbert L. Bonkovsky, Paul B. Watkins, Paul H. Hayashi, Timothy J. Davern, Victor Navarro, Rajender Reddy, Jayant A. Talwalkar, Andrew Stolz, Jiezhun Gu, Huiman Barnhart, Jay H. Hoofnagle, for the Drug‐Induced Liver Injury Network (DILIN) – 28 August 2013 – Drug‐induced liver injury (DILI) is considered to be a diagnosis of exclusion. Liver biopsy may contribute to diagnostic accuracy, but the histological features of DILI and their relationship to biochemical parameters and outcomes are not well defined.
Liver‐specific knockout of GRP94 in mice disrupts cell adhesion, activates liver progenitor cells, and accelerates liver tumorigenesis
Wan‐Ting Chen, Chun‐Chih Tseng, Kyle Pfaffenbach, Gary Kanel, Biquan Luo, Bangyan L. Stiles, Amy S. Lee – 28 August 2013 – Liver cancer is one of the most common solid tumors, with poor prognosis and high mortality. Mutation or deletion of the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is strongly correlated with human liver cancer. Glucose‐regulated protein 94 (GRP94) is a major endoplasmic reticulum (ER) chaperone protein, but its in vivo function is still emerging.