Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Kazumichi Abe, Atsushi Takahashi, Masashi Fujita, Manabu Hayashi, Ken Okai, Yoshihiro Nozawa, Hiromasa Ohira – 25 February 2019 – Interleukin (IL)‐33 was recently described as a new member of the IL‐1 family; members of this family have proinflammatory activity. IL‐33 and its soluble receptor ST2 (sST2) have been implicated in the pathogenesis of autoimmune diseases. This study investigated serum IL‐33 and sST2 in type I autoimmune hepatitis (AIH) and the relationship of these molecules with clinical and pathologic parameters.

Expression of Metastatic Tumor Antigen 1 Splice Variant Correlates With Early Recurrence and Aggressive Features of Hepatitis B Virus–Associated Hepatocellular Carcinoma

Yung‐Tsung Li, Hui‐Lin Wu, Jia‐Horng Kao, Huei‐Ru Cheng, Ming‐Chih Ho, Chih‐Chiang Wang, Pei‐Jer Chen, Ding‐Shinn Chen, Chun‐Jen Liu – 25 February 2019 – Overexpression of metastatic tumor antigen 1 (MTA1) was correlated with poor prognosis of hepatitis B virus (HBV)‐associated hepatocellular carcinoma (HBV‐HCC). The aim of this study was to examine the clinical significance of the expression of MTA1 and its exon 4‐excluded form (MTA1dE4), the most abundant spliced variant of MTA1, in patients receiving curative resection for HBV‐HCC.

Angiopoietin‐2/Tie2 Inhibition by Regorafenib Associates With Striking Response in a Patient With Aggressive Hepatocellular Carcinoma

Paola Todesca, Luca Marzi, Rosina Maria Critelli, Biagio Cuffari, Cristian Caporali, Laura Turco, Giovanni Pinelli, Filippo Schepis, Lucia Carulli, Nicola de Maria, Federico Casari, Riccardo Scaglioni, Erica Villa – 25 February 2019

PNPLA3, CGI‐58, and Inhibition of Hepatic Triglyceride Hydrolysis in Mice

Yang Wang, Nora Kory, Soumik BasuRay, Jonathan C. Cohen, Helen H. Hobbs – 25 February 2019 – A variant (148M) in patatin‐like phospholipase domain‐containing protein 3 (PNPLA3) is a major risk factor for fatty liver disease. Despite its clinical importance, the pathogenic mechanism linking the variant to liver disease remains poorly defined. Previously, we showed that PNPLA3(148M) accumulates to high levels on hepatic lipid droplets (LDs). Here we examined the effect of that accumulation on triglyceride (TG) hydrolysis by adipose triglyceride lipase (ATGL), the major lipase in the liver.

Subscribe to