HNF1B deficiency causes ciliary defects in human cholangiocytes

Philip Roelandt, Aline Antoniou, Louis Libbrecht, Werner Van Steenbergen, Wim Laleman, Chris Verslype, Schalk Van der Merwe, Frederik Nevens, Rita De Vos, Evelyne Fischer, Marco Pontoglio, Frédéric Lemaigre, David Cassiman – 18 June 2012 – Heterozygous deletion or mutation in hepatocyte nuclear factor 1 homeobox B/transcription factor 2 (HNF1B/TCF2) causes renal cyst and diabetes syndrome (OMIM #137920). Mice with homozygous liver‐specific deletion of Hnf1β revealed that a complete lack of this factor leads to ductopenia and bile duct dysplasia, in addition to mild hepatocyte defects.

Long noncoding RNA associated with microvascular invasion in hepatocellular carcinoma promotes angiogenesis and serves as a predictor for hepatocellular carcinoma patients' poor recurrence‐free survival after hepatectomy

Sheng‐Xian Yuan, Fu Yang, Yuan Yang, Qi‐Fei Tao, Jin Zhang, Gang Huang, Yun Yang, Ruo‐Yu Wang, Sen Yang, Xi‐Song Huo, Ling Zhang, Fang Wang, Shu‐Han Sun, Wei‐Ping Zhou – 18 June 2012 – Survival of patients with hepatocellular carcinoma (HCC) remains poor, which is largely attributed to active angiogenesis. However, the mechanisms underlying angiogenesis in HCC remain to be discovered. In this study, we found that long noncoding RNA associated with microvascular invasion in HCC (lncRNA MVIH) (lncRNA associated with microvascular invasion in HCC) was generally overexpressed in HCC.

HNF1B deficiency causes ciliary defects in human cholangiocytes

Philip Roelandt, Aline Antoniou, Louis Libbrecht, Werner Van Steenbergen, Wim Laleman, Chris Verslype, Schalk Van der Merwe, Frederik Nevens, Rita De Vos, Evelyne Fischer, Marco Pontoglio, Frédéric Lemaigre, David Cassiman – 18 June 2012 – Heterozygous deletion or mutation in hepatocyte nuclear factor 1 homeobox B/transcription factor 2 (HNF1B/TCF2) causes renal cyst and diabetes syndrome (OMIM #137920). Mice with homozygous liver‐specific deletion of Hnf1β revealed that a complete lack of this factor leads to ductopenia and bile duct dysplasia, in addition to mild hepatocyte defects.

Recommendations for standardized nomenclature and definitions of viral response in trials of hepatitis C virus investigational agents

Heiner Wedemeyer, Donald M. Jensen, Eliot Godofsky, Nina Mani, Jean‐Michel Pawlotsky, Veronica Miller, on behalf of the Definitions/Nomenclature Working Group* of the HCV DrAG (HCV Drug Development Advisory Group), under the auspices of the Forum for Collaborative HIV Research – 18 June 2012 – Outdated virological response terms used at key trial timepoints in clinical trials with first‐generation direct‐acting antivirals plus pegylated interferon and ribavirin have failed to keep pace with hepatitis C virus (HCV) drug development.

Liver specific inactivation of carboxylesterase 3/triacylglycerol hydrolase decreases blood lipids without causing severe steatosis in mice

Jihong Lian, Enhui Wei, Shu Pei Wang, Ariel D. Quiroga, Lena Li, Alba Di Pardo, Jelske van der Veen, Simonetta Sipione, Grant A. Mitchell, Richard Lehner – 18 June 2012 – Carboxylesterase 3/triacylglycerol hydrolase (Ces3/TGH) participates in hepatic very low‐density lipoprotein (VLDL) assembly and in adipose tissue basal lipolysis. Global ablation of Ces3/Tgh expression decreases serum triacylglycerol (TG) and nonesterified fatty acid levels and improves insulin sensitivity.

Jaundice increases the rate of complications and one‐year mortality in patients with hypoxic hepatitis

Bernhard Jäger, Andreas Drolz, Barbara Michl, Peter Schellongowski, Andja Bojic, Miriam Nikfardjam, Christian Zauner, Gottfried Heinz, Michael Trauner, Valentin Fuhrmann – 18 June 2012 – Hypoxic hepatitis (HH) is the most frequent cause of acute liver injury in critically ill patients. No clinical data exist about new onset of jaundice in patients with HH. This study aimed to evaluate the incidence and clinical effect of jaundice in critically ill patients with HH. Two hundred and six consecutive patients with HH were screened for the development of jaundice during the course of HH.

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