Serum mitochondrial biomarkers and damage‐associated molecular patterns are higher in acetaminophen overdose patients with poor outcome

Mitchell R. McGill, Vincent S. Staggs, Matthew R. Sharpe, William M. Lee, Hartmut Jaeschke, Acute Liver Failure Study Group – 13 June 2014 – Acetaminophen (APAP) overdose is a major cause of acute liver failure (ALF). Numerous studies have shown that APAP hepatotoxicity in mice involves mitochondrial dysfunction, and recent data suggest that this is also the case in humans.

The beta‐adrenoceptor agonist isoproterenol rescues acetaminophen‐injured livers through increasing progenitor numbers by Wnt in mice

Junpei Soeda, Angelina Mouralidarane, Shuvra Ray, Marco Novelli, Steven Thomas, Tania Roskams, Anna Mae Diehl, Jude A. Oben – 13 June 2014 – Acetaminophen (APAP)‐induced acute liver injury (AILI) is a major health problem. Accumulating evidence suggests that the sympathetic nervous system (SNS) regulates neuronal and hematopoietic progenitors. SNS signaling affects hepatic progenitor/oval cells (HPCs) and β‐adrenoceptor agonism will expand HPCs to reduce AILI.

Activation of the developmental pathway neurogenin‐3/microRNA‐7a regulates cholangiocyte proliferation in response to injury

Marco Marzioni, Laura Agostinelli, Cinzia Candelaresi, Stefania Saccomanno, Samuele Minicis, Luca Maroni, Eleonora Mingarelli, Chiara Rychlicki, Luciano Trozzi, Jesus M. Banales, Antonio Benedetti, Gianluca Svegliati Baroni – 13 June 2014

Increased risk of cirrhosis and its decompensation in chronic hepatitis C patients with new‐onset diabetes: A nationwide cohort study

Yi‐Wen Huang, Sien‐Sing Yang, Szu‐Chieh Fu, Ting‐Chuan Wang, Cheng‐Kai Hsu, Ding‐Shinn Chen, Jui‐Ting Hu, Jia‐Horng Kao – 11 June 2014 – The effect of diabetes on cirrhosis, its decompensation, and their time relationship in chronic hepatitis C (CHC) patients remains unclear. We conducted a nation‐wide cohort study by using the Taiwanese National Health Insurance Research Database, which is comprised of data from >99% of the entire population. Among having randomly sampled 1 million enrollees, 6,251 adult CHC patients were identified from 1997 to 2009.

Transfemoral liver biopsy using a Quick‐Core biopsy needle system in living donor liver transplantation recipients

Fen Qiang Li, Gi‐Young Ko, Kyu‐Bo Sung, Dong‐Il Gwon, Heung Kyu Ko, Jong Woo Kim, Eunsil Yu – 10 June 2014 – The purpose of this study was to evaluate the efficacy and safety of transfemoral liver biopsy with a Quick‐Core biopsy needle in select living donor liver transplantation (LDLT) recipients. Eight LDLT recipients underwent 9 transfemoral liver biopsy sessions. Six patients had undergone modified right lobe (mRL) LDLT, and 2 patients had undergone dual–left lobe LDLT.

Pnpla3I148M knockin mice accumulate PNPLA3 on lipid droplets and develop hepatic steatosis

Eriks Smagris, Soumik BasuRay, John Li, Yongcheng Huang, Ka‐man V. Lai, Jesper Gromada, Jonathan C. Cohen, Helen H. Hobbs – 10 June 2014 – A sequence polymorphism (rs738409, I148M) in patatin‐like phospholipid domain containing protein 3 (PNPLA3) is strongly associated with nonalcoholic fatty liver disease (NAFLD), but the mechanistic basis for this association remains enigmatic. Neither ablation nor overexpression of wild‐type PNPLA3 affects liver fat content in mice, whereas hepatic overexpression of the human 148M transgene causes steatosis.

Pnpla3I148M knockin mice accumulate PNPLA3 on lipid droplets and develop hepatic steatosis

Eriks Smagris, Soumik BasuRay, John Li, Yongcheng Huang, Ka‐man V. Lai, Jesper Gromada, Jonathan C. Cohen, Helen H. Hobbs – 10 June 2014 – A sequence polymorphism (rs738409, I148M) in patatin‐like phospholipid domain containing protein 3 (PNPLA3) is strongly associated with nonalcoholic fatty liver disease (NAFLD), but the mechanistic basis for this association remains enigmatic. Neither ablation nor overexpression of wild‐type PNPLA3 affects liver fat content in mice, whereas hepatic overexpression of the human 148M transgene causes steatosis.

Reply

Jacinta A. Holmes, Gail V. Matthews, Alexander J. Thompson, on behalf of the CHARIOT Study Group – 10 June 2014

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