Atrioventricular conduction disturbances immediately after hepatic graft reperfusion and their outcomes in patients undergoing liver transplantation

Sung‐Hoon Kim, Young‐Jin Moon, Sooho Lee, Sung‐Moon Jeong, Jun‐Gol Song, Gyu‐Sam Hwang – 6 February 2016 – Hemodynamic perturbation during hepatic graft reperfusion in patients undergoing liver transplantation (LT) is challenging and is frequently accompanied by bradyarrhythmia and even asystole. However, detailed data on electrocardiographic (ECG) changes during reperfusion are almost nonexistent, although the correct diagnosis by record is important for the treatment. We aimed to identify ECG rhythm disturbances during graft reperfusion and to investigate risk factors and outcomes.

Development and validation of a noninvasive prediction model for nonalcoholic steatohepatitis resolution after lifestyle intervention

Eduardo Vilar‐Gomez, Ali Yasells‐Garcia, Yadina Martinez‐Perez, Luis Calzadilla‐Bertot, Ana Torres‐Gonzalez, Bienvenido Gra‐Oramas, Licet Gonzalez‐Fabian, Oscar Villa‐Jimenez, Scott L. Friedman, Moises Diago, Manuel Romero‐Gomez – 5 February 2016 – Liver biopsy is the gold standard method to assess nonalcoholic steatohepatitis (NASH) resolution after therapeutic interventions. We developed and validated a simple and noninvasive scoring system to predict NASH resolution without fibrosis worsening after 1 year of lifestyle intervention.

Cancer Stem cells and their cellular origins in primary liver and biliary tract cancers

Tsunekazu Oikawa – 5 February 2016 – Liver and biliary tract cancers are highly aggressive, are heterogeneous in their phenotypic traits, and result in clinical outcomes that are difficult to manage. Cancers have subpopulations of cells termed “cancer stem cells” (CSCs) that share common intrinsic signaling pathways for self‐renewal and differentiation with normal stem cells. These CSCs likely have the potential to evolve over time and to give rise to new genetically and functionally diverse subclones by accumulating genetic mutations.

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Christine E. McLaren, James C. Barton, V. Nathan Subramaniam, Grant A. Ramm, Pradyumna D. Phatak, Mary J. Emond, Lyle C. Gurrin, Paul C. Adams, Lawrie W. Powell, Gregory J. Anderson, Gordon D. McLaren – 4 February 2016

Oncogenic driver genes and the inflammatory microenvironment dictate liver tumor phenotype

Matthias S. Matter, Jens U. Marquardt, Jesper B. Andersen, Cristina Quintavalle, Nikolay Korokhov, Jim K. Stauffer, Kosuke Kaji, Thomas Decaens, Luca Quagliata, Fathi Elloumi, Tanya Hoang, Alfredo Molinolo, Elizabeth A. Conner, Achim Weber, Mathias Heikenwalder, Valentina M. Factor, Snorri S. Thorgeirsson – 4 February 2016 – The majority of hepatocellular carcinoma develops in the background of chronic liver inflammation caused by viral hepatitis and alcoholic or nonalcoholic steatohepatitis.

c‐Jun N‐terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)‐dependent pathway leading to inactivation of intramitochondrial Src

Sanda Win, Tin Aung Than, Robert Win Maw Min, Mariam Aghajan, Neil Kaplowitz – 4 February 2016 – Sustained c‐Jun N‐terminal kinase (JNK) activation has been implicated in many models of cell death and tissue injury. Phosphorylated JNK (p‐JNK) interacts with the mitochondrial outer membrane SH3 homology associated BTK binding protein (Sab, or SH3BP5). Using knockdown or liver‐specific deletion of Sab, we aimed to elucidate the consequences of this interaction on mitochondrial function in isolated mitochondria and liver injury models in vivo.

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