IL‐12/Th1 and IL‐23/Th17 biliary microenvironment in primary biliary cirrhosis: Implications for therapy

Chen‐Yen Yang, Xiong Ma, Koichi Tsuneyama, Shanshan Huang, Toru Takahashi, Naga P. Chalasani, Christopher L. Bowlus, Guo‐Xiang Yang, Patrick S.C. Leung, Aftab A. Ansari, Linda Wu, Ross L. Coppel, M. Eric Gershwin – 21 December 2013 – The interleukin (IL)‐12/IL‐23‐mediated Th1/Th17 signaling pathway has been associated with the etiopathogenesis of primary biliary cirrhosis (PBC).

Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury

Justin M. Belcher, Arun J. Sanyal, Aldo J. Peixoto, Mark A. Perazella, Joseph Lim, Heather Thiessen‐Philbrook, Naheed Ansari, Steven G. Coca, Guadalupe Garcia‐Tsao, Chirag R. Parikh, for the TRIBE‐AKI Consortium – 21 December 2013 – Acute kidney injury (AKI) is common in patients with cirrhosis and associated with significant mortality. The most common etiologies of AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS). Accurately distinguishing the etiology of AKI is critical, as treatments differ markedly.

Mesenchymal stem cell therapy ameliorates diabetic hepatocyte damage in mice by inhibiting infiltration of bone marrow–derived cells

Kanna Nagaishi, Koji Ataka, Eijiro Echizen, Yoshiaki Arimura, Mineko Fujimiya – 21 December 2013 – Although mesenchymal stem cells (MSCs) have been implicated in hepatic injury, the mechanism through which they contribute to diabetic liver disease has not been clarified. In this study, we investigated the effects of MSC therapy on diabetic liver damage with a focus on the role of bone‐marrow–derived cells (BMDCs), which infiltrate the liver, and elucidated the mechanism mediating this process.

Serum immunoglobulin G4 and immunoglobulin G1 for distinguishing immunoglobulin G4‐associated cholangitis from primary sclerosing cholangitis

Kirsten Boonstra, Emma L. Culver, Lucas Maillette de Buy Wenniger, Marianne J. Heerde, Karel J. Erpecum, Alexander C. Poen, Karin M.J. Nieuwkerk, B.W. Marcel Spanier, Ben J.M. Witteman, Hans A.R.E. Tuynman, Nan Geloven, Henk Buuren, Roger W. Chapman, Eleanor Barnes, Ulrich Beuers, Cyriel Y.

MYO5B and bile salt export pump contribute to cholestatic liver disorder in microvillous inclusion disease

Muriel Girard, Florence Lacaille, Virginie Verkarre, Raphael Mategot, Gerard Feldmann, Alain Grodet, Frédérique Sauvat, Sabine Irtan, Anne Davit‐Spraul, Emmanuel Jacquemin, Frank Ruemmele, Dominique Rainteau, Olivier Goulet, Virginie Colomb, Christophe Chardot, Alexandra Henrion‐Caude, Dominique Debray – 21 December 2013 – Microvillous inclusion disease (MVID) is a congenital disorder of the enterocyte related to mutations in the MYO5B gene, leading to intractable diarrhea often necessitating intestinal transplantation (ITx).

Hepatocyte‐specific high‐mobility group box 1 deletion worsens the injury in liver ischemia/reperfusion: A role for intracellular high‐mobility group box 1 in cellular protection

Hai Huang, Gary W. Nace, Kerry‐Ann McDonald, Sheng Tai, John R. Klune, Brian R. Rosborough, Qing Ding, Patricia Loughran, Xiaorong Zhu, Donna Beer‐Stolz, Eugene B. Chang, Timothy Billiar, Allan Tsung – 21 December 2013 – High‐mobility group box 1 (HMGB1) is an abundant chromatin‐associated nuclear protein and released into the extracellular milieu during liver ischemia‐reperfusion (I/R), signaling activation of proinflammatory cascades.

Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury

Justin M. Belcher, Arun J. Sanyal, Aldo J. Peixoto, Mark A. Perazella, Joseph Lim, Heather Thiessen‐Philbrook, Naheed Ansari, Steven G. Coca, Guadalupe Garcia‐Tsao, Chirag R. Parikh, for the TRIBE‐AKI Consortium – 21 December 2013 – Acute kidney injury (AKI) is common in patients with cirrhosis and associated with significant mortality. The most common etiologies of AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS). Accurately distinguishing the etiology of AKI is critical, as treatments differ markedly.

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