Modeling viral kinetics and treatment outcome during alisporivir interferon‐free treatment in hepatitis C virus genotype 2 and 3 patients

Jeremie Guedj, Jing Yu, Micha Levi, Bin Li, Steven Kern, Nikolai V. Naoumov, Alan S. Perelson – 23 December 2013 – Alisporivir (ALV) is a cyclophilin inhibitor with pan‐genotypic activity against hepatitis C virus (HCV). Here, we characterize the viral kinetics observed in 249 patients infected with HCV genotypes 2 or 3 and treated for 6 weeks with different doses of ALV with or without ribavirin (RBV). We use this model to predict the effects of treatment duration and different doses of ALV plus RBV on sustained virologic response (SVR).

Relationship between disease severity, hyperinsulinemia, and impaired insulin clearance in patients with nonalcoholic steatohepatitis

Fernando Bril, Romina Lomonaco, Beverly Orsak, Carolina Ortiz‐Lopez, Amy Webb, Fermin Tio, Joan Hecht, Kenneth Cusi – 23 December 2013 – Hyperinsulinemia is believed to play a key role in the pathogenesis of nonalcoholic steatohepatitis (NASH) and associated cardiovascular risk. However, the relative contribution of insulin clearance to hyperinsulinemia and its relationship to liver histology have not been carefully evaluated before.

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.

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.

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).

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.

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.

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