Liver‐specific loss of glucose‐regulated protein 78 perturbs the unfolded protein response and exacerbates a spectrum of liver diseases in mice

Cheng Ji, Neil Kaplowitz, Mo Yin Lau, Eddy Kao, Lydia M. Petrovic, Amy S. Lee – 18 April 2011 – The endoplasmic reticulum (ER) chaperone protein glucose‐regulated protein 78 (GRP78)/binding immunoglobulin protein is a master regulator of ER homeostasis and stress responses, which have been implicated in the pathogenesis of metabolic disorders. By applying the locus of X‐over P1–cyclization recombination strategy, we generated mice with liver‐specific GRP78 loss.

Schistosoma mansoni infection in the liver graft: The impact on donor and recipient outcomes after transplantation

Rodrigo Vincenzi, João Seda Neto, Eduardo A. Fonseca, Vincenzo Pugliese, Katia R. M. Leite, Marcel R. Benavides, Helry Lopes Cândido, Gilda Porta, Irene K. Miura, Renata Pugliese, Vera B. Danesi, Teresa C. Guimarães, Adriana Porta, Mario Kondo, Eduardo Carone, Paulo Chapchap – 18 April 2011 – The increasing number of transplants performed each year has led to the identification of unusual diseases in liver grafts from asymptomatic donors that were unrecognized before liver transplantation. Here we report our experience with patients who received liver grafts infected with schistosomiasis.

Clinical utility of hepatitis B surface antigen quantitation in patients with chronic hepatitis B: A review

Yun‐Fan Liaw – 18 April 2011 – This clinically relevant review focuses on recent findings concerning hepatitis B surface antigen (HBsAg) quantitation in untreated patients and treated patients with chronic hepatitis B. Recent studies and emerging data have shown that both HBsAg and hepatitis B virus (HBV) DNA levels decline during the natural course of a chronic HBV infection; they are lowest in the inactive phase, which is also characterized by the highest HBsAg/HBV DNA ratio.

Efficacy and safety of entecavir versus adefovir in chronic hepatitis B patients with hepatic decompensation: A randomized, open‐label study

Yun‐Fan Liaw, Maria Raptopoulou‐Gigi, Hugo Cheinquer, Shiv Kumar Sarin, Tawesak Tanwandee, Nancy Leung, Cheng‐Yuan Peng, Robert P. Myers, Robert S. Brown, Lennox Jeffers, Naoky Tsai, Jolanta Bialkowska, Shijie Tang, Suzanne Beebe, Elizabeth Cooney – 18 April 2011 – A randomized, open‐label comparative study of entecavir versus adefovir therapy was performed in subjects with chronic hepatitis B who had hepatic decompensation (Child‐Turcotte‐Pugh score ≥7).

Hepatic B7 homolog 1 expression is essential for controlling cold ischemia/reperfusion injury after mouse liver transplantation

Shinya Ueki, Antonino Castellaneta, Osamu Yoshida, Kikumi Ozaki, Matthew Zhang, Shoko Kimura, Kumiko Isse, Mark Ross, Lifang Shao, Donna B. Stolz, Angus W. Thomson, Anthony J. Demetris, David A. Geller, Noriko Murase – 18 April 2011 – Ischemia/reperfusion (I/R) injury remains a key risk factor significantly affecting morbidity and mortality after liver transplantation (LT). B7 homolog 1 (B7‐H1), a recently identified member of the B7 family, is known to play important roles in regulating local immune responses.

Mixed phenotype hepatocellular carcinoma after transarterial chemoembolization and liver transplantation

Chikako Zen, Yoh Zen, Ragai R. Mitry, Denis Corbeil, Jana Karbanová, John O'Grady, John Karani, Pauline Kane, Nigel Heaton, Bernard C. Portmann, Alberto Quaglia – 13 April 2011 – We investigated the phenotype of hepatocellular carcinoma (HCC) in livers removed during transplantation after local ablation therapy by transarterial chemoembolization (TACE).

Risk factors for cholangiocarcinoma

Gia L. Tyson, Hashem B. El‐Serag – 12 April 2011 – Cholangiocarcinoma (CC) is the second most common primary hepatic malignancy after hepatocellular cancer. CC accounts for approximately 10%‐25% of all hepatobiliary malignancies. There are considerable geographic and demographic variations in the incidence of CC. There are several established risk factors for CC, including parasitic infections, primary sclerosing cholangitis, biliary‐duct cysts, hepatolithiasis, and toxins.

Lack of de novo phosphatidylinositol synthesis leads to endoplasmic reticulum stress and hepatic steatosis in cdipt‐deficient zebrafish

Prakash C. Thakur, Carsten Stuckenholz, Marcus R. Rivera, Jon M. Davison, Jeffrey K. Yao, Adam Amsterdam, Kirsten C. Sadler, Nathan Bahary – 12 April 2011 – Hepatic steatosis is the initial stage of nonalcoholic fatty liver disease (NAFLD) and may predispose to more severe hepatic disease, including hepatocellular carcinoma. Endoplasmic reticulum (ER) stress has been recently implicated as a novel mechanism that may lead to NAFLD, although the genetic factors invoking ER stress are largely unknown.

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