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.

Impact of patatin‐like phospholipase‐3 (rs738409 C>G) polymorphism on fibrosis progression and steatosis in chronic hepatitis C

Eric Trépo, Pierre Pradat, Andrej Potthoff, Yukihide Momozawa, Eric Quertinmont, Thierry Gustot, Arnaud Lemmers, Pascale Berthillon, Leila Amininejad, Michéle Chevallier, Jerome Schlué, Hans Kreipe, Jacques Devière, Michael Manns, Christian Trépo, John Sninsky, Heiner Wedemeyer, Denis Franchimont, Christophe Moreno – 12 April 2011 – Only 20% of patients with chronic hepatitis C (CHC) will develop cirrhosis, and fibrosis progression remains highly unpredictable.

Apoptosis signal‐regulating kinase 1 inhibits hepatocarcinogenesis by controlling the tumor‐suppressing function of stress‐activated mitogen‐activated protein kinase

Hayato Nakagawa, Yoshihiro Hirata, Kohsuke Takeda, Yoku Hayakawa, Takehiro Sato, Hiroto Kinoshita, Kei Sakamoto, Wachiko Nakata, Yohko Hikiba, Masao Omata, Haruhiko Yoshida, Kazuhiko Koike, Hidenori Ichijo, Shin Maeda – 12 April 2011 – The stress‐activated mitogen‐activated protein kinases (MAPKs), c‐Jun NH2‐terminal kinase (JNK), and p38 have been implicated in hepatocarcinogenesis. Although the many interrelated functions of JNK and p38 are precisely regulated by upstream signaling molecules, little is known about upstream regulators.

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