Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells

Timea Csak, Michal Ganz, Justin Pespisa, Karen Kodys, Angela Dolganiuc, Gyongyi Szabo – 12 April 2011 – The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome activation involves sequential hits. The inflammasome, which cleaves pro–interleukin‐1β (pro–IL‐1β) into secreted IL‐1β, is induced by endogenous and exogenous danger signals. Lipopolysaccharide (LPS), a toll‐like receptor 4 ligand, plays a role in NASH and also activates the inflammasome.

The metastasis‐associated protein‐1 gene encodes a host permissive factor for schistosomiasis, a leading global cause of inflammation and cancer

Sujit S. Nair, Anitha Bommana, Jeffrey M. Bethony, Amanda J. Lyon, Kazufumi Ohshiro, Suresh B. Pakala, Gabriel Rinaldi, Brian Keegan, Sutas Suttiprapa, Maria V. Periago, Peter J. Hotez, Paul J. Brindley, Rakesh Kumar – 12 April 2011 – Schistosoma haematobium is responsible for two‐thirds of the world's 200 million to 400 million cases of human schistosomiasis. It is a group 1 carcinogen and a leading cause of bladder cancer that occurs after years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

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.

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.

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.

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.

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