Risk stratification and targeted antifungal prophylaxis for prevention of aspergillosis and other invasive mold infections after liver transplantation

Walter C. Hellinger, Hugo Bonatti, Joseph D. Yao, Salvador Alvarez, Lisa M. Brumble, Michael R. Keating, Julio C. Mendez, David J. Kramer, Rolland C. Dickson, Denise M. Harnois, James R. Spivey, Christopher B. Hughes, Justin H. Nguyen, Jeffery L. Steers – 24 May 2005 – Antifungal prophylaxis has been proposed for liver transplant recipients at increased risk for invasive mold infection.

NAD(P)H oxidase plays a crucial role in PDGF‐induced proliferation of hepatic stellate cells

Tohru Adachi, Hitoshi Togashi, Akihiko Suzuki, Shigenobu Kasai, Junitsu Ito, Kazuhiko Sugahara, Sumio Kawata – 24 May 2005 – The proliferation of hepatic stellate cells (HSCs) is a critical step in hepatic fibrogenesis. Platelet‐derived growth factor (PDGF) is the most potent mitogen for HSCs. We investigated the role of nonphagocytic NAD(P)H oxidase–derived reactive oxygen species (ROS) in PDGF‐induced HSC proliferation. The human HSC line, LI‐90 cells, murine primary‐cultured HSCs, and PDGF‐BB were used in this study.

Design and validation of a histological scoring system for nonalcoholic fatty liver disease

David E. Kleiner, Elizabeth M. Brunt, Mark Van Natta, Cynthia Behling, Melissa J. Contos, Oscar W. Cummings, Linda D. Ferrell, Yao‐Chang Liu, Michael S. Torbenson, Aynur Unalp‐Arida, Matthew Yeh, Arthur J. McCullough, Arun J. Sanyal, Nonalcoholic Steatohepatitis Clinical Research Network – 24 May 2005 – Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis in the absence of a history of significant alcohol use or other known liver disease. Nonalcoholic steatohepatitis (NASH) is the progressive form of NAFLD.

Liver transplantation for severe intrahepatic noncirrhotic portal hypertension

Alyssa M. Krasinskas, Bijan Eghtesad, Patrick S. Kamath, Anthony J. Demetris, Susan C. Abraham – 24 May 2005 – Intrahepatic noncirrhotic portal hypertension can be idiopathic or associated with known toxic, developmental, vascular, or biliary tract diseases. Most patients are successfully managed medically or with shunting procedures. The goal of this study was to explore the reasons some patients require orthotopic liver transplantation (OLT).

Liver transplant recipient selection: MELD vs. clinical judgment

Michael A. Fink, Peter W. Angus, Paul J. Gow, S. Roger Berry, Bao‐Zhong Wang, Vijayaragavan Muralidharan, Christopher Christophi, Robert M. Jones – 24 May 2005 – Minimization of death while waiting for liver transplantation involves accurate prioritization according to clinical status and appropriate allocation of donor livers. Clinical judgment in the Liver Transplant Unit Victoria (LTUV) was compared with Model for End‐Stage Liver Disease (MELD) in a retrospective analysis of the LTUV database over the 2‐year period August 1, 2002, through July 31, 2004.

Intraoperative direct measurement of hepatic arterial buffer response in patients with or without cirrhosis

Taku Aoki, Hiroshi Imamura, Junichi Kaneko, Yoshihiro Sakamoto, Yutaka Matsuyama, Norihiro Kokudo, Yasuhiko Sugawara, Masatoshi Makuuchi – 24 May 2005 – The hepatic arterial buffer response (HABR) is an intrinsic regulatory mechanism of the hepatic artery (HA) that compensates for reductions in portal venous (PV) blood flow. Whether this response is maintained in patients with cirrhosis (LC) is unclear. The aim of the present study was to examine whether HABR is maintained in patients with LC using direct blood flow measurements.

Chronic liver injury during obstructive sleep apnea

Florence Tanné, Frédéric Gagnadoux, Olivier Chazouillères, Bernard Fleury, Dominique Wendum, Elisabeth Lasnier, Bernard Lebeau, Raoul Poupon, Lawrence Serfaty – 24 May 2005 – Patients with obstructive sleep apnea (OSA) are at risk for the development of fatty liver as a result of being overweight. Several data suggest that OSA per se could be a risk factor of liver injury; ischemic hepatitis during OSA has been reported, and OSA is an independent risk factor for insulin resistance.

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