The global burden of hepatitis E virus genotypes 1 and 2 in 2005

David B. Rein, Gretchen A. Stevens, Jordan Theaker, John S. Wittenborn, Steven T. Wiersma – 26 November 2011 – We estimated the global burden of hepatitis E virus (HEV) genotypes 1 and 2 in 2005. HEV is an emergent waterborne infection that causes source‐originated epidemics of acute disease with a case fatality rate thought to vary by age and pregnancy status.

Hypoxia and hypoxia inducible factors: Diverse roles in liver diseases

Bharath Nath, Gyongyi Szabo – 26 November 2011 – Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology.

Toll‐like receptor 4–dependent Kupffer cell activation and liver injury in a novel mouse model of parenteral nutrition and intestinal injury

Karim C. El Kasmi, Aimee L. Anderson, Michael W. Devereaux, Sophie A. Fillon, J. Kirk Harris, Mark A. Lovell, Milton J. Finegold, Ronald J. Sokol – 26 November 2011 – Infants with intestinal failure who are parenteral nutrition (PN)‐dependent may develop cholestatic liver injury and cirrhosis (PN‐associated liver injury: PNALI). The pathogenesis of PNALI remains incompletely understood.

Phospholipid transfer activity of microsomal triglyceride transfer protein produces apolipoprotein B and reduces hepatosteatosis while maintaining low plasma lipids in mice

Irani Khatun, Sebastian Zeissig, Jahangir Iqbal, Minghui Wang, David Curiel, Gregory S. Shelness, Richard S. Blumberg, M.Mahmood Hussain – 26 November 2011 – Microsomal triglyceride transfer protein (MTP), essential for apolipoprotein B (apoB) biosynthesis, evolved as a phospholipid transfer protein and acquired triglyceride transfer activity during a transition from invertebrates to vertebrates. But it is unknown whether MTP directly transfers lipids onto apoB in vivo and, if it does, whether both neutral and polar lipid transfer activities of MTP are critical for lipoprotein assembly.

The microenvironment in hepatocyte regeneration and function in rats with advanced cirrhosis

Liping Liu, Govardhana Rao Yannam, Taichiro Nishikawa, Toshiyuki Yamamoto, Hesham Basma, Ryotaro Ito, Masaki Nagaya, Joyeeta Dutta‐Moscato, Donna B. Stolz, Fenghai Duan, Klaus H. Kaestner, Yoram Vodovotz, Alejandro Soto‐Gutierrez, Ira J. Fox – 23 November 2011 – In advanced cirrhosis, impaired function is caused by intrinsic damage to the native liver cells and from the abnormal microenvironment in which the cells reside. The extent to which each plays a role in liver failure and regeneration is unknown.

Extrahepatic metastases occur in a minority of hepatocellular carcinoma patients treated with locoregional therapies: Analyzing patterns of progression in 285 patients

Seanthan Senthilnathan, Khairuddin Memon, Robert J. Lewandowski, Laura Kulik, Mary F. Mulcahy, Ahsun Riaz, Frank H. Miller, Vahid Yaghmai, Paul Nikolaidis, Edward Wang, Talia Baker, Michael Abecassis, Al B. Benson, Reed A. Omary, Riad Salem – 23 November 2011 – Although most cancers are considered predominantly systemic processes, this may not hold true for hepatocellular carcinoma (HCC). The literature regarding patterns of progression of HCC (local versus systemic) has been relatively sparse.

Connecting liver and gut: Murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid

Katrin Neumann, Nils Kruse, Balint Szilagyi, Ulrike Erben, Christine Rudolph, Anne Flach, Martin Zeitz, Alf Hamann, Katja Klugewitz – 23 November 2011 – Gut‐activated T cells migrating into the liver can cause extraintestinal manifestations of inflammatory bowel disease. T cells acquire a gut‐homing phenotype dependent on retinoic acid (RA) provided by intestinal dendritic cells (DC). We investigated whether liver antigen‐presenting cells can induce gut tropism supporting an enterohepatic lymphocyte circulation.

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