Hepatocyte nuclear factor 1β is a novel prognostic marker independent of the milan criteria in transplantable hepatocellular carcinoma: A retrospective analysis based on tissue microarrays

Ju Hyun Shim, Han Chu Lee, Seungbong Han, Hyo Jeong Kang, Eunsil Yu, Sung‐Gyu Lee – 2 December 2012 – We retrospectively investigated the prognostic value of hepatocyte nuclear factor 1 (HNF1) proteins in 159 liver transplant patients with hepatocellular carcinoma (HCC), including 36 (22.6%) exceeding the Milan criteria. The expression of alpha‐fetoprotein (AFP), HNF1α, and HNF1β was examined with immunohistochemistry on duplicate tissue microarray slides containing HCC tumor explants.

Clinical experience with microdialysis catheters in pediatric liver transplants

Håkon Haugaa, Runar Almaas, Ebbe Billmann Thorgersen, Aksel Foss, Pål Dag Line, Truls Sanengen, Gísli Björn Bergmann, Per Ohlin, Lars Wælgaard, Guro Grindheim, Soeren Erik Pischke, Tom Eirik Mollnes, Tor Inge Tønnessen – 29 November 2012 – Ischemic vascular complications and rejection occur more frequently with pediatric liver transplants versus adult liver transplants. Using intrahepatic microdialysis catheters, we measured lactate, pyruvate, glucose, and glycerol values at the bedside for a median of 10 days in 20 pediatric liver grafts.

Mesenchymal Stem Cells Overexpressing C‐X‐C Chemokine Receptor Type 4 Improve Early Liver Regeneration of Small‐for‐Size Liver Grafts

Zhiyong Du, Cuifeng Wei, Jiqi Yan, Baosan Han, Mingjun Zhang, Chenghong Peng, Yingbin Liu – 29 November 2012 – Mesenchymal stem cell (MSC) therapy can prevent hepatic parenchymal cell loss and promote tissue repair. However, poor MSC engraftment is one of the primary barriers to the effectiveness of cell therapy because culture‐expanded MSCs progressively down‐regulate C‐X‐C chemokine receptor type 4 (CXCR4) expression and lose their ability to migrate toward a concentration gradient of stromal cell–derived factor 1a (SDF1a).

Endoplasmic reticulum polymers impair luminal protein mobility and sensitize to cellular stress in alpha1‐antitrypsin deficiency

Adriana Ordóñez, Erik L. Snapp, Lu Tan, Elena Miranda, Stefan J. Marciniak, David A. Lomas – 29 November 2012 – Point mutants of alpha1‐antitrypsin (α1AT) form ordered polymers that are retained as inclusions within the endoplasmic reticulum (ER) of hepatocytes in association with neonatal hepatitis, cirrhosis, and hepatocellular carcinoma. These inclusions cause cell damage and predispose to ER stress in the absence of the classical unfolded protein response (UPR).

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