Explanted liver inflammatory grade predicts fibrosis progression in hepatitis C recurrence

Marwan Ghabril, Rolland C. Dickson, Murli Krishna, Victor Machicao, Jaime Aranda‐Michel, Hugo Bonatti, Justin H. Nguyen – 10 January 2011 – Factors present prior to liver transplantation (LT) that predict fibrosis progression in recurrent hepatitis C infection (HCV) after LT would be important to identify. This study sought to determine if histologic grade of HCV in the explant predicts fibrosis progression in recurrent HCV.

Noncirrhotic presinusoidal portal hypertension is common in cystic fibrosis–associated liver disease

Peter Witters, Louis Libbrecht, Tania Roskams, Kris De Boeck, Lieven Dupont, Marijke Proesmans, François Vermeulen, Birgitta Strandvik, Anders Lindblad, Xavier Stéphenne, Etienne Sokal, Serge Gosseye, Sam Heye, Geert Maleux, Raymond Aerts, Diethard Monbaliu, Jacques Pirenne, Ilse Hoffman, Frederik Nevens, David Cassiman – 10 January 2011

Outcomes in children who underwent transplantation for autoimmune hepatitis

Steven R. Martin, Fernando Alvarez, Ravinder Anand, Changhong Song, Wanrong Yin – 6 January 2011 – The outcomes of 113 children with autoimmune hepatitis (AIH), registered with Studies of Pediatric Liver Transplantation and who underwent transplantation between 1995 and 2006, were compared with those who underwent transplantation for other diagnoses (non‐AIH). A total of 4.9% of liver transplants were for AIH; 81% of these patients had AIH type 1 and most underwent transplantation for complications of chronic disease (60%), the majority in females (72%).

The GRACILE mutation introduced into Bcs1l causes postnatal complex III deficiency: A viable mouse model for mitochondrial hepatopathy

Per Levéen, Heike Kotarsky, Matthias Mörgelin, Riitta Karikoski, Eskil Elmér, Vineta Fellman – 28 December 2010 – Mitochondrial dysfunction is an important cause for neonatal liver disease. Disruption of genes encoding oxidative phosphorylation (OXPHOS) components usually causes embryonic lethality, and thus few disease models are available. We developed a mouse model for GRACILE syndrome, a neonatal mitochondrial disease with liver and kidney involvement, caused by a homozygous BCS1L mutation (232A>G).

Molecular therapy for obesity and diabetes based on a long‐term increase in hepatic fatty‐acid oxidation

Josep M. Orellana‐Gavaldà, Laura Herrero, Maria Ida Malandrino, Astrid Pañeda, Maria Sol Rodríguez‐Peña, Harald Petry, Guillermina Asins, Sander Van Deventer, Fausto G. Hegardt, Dolors Serra – 22 December 2010 – Obesity‐induced insulin resistance is associated with both ectopic lipid deposition and chronic, low‐grade adipose tissue inflammation. Despite their excess fat, obese individuals show lower fatty‐acid oxidation (FAO) rates. This has raised the question of whether burning off the excess fat could improve the obese metabolic phenotype.

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