Inhibiting pathway activity in Hh-responsive target cells reduced fibrogenesis, angiogenesis, and growth. In conclusion, HBV/HCV infection increases hepatocyte production of Hh ligands and expands the types of Hh-responsive cells that promote liver fibrosis and cancer. Laboratory Investigation (2010) 90, 1690-1703; doi:10.1038/labinvest.2010.147; published online 9 August 2010″
“Hippocampal (HC) atrophy and atrophy rates are putative clinical markers of progression to Alzheimer’s disease (AD). We compared results given by two different automated HC segmentation techniques in the Alzheimer’s Disease Neuroimaging Initiative

dataset between two time intervals. We used HC volumetric automated segmentation data for a total of 683 patients at baseline (198 controls, 331 with mild cognitive impairment (MCI) and 154 with AD), 684 at 6 months (198 controls, PRT062607 datasheet 332 with MCI and 154 with AD) and 587 at 12 months (176 controls, 280 with MCI and 131 with AD). Segmentation techniques included FreeSurfer and SNT. We calculated HC monthly atrophy rates between baseline and 6 months and between 6 and 12 months, and used a multiple-way ANOVA for repeated measures. Mean HC volumes decrease with time.

The only significant (p < 0.05) main effect was diagnosis. We measured strong interaction between technique and scan interval and weak interaction between diagnoses and scan interval. When compared to mean rates from largely manual segmentation, automated segmentation results show BIBW2992 datasheet increased atrophy rates for both SNT and FreeSurfer techniques. While sensitive, there remains substantial

technique variability, likely due to differences in methodological approaches and especially neuroanatomical HC definitions. These fundamental metrological problems need to be resolved before concluding with certainty on the accuracy and reliability of automated techniques. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“In nonalcoholic fatty liver disease (NAFLD), depletion of hepatic antioxidants may contribute to the progression of steatosis to nonalcoholic steatohepatitis (NASH) by increasing oxidative stress that produces lipid peroxidation, inflammation, and fibrosis. We investigated whether depletion of glutathione Bcl-w (GSH) increases NASH-associated hepatic pathology in mice fed a diet deficient in methionine and choline (MCD diet). Wild-type (wt) mice and genetically GSH-deficient mice lacking the modifier subunit of glutamate cysteine ligase (Gclm null mice), the rate-limiting enzyme for de novo synthesis of GSH, were fed the MCD diet, a methionine/choline-sufficient diet, or standard chow for 21 days. We assessed NASH-associated hepatic pathology, including steatosis, fibrosis, inflammation, and hepatocyte ballooning, and used the NAFLD Scoring System to evaluate the extent of changes.