Over this period, deterioration of verbal abilities such as picture naming, story retelling, and semantic word recall was found, and the individual decline was quantified and compared between the three patients. Furthermore, decrease

in non-verbal skills such as divided attention and increasing apraxia was observed in all three patients. In addition, inter-subject variability in the progression with different focuses was observed, with one patient developing a non-fluent PPA variant. The longitudinal, multivariate investigation of logopenic PPA thus provides novel insights into the progressive deterioration of verbal as well as non-verbal abilities. These deficits may further interact and Saracatinib thus form a multi-causal

basis for the patients’ problems in every-day life which need to be considered when planning individually targeted intervention in PPA (C) 2012 Elsevier Ltd. All rights reserved.”
“Objectives: Esophageal adenocarcinoma is an aggressive malignancy generally diagnosed after metastatic spread and currently lacks effective medical therapy. Expression of intracellular adhesion molecule-1 (ICAM-1) is an adverse prognostic indicator in various human tumor cells and contributes significantly to their metastatic potential. Statin therapy reduces circulating ICAM-1 levels in patients with coronary heart disease and is associated with reduction in progression from Barrett esophagus to esophageal adenocarcinoma. We hypothesize that statin therapy may attenuate growth and malignant potential via ICAM-1 expression and nuclear factor-kappa beta activation in human esophageal adenocarcinoma selleck inhibitor Electron transport chain cells.

Methods: Verified human esophageal

adenocarcinoma cells (FLO-1) were treated with simvastatin, atorvastatin, or pravastatin (10-, 30-, and 50-mu mol/L concentrations). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide viability, 5-bromo-2′-deoxyuridine proliferation, or annexin V apoptosis assays were performed, or cells were stimulated with tumor necrosis factor-alpha and collected for immunoblotting and flow cytometry.

Results: Simvastatin decreased cell viability and proliferation while increasing apoptosis in a dose-dependent manner (P < .05). Simvastatin attenuated total cellular and cell-surface ICAM-1 expression as well as nuclear factor-kappa beta activation (P < .05). Atorvastatin had mild effects and pravastatin had essentially no effect on growth and metastatic potential of these cells.

Conclusions: We demonstrate that treatment of human esophageal adenocarcinoma cells with simvastatin attenuates growth, by decreasing cell viability, decreasing cell proliferation, and increasing apoptosis, and attenuates metastatic potential, by decreasing expression of key metastatic markers. These findings identify simvastatin as a potential therapeutic and chemopreventive modality to thwart the progression of esophageal adenocarcinoma.