The primary outcomes were in-hospital mortality, stroke, hospital charges, and discharge disposition. Subgroup analyses were performed to evaluate these outcomes by neurologic presentation using chi(2) and multivariable logistic regression.

Results: Of the 404,256 discharges for carotid revascularization,

CAS utilization was 66% higher in 2006 than in 2005 (9.3% vs 14%, P = .0004). Crude mortality, stroke, and median charges remained higher for CAS than for CEA; discharge to home was more common after CEA. Results improved from 2005 to 2007. By logistic regression of the total cohort from 2005 to CH5183284 datasheet 2006, CAS was independently predictive of mortality (odds ratio [OR], 1.47; 95% confidence interval [CI], 1.08-2.00; P < .0001). Independent predictors of stroke included CAS (OR, 1.43; 95% CI, 1.18-1.73; P < .0001) and symptomatic disease (OR, 2.4; 95% CI, 2.06-2.93;P < .0001). Among subgroups based on neurological presentation, regression showed that

CAS significantly increased the odds of stroke in asymptomatic patients (OR, 1.6; 95% CI, 1.2-2.0; P = .0003). Among symptomatic patients, CAS increased the odds of in-hospital death (OR, 3.0; 95% CI, 1.7-5.1, P < .0001) and trended toward significance for stroke CP 690550 (OR, 1.7; 95% CI, 1.0-2.8; P = .0569).

Conclusion: Utilization of CAS has increased from the years 2005 to 2007 with some improvements in the outcome. Despite improvements in outcome, resource utilization remains significantly higher for CAS than CEA. (J Vasc Surg 2011;53:307-15.)”
“Amyloid beta peptide 1-40 (A beta(1-40)) is closely associated

with the progressive neuronal loss and cognitive decline observed in Alzheimer’s disease (AD). This study aimed to establish a proteomic strategy for the profiling of AD tissues for disease-specific changes in protein abundance. Intrahippocampal injection of A beta(1-40) Tryptophan synthase induced spatial memory and learning decline in rats. Proteomic analysis revealed the changes in protein expression in the rat hippocampus treated with A beta(1-40). Four proteins of interest which was in abundance was significantly altered in A beta(1-40)-treated rats were identified by peptide mass fingerprint (PMF). These proteins corresponded to synapsin Ib, protein disulfide-isomerase A3 precursor, tubulin beta chain and ATP synthase beta subunit. Our results provide new insights into the relationship between A beta and the pathogenesis of AD, and suggest potential targets for the therapy of AD. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Background: Current data suggest microembolization to the brain may result in long-term cognitive dysfunction despite the absence of immediate clinically obvious cerebrovascular events.