Functional connectivity analysis using time series correlation, factor analysis, and beta series correlation methods provided convergent evidence that the ASD group exhibited lower levels of functional connectivity and less network integration between frontal, parietal, and occipital regions. In the typically developing P5091 cell line group, fronto-parietal connectivity was related to lower error rates on high control trials. In the autism group, reduced fronto-parietal connectivity was related to attention deficit hyperactivity disorder symptoms. (C) 2009 Elsevier Ltd. All rights reserved.”
“Vaccines that elicit CD8(+) T-cell responses are routinely tested for immunogenicity in nonhuman primates before advancement

to clinical trials. Unfortunately, the magnitude and specificity of vaccine-elicited T-cell responses are variable in currently utilized nonhuman primate populations, owing to heterogeneity in major histocompatibility (MHC) class I genetics. SB431542 mw We recently showed that Mauritian cynomolgus macaques (MCM) have unusually simple MHC genetics, with three common haplotypes encoding a shared pair of MHC class IA alleles, Mafa-A*25 and Mafa-A*29.

Based on haplotype frequency, we hypothesized that CD8(+) T-cell responses restricted by these MHC class I alleles would be detected in nearly all MCM. We examine here the frequency and functionality of these two alleles, showing that 88% of MCM express Mafa-A*25 and Mafa-A*29 and that animals carrying these alleles mount three newly defined simian immunodeficiency virus-specific CD8(+) T-cell responses. The epitopes recognized by each of these responses accumulated substitutions consistent with immunologic escape, suggesting these responses exert antiviral selective pressure. The demonstration that Mafa-A*25 and Mafa-A*29 restrict CD8(+) T-cell responses that are shared among nearly all MCM indicates that these animals are an advantageous nonhuman primate model for comparing the immunogenicity of HSP90 vaccines that elicit CD8(+)

T-cell responses.”
“It is well known that the occurrence of false memories increases with aging, but the results remain inconsistent concerning Alzheimer’s disease (AD). Moreover, the mechanisms underlying the production of false memories are still unclear. Using an experimental episodic memory test with material based on the names of famous people in a procedure derived from the DRM paradigm [Roediger, H. L, III, & McDermott, K. B. (1995). Creating false memories: Remembering words not presented in lists. Journal of Experimental Psychology: Learning, Memory & Cognition, 21, 803-814], we examined correct and false recall and recognition in 30 young adults, 40 healthy older adults, and 30 patients with AD. Moreover, we evaluated the relationships between false memory performance, correct episodic memory performance, and a set of neuropsychological assessments evaluating the semantic memory and executive functions.