This disease represents a particular challenge for researchers and clinicians, due to its insidious onset and ambiguous clinical features, which frequently render difficult a precise and timely diagnosis. The paper proposes a way to shed
new light on the hypothesis that the neuropsychiatric profile of individuals with bv-FTD can be at least partially explained by a deficit in ToM ability. We examined both neuroimaging data on the neural correlates of ToM ability in healthy participants and studies investigating the progressive cerebral atrophy in patients with bv-FTD. Our findings suggest a link between the progressive degeneration of the anterior regions of medial frontal structures characterising the early stages of the bv-FTD PD173074 clinical trial and the ToM deficit these patients show. They also suggest the importance of using ToM tests during the diagnostic process of bv-FTD. (C) 2009 Elsevier Ltd. HSP990 All rights reserved.”
“Human parvovirus B19 (B19V) is a member of the genus Erythrovirus in the family Parvoviridae. In vitro, autonomous B19V replication is limited to human erythroid progenitor cells and in a small number of erythropoietin-dependent human
megakaryoblastoid and erythroid leukemic cell lines. Here we report that the failure of B19V DNA replication in nonpermissive 293 cells can be overcome by adenovirus infection. More specifically, the replication of B19V DNA in the 293 cells and the production of infectious progeny virus were made check details possible by the presence of the adenovirus E2a, E4orf6, and VA RNA genes that emerged during the transfection of the pHelper plasmid. Using this replication system, we identified the terminal resolution site and the nonstructural protein 1 (NS1) binding site on the right terminal palindrome of the viral genome, which is composed of a minimal origin of replication spanning 67 nucleotides. Plasmids or DNA fragments containing an NS1 expression
cassette and this minimal origin were able to replicate in both pHelper-transfected 293 cells and B19V-semipermissive UT7/Epo-S1 cells. Our results have important implications for our understanding of native B19V infection.”
“Declines in neural processing speed have been proposed to underlie a broad range of cognitive deficits in older adults. However, the impact of delays in neural processing during stimulus encoding on working memory (WM) performance is not well understood. In the current study. we assessed the influence of aging on the relationship between neural measures of processing speed and WM performance during a selective delayed-recognition task for color and motion stimuli, while electroencephalography (EEG) was recorded in young and older adults.