Working memory dysfunctions in schizophrenia correlated with grey matter in both cerebellar hemispheres and vermis. Mental flexibility dysfunctions also correlated with reductions in white matter volume in bilateral cerebellum. This evidence supports the contribution of cerebellar grey and white matter deficits to

executive dysfunctions observed in schizophrenia.”
“Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of the aggressive and fatal disease adult T-cell leukemia. Previous studies have demonstrated that the HTLV-1-encoded Tax protein inhibits the function of tumor suppressor p53 through a Tax-induced NF-kappa B pathway. Given these Silmitasertib concentration attributes, we were interested in the activity of small-molecule inhibitor 9-aminoacridine (9AA), an anticancer drug that targets two important stress response pathways, NF-kappa B and p53. In the present study, we have examined the effects of 9AA on HTLV-1 -transformed cells. Treatment of HTLV-1-transformed cells with 9AA resulted in a dramatic decrease in cell viability. Consistent with

these results, we observed an increase in the percentage of cells in sub-G, and an increase in the number of cells positive by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling assay following treatment of HTLV-1-transformed cells with 9AA. In each assay, HTLV-1-transformed cells C8166, selleck compound Hut102, Carteolol HCl and MT2 were more sensitive to treatment with 9AA than control CEM and peripheral blood mononuclear cells. Analyzing p53 function, we demonstrate that treatment of HTLV-1 -transformed cells

with 9AA resulted in an increase in p53 protein and activation of p53 transcription activity. Of significance, 9AA-induced cell death could be blocked by introduction of a p53 small interfering RNA, linking p53 activity and cell death. These results suggest that Tax-repressed p53 function in HTLV-1-transformed cells is “”druggable”" and can be restored by treatment with 9AA. The fact that 9AA induces p53 and inhibits NF-kappa B suggests a promising strategy for the treatment of HTLV-1-transformed cells.”
“Sensory gating refers to the suppression of the neuronal response to a repeating stimulus and is considered a protection mechanism in the brain. In this study, we assessed gating of the mid-latency components of the visual evoked potentials (N75, P100, N1150) in II healthy individuals using a paired-flash paradigm. A significant decrease of P100 and NISO amplitudes was shown; additionally, a significant increase in the latency of N75 and P100 for the second stimulus of the pair compared with the first one was also observed. Absolute power of the stimulus 2 signal at 0 frequency was significantly suppressed as compared with the stimulus I signal. These results indicate a gating effect in the visual modality, reflected in both time-domain and frequency-domain measures.