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“Neurological soft signs (NSS) comprise a broad range of minor motor and sensory deficits which are frequently found in schizophrenia. However, the cerebral changes underlying NSS are only partly understood. We therefore investigated the cerebral correlates of NSS by using magnetic resonance imaging (MRI) in 102 patients with first episode schizophrenia. NSS were assessed after remission of acute psychotic symptoms using the Heidelberg scale (HS), which consists of five NSS subscales (“motor coordination”, “complex motor tasks”, “orientation”, “integrative functions”, and “hard signs”). Correlations between NSS scores this website and cerebral changes

were established by optimized voxel-based morphometry. NSS total scores were significantly associated with

reduced gray matter densities in the precentral and postcentral gyri, the inferior parietal lobule and the inferior occipital gyrus. Both check details of the NSS subscales “motor coordination” and “complex motor tasks”, referred to motor strip changes but showed differential correlations with parietal, insular, cerebellar or frontal sites, respectively. The NSS subscales “orientation” and “integrative functions” were associated with left frontal, parietal, and occipital changes or bihemispheric frontal changes, respectively. The NSS subscale “hard signs” was associated with deficits in the right cerebellum and right parastriate cortex. Repeated analyses for white matter changes revealed similar results. These findings confirm the associations between NSS and cerebral changes in areas important for motor and sensory functioning. This variety of cerebral sites corresponds to the heterogeneity of NSS and are consistent with the hypothesis that NSS reflect both a rather generalized cerebral dysfunction and localized deficits specific for particular signs. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Previous studies have shown that 7-b (6-(dodecylamino)-2-(3-(4-methylpiperazin-1-yl)propyl)-1H-benzo-[de]isoquinoline-1,3(2H)-dione), Caspase inhibitor a novel amonafide-based DNA intercalator, was generated as a new anticancer candidate. However, the effects induced by 7-b and the molecular mechanisms

involved remain poorly understood in Burkitt’s lymphoma. To shed light on these issues, we have investigated the effects of 7-b on proliferation, cell cycle progression, apoptosis activity and oxidative stress levels of lymphoma Raji cells in vitro. Our results showed that 7-b inhibited the proliferation of Raji cells and induced G1 cell cycle arrest in a dose-dependent manner. Moreover, 7-b treatment triggered programmed cell death, production of reactive oxygen species (ROS) and alteration of the mitochondrial membrane potential (Delta psi m). Altogether our results showed that 7-b mediated its growth inhibitory effects on Raji cells via the activation of a ROS-mediated mitochondrial pathway and cell cycle checkpoint signaling pathway which subsequently targeted p21.