Group differences in whole-brain grey matter were compared voxel by voxel, using Brain Activation and Morphological Mapping (BAMM) software. We also conducted testing of group differences with region-of-interest (ROI) measurements of the caudate nucleus.

Results. Relative to the untreated group, those receiving antipsychotic medication for 3-4 weeks had significantly greater grey-matter Volumes in the bilateral caudate and cingulate gyri, extending to the left medial Quizartinib order frontal gyros. ROI analysis confirmed that, in treated patients, the right and left caudate nuclei were significantly larger by 10%, (p<0.039, two-tailed) and 9%, (p<0.048, two-tailed)

respectively.

Conclusions. Early striatal grey-matter enlargement may occur within the first 3-4, weeks of antipsychotic treatment. Possible reasons for putative striatal hypertrophy and its implications are discussed.”
“Tenascin-R (TN-R) is a neural specific protein and an important Neuronal Signaling inhibitor molecule involved in inhibition of axonal regeneration after spinal cord injury (SCI). Here we report on rabbit-derived TN-R polyclonal antibody, which acts as a TN-R antagonist with high titer and high specificity, promoted neurite outgrowth and sprouting of rat cortical neurons cultured on the inhibitory TN-R substrate in

vitro. When locally administered into the lesion sites of rats received spinal cord dorsal hemisection, these TN-R antibodies could significantly decrease RhoA activation

and improve functional recovery from corticospinal tract (CST) transection. Thus, passive immunotherapy with specific TN-R antagonist may represent a promising repair strategy following acute SCI. (C) 2012 Elsevier Ireland Ltd. All rights reserved.”
“DNA DNA ligase within cells is subject to damage from various sources. Organisms have evolved a number of mechanisms to repair DNA damage. The activity of repair enzymes carries its own risk, however, because the repair of two nearby lesions may lead to the breakup of DNA and result in cell death. We propose a mathematical theory of the damage and repair process in the important scenario where lesions are caused in bursts. We use this model to show that there is an optimum level of repair enzymes within cells which optimises the cell’s response to damage. This optimal level is explained as the best trade-off between fast repair and a low probability of causing double-stranded breaks. We derive our results analytically and test them using stochastic simulations, and compare our predictions with current biological knowledge. (C) 2011 Elsevier Ltd. All rights reserved.”
“Retrograde signaling is a fundamental means by which neurons communicate. The acceptance of this statement has required a revision of how we view transmission and storage of information at the synapse.