The authors discuss potential differences between neural mechanisms of sexual abuse-related PTSD and war-related PTSD. (c) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Object: The aim of this study is to explore the changes of inter-hemispheric functional connectivity in patients with

unilateral brachial plexus injury.

Methods: Nine patients with five Mocetinostat manufacturer roots of unilateral brachial plexus avulsion injury and 11 healthy controls were recruited in this study. Resting-state functional connectivity magnetic resonance image was used to study the differences of inter-hemispheric functional connectivity between patients and healthy controls. Four areas were defined as regions of interest (ROI): the two primary motor areas (M1 areas) and two supplementary motor areas (SMAs) in the two hemispheres activated when the healthy

controls performed unilateral hand grasping movement of the two hands, respectively. Functional connectivity maps were generated by correlating the regional time course of each ROI with that of every voxel in the whole brain. Then, functional connectivity was calculated by correlating the functional magnetic resonance image signal time courses of every two ROIs.

Results: Resting-state inter-hemispheric functional connectivity of the primary motor areas was reduced following brachial plexus avulsion injury. The selleck inhibitor correlation coefficients of the SMAs showed no difference between the brachial plexus patients and healthy volunteers.

Conclusions: Our results indicate that brachial plexus injury decreases resting-state inter-hemispheric functional connectivity of the two primary motor areas. These results provide new insight into functional reorganization of the cerebral cortex after brachial plexus GPX6 injury. (c) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The activation of the interferon (IFN) system, which is triggered largely by the recognition of viral nucleic

acids, is one of the most important host defense reactions against viral infections. Although influenza A and B viruses, which both have segmented negative-strand RNA genomes, share major structural similarities, they have evolutionarily diverged, with total genetic incompatibility. Here we compare antiviral-inducing mechanisms during infections with type A and B influenza viruses in human dendritic cells. We observed that IFN responses are induced significantly faster in cells infected with influenza B virus than in cells infected with type A influenza virus and that the early induction of antiviral gene expression is mediated by the activation of the transcription factor IFN regulatory factor 3 (IRF3). We further demonstrate that influenza A virus infection activates IFN responses only after viral RNA (vRNA) synthesis, whereas influenza B virus induces IFN responses even if its infectivity is destroyed by UV treatment.