Data on diagnoses, symptom severity, and affective information processing using a facial recognition task were collected from 66 participants, male and female between selleck compound ages 18 and 54 years, grouped by major depressive disorder (N=37) or healthy non-psychiatric (N=29) status. Findings from MANCOVAs revealed that major depression was associated with a significantly longer reaction time to sad facial expressions compared with healthy status. Also, depressed participants demonstrated a negative bias towards interpreting neutral facial

expressions as sad significantly more often than healthy participants. In turn, healthy participants interpreted neutral Citarinostat cell line faces as happy significantly more often than depressed participants. No group differences were observed for facial expression recognition

and intensity categorization: The observed effects suggest that depression has significant effects on the perception of the intensity of negative affective stimuli, delayed speed of processing sad affective information, and biases towards interpreting neutral faces as sad. (c) 2007 Elsevier Ireland Ltd. All rights reserved.”
“BACKGROUND: Traumatic brain injury (TBI) remains a devastating condition for which extracranial protection traditionally has been in the form of helmets, which largely fail to protect against intracranial injury.

OBJECTIVE: To determine whether the pathological outcome after traumatic brain injury can be improved via slosh mitigation by internal jugular vein (IJV) compression.

METHODS: Two groups of 10 adult male Sprague-Dawley rats were subjected to impact-acceleration traumatic brain injury. One group underwent IJV compression via application of a collar before injury; the second group did not. Intracranial pressure and intraocular pressure were measured before and after IJV compression Mephenoxalone to assess collar performance. All rats were killed after a 7-day recovery period, and brainstem white matter tracts underwent fluorescent

immunohistochemical processing and labeling of beta-amyloid precursor protein, a marker of axonal injury. Digital imaging and statistical analyses were used to determine whether IJV compression resulted in a diminished number of injured axons.

RESULTS: Compression of the IJV resulted in an immediate 30% increase in intraocular and intracranial pressures. Most notably, IJV compression resulted in. 80% reduction in the number of amyloid precursor protein-positive axons as indicated by immunohistochemical analysis.

CONCLUSION: Using a standard acceleration-deceleration laboratory model of mild traumatic brain injury, we have shown successful prevention of axonal injury after IJV compression as indicated by immunohistochemical staining of amyloid precursor protein.