Articles: function.
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Journal of neurotrauma · May 2014
Agreement on and predictors of long term psychosocial development 16 years post childhood traumatic brain injury.
Childhood traumatic brain injury (CTBI) is one of the most common causes of childhood mortality and morbidity, with psychosocial impairment being among the most debilitating persisting consequences. Child and adolescent survivors of CTBI have fewer friends and lower self-esteem with a higher risk of developing a psychiatric disorder. In most research to date, findings in the psychosocial domain have been based on parent reports, with the child or adolescent only consulted infrequently. ⋯ On the scales with poor agreement, there was no consistent contribution identified for any injury or preinjury factors. Preinjury adaptive behavior partly predicted withdrawn and overall internalizing symptoms, with a trend to also partly predict anxious/depressed and rule-breaking behavior reported by the significant other. Because young adults and significant others had poor agreement on the less-overt symptoms, these young adults may be at a higher risk of developing more-severe symptoms or disorders if it is not identified in time.
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Journal of neurotrauma · May 2014
Prehospital Heart Rate and Blood Pressure Increase the Positive Predictive Value of the Glasgow Coma Scale for High-Mortality Traumatic Brain Injury.
We hypothesized that vital signs could be used to improve the association between a trauma patient's prehospital Glasgow Coma Scale (GCS) score and his or her clinical condition. Previously, abnormally low and high blood pressures have both been associated with higher mortality for patients with traumatic brain injury (TBI). We undertook a retrospective analysis of 1384 adult prehospital trauma patients. ⋯ When the GCS was <15, ROC AUCs were significantly higher for a multi-variate regression model (GCS, SBP, and HR) versus GCS alone. In particular, patients with abnormalities in all parameters (GCS, SBP, and HR) were significantly more likely to have high-mortality TBI versus those with abnormalities in GCS alone. This could be useful for mobilizing resources (e.g., neurosurgeons and operating rooms at the receiving hospital) and might enable new prehospital management protocols where therapies are selected based on TBI mortality risk.
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Journal of neurotrauma · May 2014
Repeated Primary Blast Injury Causes Delayed Recovery, But Not Additive Disruption, in an In Vitro Blood-Brain Barrier Model.
Recent studies have demonstrated increased susceptibility to breakdown of the cerebral vasculature associated with repetitive traumatic brain injury. We hypothesized that exposure to two consecutive blast injuries would result in exacerbated damage to an in vitro model of the blood-brain barrier (BBB) compared with exposure to a single blast of the same severity. Contrary to our hypothesis, however, repeated mild or moderate primary blast delivered with a 24 or 72 h interval between injuries did not significantly exacerbate reductions in transendothelial electrical resistance (TEER) across a brain endothelial monolayer compared with sister cultures receiving a single exposure of the same intensity. ⋯ Similarly, recovery of hydraulic conductivity through the BBB was delayed by a second exposure. Extending the interinjury interval to 72 h, the effects of multiple injuries on the BBB were found to be independent given sufficient recovery time between consecutive exposures. Careful investigation of the effects of repeated blast on the BBB will help identify injury levels and a temporal window of vulnerability associated with BBB dysfunction, ultimately leading to improved strategies for protecting warfighters against repeated blast-induced disruption of the cerebral vasculature.
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Am. J. Respir. Crit. Care Med. · May 2014
Revealing the pathogenic and aging-related mechanisms of the enigmatic idiopathic pulmonary fibrosis: An integral model.
A growing body of evidence indicates that aberrant activation of alveolar epithelial cells and fibroblasts in an aging lung plays a critical role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the biopathological processes linking aging with IPF and the mechanisms responsible for the abnormal activation of epithelial cells and fibroblasts have not been elucidated. ⋯ Therefore, an unanswered question is why a current/former smoker of about 60 years of age with shorter telomeres, alveolar epithelial senescence, excessive oxidative stress, and mitochondrial dysfunction develops IPF and not COPD; in other words, what makes old lungs specifically susceptible to develop IPF? In this Perspective, we propose an integral model in which the combination of some gene variants and/or gene expression in the aging lung results in the loss of epithelial integrity and consequently in the failure of the alveoli to correctly respond to injury and to face the stress associated with mechanical stretch. Afterward, a distinctive epigenetic "reprogramming" that affects both epithelial cells and fibroblasts provokes, among others, the recapitulation of developmental pathways and the aberrant activation and miscommunication between both cell types, resulting in the exaggerated production and accumulation of extracellular matrix and the subsequent destruction of the lung architecture.