Journal of neurotrauma
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Journal of neurotrauma · Nov 2013
Brain Injury: Neuro-Inflammation, Cognitive Deficit, and Magnetic Resonance Imaging in a Model of Blast Induced Traumatic Brain Injury.
Blast wave-induced traumatic injury from terrorist explosive devices can occur at any time in either military or civilian environments. To date, little work has focused on the central nervous system response to a non-penetrating blast injury. We have evaluated the effect of a single 80-psi blast-overpressure wave in a rat model. ⋯ These data indicate an early and lasting response of brain tissue to non-penetrating blast over-pressure injury. This early inflammatory response is indicative of a mild traumatic brain injury. There is evidence of early hippocampal dysfunction.
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Journal of neurotrauma · Nov 2013
Multicenter Study Clinical Trial Observational StudyTransforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot: Multicenter Implementation of the Common Data Elements for Traumatic Brain Injury.
Traumatic brain injury (TBI) is among the leading causes of death and disability worldwide, with enormous negative social and economic impacts. The heterogeneity of TBI combined with the lack of precise outcome measures have been central to the discouraging results from clinical trials. Current approaches to the characterization of disease severity and outcome have not changed in more than three decades. ⋯ Risk factors for poor follow-up, TBI-CDE limitations, and implementation strategies are described. Having demonstrated the feasibility of implementing the TBI-CDEs through successful recruitment and multidimensional data collection, we aim to expand to additional study sites. Furthermore, interested researchers will be provided early access to the Transforming Research and Clinical Knowledge in TBI (TRACK-TBI) data set for collaborative opportunities to more precisely characterize TBI and improve the design of future clinical treatment trials. (ClinicalTrials.gov Identifier NCT01565551.).
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Journal of neurotrauma · Nov 2013
Injury-Induced Expression of Glial Androgen Receptor in the Zebra Finch Brain.
Astrogliosis occurs following injury to the zebra finch brain. To date, only estrogen synthase (aromatase) has been identified in injury-induced astrocytes. The expression of other steroidogenic enzymes or their receptors remains unknown in the avian brain. ⋯ Finches were given a single penetrating injury and brain tissue was collected 24 or 72 h later. Expression of androgen receptor was examined using immunohistochemistry and quantified using quantitative polymerase chain reaction (qPCR) analysis. Androgen receptors were localized to astrocytes versus neurons, further solidifying the role for astrocytes in neural recovery.
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Journal of neurotrauma · Nov 2013
tPA-S(481)A Prevents Impairment of Cerebrovascular Autoregulation by Endogenous tPA after Traumatic Brain Injury by Upregulating p38 MAPK and Inhibiting ET-1.
Traumatic brain injury (TBI) is associated with loss of cerebrovascular autoregulation, which leads to cerebral hypoperfusion. Mitogen activated protein kinase (MAPK) isoforms ERK, p38, and JNK and endothelin-1 (ET-1) are mediators of impaired cerebral hemodynamics after TBI. ⋯ We investigated the ability of variants that lack proteolytic activity but bind/block activation of NMDA-Rs by wt tPA (tPA-S(481)A), do not bind/block activation of NMDA-Rs but are proteolytic (tPA-A(296-299)), or neither bind/block NMDA-Rs nor are proteolytic (tPA-A(296-299)S(481)A) to prevent impairment of autoregulation after TBI and the role of MAPK and ET-1 in such effects. Results show that tPA-S(481)A given 3 h post-TBI, but not tPA-A(296-299) or tPA-A(296-299)S(481)A prevents impaired autoregulation by upregulating p38 and inhibiting ET-1, suggesting that tPA-S(481)A has a realistic therapeutic window and focuses intervention on NMDA-Rs to improve outcome.
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Journal of neurotrauma · Nov 2013
Health-Related Quality of Life in Traumatic Brain Injury: Is a Proxy Report Necessary?
Despite its importance to care, clinicians and researchers often discount patient-reported outcomes in favor of proxy reports, in persons with traumatic brain injury (TBI). The rationale relates to concerns about lack of awareness of patients regarding their functioning. However, although lack of awareness occurs in some patients with severe TBI, or in TBI involving certain lesion locations, or very soon after injury, this conclusion has been overgeneralized. ⋯ Dissatisfaction significantly related to the functional limitation in that area as judged by the patients themselves (p<0.001) or by someone who knew them well (p≤0.001). The most severely injured group reported the most dissatisfaction for 13 out of 17 areas assessed. Patients with TBI, in general, do not need a proxy to report on their behalf regarding their functional limitations or health-related quality of life.