Journal of neurotrauma
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Journal of neurotrauma · Aug 2014
Subtypes of Post-Traumatic Epilepsy: Clinical, Electrophysiologic, and Imaging Features.
Post-traumatic epilepsy (PTE) is a consequence of traumatic brain injury (TBI), occurring in 10-25% of patients with moderate to severe injuries. The development of animal models for testing antiepileptogenic therapies and validation of biomarkers to follow epileptogenesis in humans necessitates sophisticated understanding of the subtypes of PTE, which is the objective of this study. In this study, retrospective review was performed of patients with moderate to severe TBI with subsequent development of medically refractory epilepsy referred for video-electroencephalography (EEG) monitoring at a single center over a 10-year period. ⋯ At a mean follow-up of 2.5 years, Engel Class I outcomes were seen in 69% of those with TLE and 33% of those with FLE. Our findings suggest PTE is a heterogeneous condition, and careful evaluation with video-EEG monitoring and high resolution MRI can identify distinct syndromes. These results have implications for the design of clinical trials of antiepileptogenic therapies for PTE.
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Journal of neurotrauma · Aug 2014
Hemorrhagic shock shifts the serum cytokine profile from pro-to anti-inflammatory after experimental traumatic brain injury in mice.
Secondary insults, such as hemorrhagic shock (HS), worsen outcome from traumatic brain injury (TBI). Both TBI and HS modulate levels of inflammatory mediators. We evaluated the addition of HS on the inflammatory response to TBI. ⋯ There were no significant differences between levels after CCI alone and CCI+HS in any mediator. Addition of HS to experimental TBI led to a shift toward an anti-inflammatory serum profile--specifically, a marked increase in IL-10 levels. The brain cytokine and chemokine profile after TBI was minimally affected by the addition of HS.
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Journal of neurotrauma · Aug 2014
Neurotherapeutic Effect of Cord Blood Derived CD45+ Hematopoietic Cells in Mice after Traumatic Brain Injury.
Treatment of traumatic brain injury (TBI) is still an unmet need. Cell therapy by human umbilical cord blood (HUCB) has shown promising results in animal models of TBI and is under evaluation in clinical trials. HUCB contains different cell populations but to date, only mesenchymal stem cells have been evaluated for therapy of TBI. ⋯ At the site of brain injury, 1.5-2 h after transplantation, HUCB-derived cells were identified by near infrared scanning and immunohistochemistry using anti-human-CD45 and anti-human-nuclei antibodies. Nerve growth factor and vascular endothelial growth factor levels were differentially expressed in both ipsilateral and contralateral brain hemispheres, thirty-five days after CHI, measured by enzyme-linked immunosorbent assay. These findings indicate the neurotherapeutic potential of HUCB-derived CD45(+) cell population in a mouse model of TBI and propose their use in the clinical setting of human TBI.
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Journal of neurotrauma · Aug 2014
Engineering In Situ Crosslinkable, Injectable, and Neurocompatible Hydrogels.
Physical injuries of the central nervous system (CNS) are prevalent and very severe because the CNS has limited capacity to replace neuronal loss from the injury. A growing body of evidence has suggested that exogenous cell transplantation is one promising strategy to promote CNS regeneration. Direct injection of neural stem cells (NSCs) to the lesion site, however, may not be an optimal therapeutic strategy because of poor viability and functionality of transplanted cells resulting from the local hostile tissue environment. ⋯ By controlling the cross-linking density via varying the amount of cross-linker (PEGDA) and the concentration of the adhesive component gelatin, an optimal microenvironment for the survival, proliferation, and neuronal differentiation of NSCs was created in vitro. The soft hydrogel of less than 10 Pa with Gtn-SH content (50%) is one of the optimal conditions to support NSCs growth and neuronal differentiation in vitro. The optimized hydrogel holds great potential as a carrier of stem cells to treat CNS injuries and diseases in which cell therapies may be essential.
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Journal of neurotrauma · Aug 2014
ReviewALTERATION IN SYNAPTIC JUNCTION PROTEINS FOLLOWING TRAUMATIC BRAIN INJURY.
Extensive research and scientific efforts have been focused on the elucidation of the pathobiology of cellular and axonal damage following traumatic brain injury (TBI). Conversely, few studies have specifically addressed the issue of synaptic dysfunction. ⋯ A Synapse Protein Database on synapse ontology identified 109 domains implicated in synaptic activities and over 5000 proteins, but few of these demonstrated to play a role in the synaptic dysfunction after TBI. These proteins are involved in neuroplasticity and neuromodulation and, most importantly, may be used as novel neuronal markers of TBI for specific intervention.