Journal of neurotrauma
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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
Risk factors for posttraumatic massive cerebral infarction secondary to space-occupying epidural haematoma.
Post-traumatic massive cerebral infarction (MCI) is a fatal complication of concurrent epidural hematoma (EDH) and brain herniation that commonly requires an aggressive decompressive craniectomy. The risk factors and surgical indications of MCI have not been fully elucidated. In this retrospective study, post-traumatic MCI was diagnosed in 32 of 176 patients. ⋯ Incidence of post-traumatic MCI increased from 16.4% in those having any two of the six risk factors to 47.7% in those having any three or more of the six risk factors (p<0.001). Patients with concurrent EDH and brain herniation exhibited an increased risk for post-traumatic MCI with the accumulation of several critical clinical factors. Early decompressive craniectomy based on accurate risk estimation is recommended in efforts to improve patient functional outcomes.
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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
Eotaxin-3 activates Smad through the TGF-β1 pathway in chronic subdural hematoma outer membranes.
Chronic subdural hematoma (CSDH) is considered to be an inflammatory disease. Eosinophils are frequently expressed in the outer membrane of CSDH and are major sources of transforming growth factor beta (TGF-β). The mothers against decapentaplegic (Smad)-signaling pathway, which is activated by TGF-β, has been shown to be involved with fibrosis. ⋯ Smad3 was shown to be present in fibroblasts. These findings indicate that eotaxin-3 is expressed in CSDH fluid, inducing eosinophils into the outer membrane and resulting in elevation of TGF-β with the Smad pathway activated by TGF-β. These data suggest a potential mechanism for CSDH formation and growth.
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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.