Journal of neurotrauma
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Journal of neurotrauma · May 2007
Diffuse axonal injury in severe traumatic brain injury visualized using high-resolution diffusion tensor imaging.
Traumatic brain injury (TBI) is the most common cause of death and disability in young people. The functional outcome in patients with TBI cannot be explained by focal pathology alone, and diffuse axonal injury (DAI) is considered a major contributor to the neurocognitive deficits experienced by this group. The aim of the present study was to investigate whether diffusion tensor imaging (DTI) offers additional information as to the extent of damage not visualized with standard magnetic resonance imaging (MRI) in patients with severe TBI. ⋯ The findings of this study support the hypothesis that severe TBI is accompanied by DAI. The DTI changes were more prominent on the right side that contained the focal pathology in most of the patients and accurately reflected differences in both hemispheres. In conclusion, DTI holds great promise as a diagnostic tool to identify and quantify the degree of white matter injury in TBI patients.
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Journal of neurotrauma · May 2007
Transplantation of adult rat spinal cord stem/progenitor cells for spinal cord injury.
Stem/progenitor cells derived from the ependymal region of the spinal cord have the ability to self-renew and are multipotential for neurons and glia. These cells may have the ability to regenerate the injured mammalian spinal cord as they do in some lower vertebrates. However, the optimal conditions for transplantation and the fate of transplanted cells are not fully known. ⋯ A significant increase in cell survival was also seen in rats receiving subacute transplants at 9 days after injury. Transplanted cells differentiated primarily into astrocytes (31.2%) and oligodendrocytes (50.3%), and a small number of neurons (1%). No improvement was seen in the Basso, Beattie and Bresnahan (BBB) locomotor rating scale after acute transplantation as compared with injury only, although surviving transplanted cells were identified that had migrated across the injury site from the rostral and caudal injection sites.
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Journal of neurotrauma · May 2007
Proteomic identification of oxidized mitochondrial proteins following experimental traumatic brain injury.
Experimental traumatic brain injury (TBI) results in a significant loss of cortical tissue at the site of injury, and in the ensuing hours and days a secondary injury exacerbates this primary injury, resulting in significant neurological dysfunction. The mechanism of the secondary injury is not well understood, but evidence implicates a critical role for mitochondria in this cascade. This mitochondrial dysfunction is believed to involve excitotoxicity, disruption of Ca(2+) homeostasis, production of reactive oxygen species (ROS), ATP depletion, oxidative damage of mitochondrial proteins, and an overall breakdown of mitochondrial bioenergetics. ⋯ In addition, we have also shown that, following TBI, there is a reduction in the activities of pyruvate dehydrogenase (PDH), complex I, and complex IV. These findings demonstrate that, following TBI, several proteins involved in mitochondrial bioenergetics are highly oxidatively modified, which may possibly underlie the massive breakdown of mitochondrial energetics and eventual cell death known to occur in this model. The identification of these proteins provides new insights into the mechanisms that take place following TBI and may provide avenues for possible therapeutic interventions after TBI.