Journal of neurotrauma
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Journal of neurotrauma · Jul 2010
Pyridoxine administration improves behavioral and anatomical outcome after unilateral contusion injury in the rat.
The purpose of this project was to evaluate the preclinical efficacy of pyridoxine, or vitamin B(6). Rats received a 3.0 mm unilateral controlled cortical impact (CCI) injury of the sensorimotor cortex or sham surgery. Treatment with vitamin B(6) (600 or 300 mg/kg IP) or vehicle was administered at 30 min and 24 h post-CCI. ⋯ Finally, the 600-mg/kg dose resulted in significant cortical sparing compared to the vehicle-treated group. In general, the effects of vitamin B(6) on recovery of function were dose-dependent, with the 600-mg/kg dose consistently showing greater recovery than the 300-mg/kg dose. More experimental analyses are warranted to evaluate the potential preclinical efficacy and mechanistic action of vitamin B(6).
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Journal of neurotrauma · Jul 2010
Multicenter StudyQuality of Life after Brain Injury (QOLIBRI): scale validity and correlates of quality of life.
The QOLIBRI (Quality of Life after Brain Injury) is a novel health-related quality-of-life (HRQoL) instrument specifically developed for traumatic brain injury (TBI). It provides a profile of HRQoL in six domains together with an overall score. Scale validity and factors associated with HRQoL were investigated in a multi-center international study. ⋯ The main correlates of the total QOLIBRI score were emotional state (HADS depression and anxiety), functional status (amount of help needed and outcome on the GOSE), and comorbid health conditions. Together these five variables accounted for 58% of the variance in total QOLIBRI scores. The QOLIBRI is the first tool developed to assess disease-specific HRQoL in brain injury, and it contains novel information not given by other currently available assessments.
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Journal of neurotrauma · Jul 2010
Upregulation of EphA4 on astrocytes potentially mediates astrocytic gliosis after cortical lesion in the marmoset monkey.
Glial scar formation occurs in response to brain injury in mammalian models and inhibits axonal growth. Identification of molecules that may mediate reactivity of astrocytes has become a leading therapeutic goal in the field of neurotrauma. In adult rodent brain and spinal cord, many of the Eph receptors and their ephrin ligands have been demonstrated to be upregulated on reactive astrocytes at the injury site; however, little is known about the expression of these molecules in nonhuman primate injury models. ⋯ This astrocyte reactivity was also associated with neuronal death in the area adjacent to the lesion site. EphA4 activation induced by clustered ephrin A5-Fc-mediated astrocyte proliferation and glial fibrillary acidic protein expression in vitro, as demonstrated by closure of scratched wound and MTT assays, occurs via two potential signaling pathways, the mitogen-activated protein kinase and Rho pathways. These results in a nonhuman primate model highlight the importance of developing pharmacotherapeutic approaches to block these molecules following brain injury.
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Journal of neurotrauma · Jul 2010
αII-spectrin breakdown products (SBDPs): diagnosis and outcome in severe traumatic brain injury patients.
In this study we assessed the clinical utility of quantitative assessments of alphaII-spectrin breakdown products (SBDP145 produced by calpain, and SBDP120 produced by caspase-3) in cerebrospinal fluid (CSF) as markers of brain damage and outcome after severe traumatic brain injury (TBI). We analyzed 40 adult patients with severe TBI (Glasgow Coma Scale [GCS] score
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Journal of neurotrauma · Jul 2010
Genetic deletion and pharmacological inhibition of Nogo-66 receptor impairs cognitive outcome after traumatic brain injury in mice.
Functional recovery is markedly restricted following traumatic brain injury (TBI), partly due to myelin-associated inhibitors including Nogo-A, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp), that all bind to the Nogo-66 receptor-1 (NgR1). In previous studies, pharmacological neutralization of both Nogo-A and MAG improved outcome following TBI in the rat, and neutralization of NgR1 improved outcome following spinal cord injury and stroke in rodent models. However, the behavioral and histological effects of NgR1 inhibition have not previously been evaluated in TBI. ⋯ In the sNgR1 study, we evaluated hippocampal mossy fiber sprouting using the Timm stain and found it to be increased at 5 weeks following TBI. Neutralization of NgR1 significantly increased mossy fiber sprouting in sham-injured animals, but not in brain-injured animals. Our data suggest a complex role for myelin-associated inhibitors in the behavioral recovery process following TBI, and urge caution when inhibiting NgR1 in the early post-injury period.