Journal of neurotrauma
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Journal of neurotrauma · Oct 2007
Omega-3 fatty acids supplementation restores mechanisms that maintain brain homeostasis in traumatic brain injury.
Traumatic brain injury (TBI) produces a state of vulnerability that reduces the brain capacity to cope with secondary insults. The silent information regulator 2 (Sir2) has been implicated with maintaining genomic stability and cellular homeostasis under challenging situation. Here we explore the possibility that the action of Sir2alpha (mammalian Sir2) in the brain can extend to serve neuronal plasticity. ⋯ Furthermore, we found that the correlation between Sir2alpha and AMPK or p-AMPK was disrupted by TBI, but restored by omega-3 fatty acids supplements. Our results suggest that TBI may compromise neuronal protective mechanisms by involving the action of Sir2alpha. In addition, results show the capacity of omega-3 fatty acids to counteract some of the effects of TBI by normalizing levels of molecular systems associated with energy homeostasis.
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Journal of neurotrauma · Oct 2007
Effects of erythropoietin on posttraumatic place learning in fimbria-fornix transected rats after a 30-day postoperative pause.
Human recombinant erythropoietin (EPO) has been shown to exert neuroprotective effects following both vascular and mechanical brain injury. Previously, we showed that behavioral symptoms associated with mechanical lesions of the hippocampus are nearly abolished due to EPO treatment. In these studies, the EPO administration took place simultaneously with the infliction of brain injury and the rehabilitation training started 6-7 days postoperatively. ⋯ Subsequently, the animals were given behavioral challenges during which the cue constellation in the room was changed. The challenges revealed that, although the EPO-treated lesion group had achieved the same level of task proficiency as the control group, the cognitive mechanisms mediating the task performance in the EPO-treated lesion group (as well as in the saline-treated lesion group) were dissimilar from those mediating the task in the control group. Both the EPO-treated and the saline-treated lesion group demonstrated an increased dependency on the original cue configuration.
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Journal of neurotrauma · Oct 2007
Effect of penetrating brain injury on aquaporin-4 expression using a rat model.
Cerebral edema (CE) is a frequent and potentially lethal consequence of various neurotraumas, including penetrating brain injury (PBI). Aquaporin-4 (AQP4) water channel is predominantly expressed by astrocytes and plays an important role in regulating water balance in the normal and injured brain. Using a rat model of PBI, we show that AQP4 immunoreactivity was substantially increased in the peri-injury area at both 24 and 72 h after PBI. ⋯ Western analysis confirmed the increase in AQP4 immunoreactivity observed in the injured tissue. The apparent increase in AQP4 immunoreactivity was likely due to de novo AQP4 protein synthesis, as most of the increased AQP4 immunoreactivity was found in the soluble (cytosolic) fraction. Our results demonstrate dynamic spatial and temporal changes in AQP4 expression that contribute to the molecular pathophysiology of PBI.
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Journal of neurotrauma · Oct 2007
Diffusion-weighted magnetic resonance imaging improves outcome prediction in adult traumatic brain injury.
In patients with traumatic brain injury (TBI), diffuse axonal injury (DAI) accounts for a significant amount of parenchymal injury. Diffusion weighted magnetic resonance imaging (DWI) is known to be sensitive for detecting visible DAI lesions. We focused on detection of non-visible, quantifiable diffusion changes in specific normal-appearing brain regions, using apparent diffusion coefficient (ADC) maps. ⋯ Patients with more severe injury (i.e., GCS 3-8) had significantly different mean ADC values than control patients (p
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Journal of neurotrauma · Oct 2007
Diffuse brain injury in the immature rat: evidence for an age-at-injury effect on cognitive function and histopathologic damage.
Diffuse axonal injury is a significant component of the pathology of moderate-severe pediatric traumatic brain injury in children less than 4 years of age, and is associated with poor cognitive outcome. However, cognitive deficits or gross histopathologic abnormalities are typically not observed following moderate-severe diffuse brain injury in the immature (17-day-old) rat. In order to test whether the age of the immature animal may influence post-traumatic outcome, non-contusive brain trauma was induced in post-natal day (PND) 11 or 17 rats. ⋯ Quantitative analysis revealed a time-dependent increase in tissue loss in the injured hemisphere (7-10%) in the younger animals, and a modest extent of tissue loss in the older animals (3-4%). Traumatic axonal injury was observed to similar extents in the white matter and thalamus below the impact site in both brain-injured PND11 and 17 rats. These data demonstrate that non-contusive (diffuse) brain injury of moderate severity in the immature rat is associated with chronic cognitive deficits and long-term histopathologic alterations and suggest that the age-at-injury is an important parameter of behavioral and pathologic outcome following closed head injury in the immature age group.