Journal of neurotrauma

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• Journal of neurotrauma · Aug 2009

  Conditional knockout of brain-derived neurotrophic factor in the hippocampus increases death of adult-born immature neurons following traumatic brain injury.

  It has been reported that the hippocampus is particularly vulnerable to traumatic brain injury (TBI), the consequence of which results in hippocampal-dependent cognitive impairment. In the previous study we found that adult-born immature neurons in the hippocampal dentate gyrus are the most vulnerable cell type to moderate TBI insult. ⋯ The results showed that the amount of adult-born immature neuron death in the hippocampal dentate gyrus significantly increased in the BDNF conditional knockout mice. This result suggests that BDNF is involved in regulating the survival of adult-born immature neurons in the hippocampus following TBI, and potentially might be a useful target for preventing the adult-born immature neurons from death following TBI.

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• Journal of neurotrauma · Aug 2009

  P43/pro-EMAPII: a potential biomarker for discriminating traumatic versus ischemic brain injury.

  To gain additional insights into the pathogenic cellular and molecular mechanisms underlying different types of brain injury (e.g., trauma versus ischemia), recently attention has focused on the discovery and study of protein biomarkers. In previous studies, using a high-throughput immunoblotting (HTPI) technique, we reported changes in 29 out of 998 proteins following acute injuries to the rat brain (penetrating traumatic versus focal ischemic). Importantly, we discovered that one protein, endothelial monocyte-activating polypeptide II precursor (p43/pro-EMAPII), was differentially expressed between these two types of brain injury. ⋯ Changes in protein expression were assessed by Western blot analysis and immunohistochemistry. Our results indicated that p43/pro-EMAPII was significantly increased in brain tissues, CSF, and plasma following PBBI, but decreased after MCAo injury compared to their respective sham control samples. This differential expression of p43/pro-EMAPII may be a useful injury-specific biomarker associated with the underlying pathologies of traumatic versus ischemic brain injury, and provide valuable information for directing injury-specific therapeutics.

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• Journal of neurotrauma · Aug 2009

  Increased cerebral uptake of [18F]fluoro-deoxyglucose but not [1-14C]glucose early following traumatic brain injury in rats.

  Following experimental and clinical traumatic brain injury (TBI), the local cerebral metabolic rate of glucose (lCMR(Glc)) is commonly estimated using the 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG) method. The adequate estimation of lCMR(Glc) using FDG requires a correction factor, the lumped constant (LC), to convert FDG net uptake into lCMR(Glc). The LC, and thus lCMR(Glc) calculations, require a steady-state that may be disrupted following TBI. ⋯ At 12 h following FPI, the ipsilateral FDG and [1-(14)C]glucose uptake were decreased in the cortex and hippocampus, and the ipsilateral cortical ATP concentration was decreased in comparison to sham-injured controls (p < 0.05). Under the present experimental conditions, the rate of cerebral uptake of FDG and of [1-(14)C]glucose differed, and indicated that following TBI, regional changes in the LC may occur in the immediate, but not in the late, post-injury phase. These results should be considered when interpreting results obtained using FDG for the estimation of lCMR(Glc) early following experimental TBI.

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• Journal of neurotrauma · Aug 2009

  Randomized Controlled Trial

  Prostacyclin treatment in severe traumatic brain injury: a microdialysis and outcome study.

  Prostacyclin (PGI(2)) is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation. In trauma the balance between PGI(2) and thromboxane A(2) (TXA(2)) is shifted towards TXA(2). Externally provided PGI(2) would, from a theoretical and experimental point of view, improve the microcirculation in injured brain tissue. This study is a prospective consecutive double-blinded randomized study on the effect of PGI(2) versus placebo in severe traumatic brain injury (sTBI). All patients with sTBI were eligible. ⋯ verified sTBI, Glasgow Coma Score (GCS) at intubation and sedation of or=10 mm Hg, and arrival within 24 h of trauma. All subjects received an intracranial pressure (ICP) measuring device, bilateral intracerebral microdialysis catheters, and a microdialysis catheter in the abdominal subcutaneous adipose tissue. Subjects were treated according to an ICP-targeted therapy based on the Lund concept. 48 patients (mean age of 35.5 years and a median GCS of 6 [3-8]) were included. We found no significant effect of prostacyclin (epoprostenol, Flolan) on either the lactate-pyruvate ratio (L/P) at 24 h or the brain glucose levels. There was no significant difference in clinical outcome between the two groups. The median Glasgow Outcome Score (GOS) at 3 months was 4, and mortality was 12.5%. The favorable outcome (GOS 4-5) was 52%. The initial L/P did not prognosticate for outcome. Thus our results indicate that there is no effect of PGI(2) at a dose of 0.5 ng/kg/min on brain L/P, brain glucose levels, or outcome at 3 months.

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• Journal of neurotrauma · Aug 2009

  Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation and cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.

  Preliminary evidence suggests local brain tissue oxygenation (PbtO(2)) values of or=20 mm Hg to avoid hypoxia. This study tested the impact of a short (2 h) trial of normobaric hyperoxia on measures of oxidative stress. ⋯ Oxidative stress markers, antioxidant reserve defenses, and ICP, MAP, and CPP did not significantly change for any time period. These preliminary findings suggest that brief periods of normobaric hyperoxia do not produce oxidative stress and/or change antioxidant reserves in CSF. Additional studies are required to examine extended periods of normobaric hyperoxia in a larger sample.

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