Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
The serum phosphorylated neurofilament heavy subunit as a predictive marker for outcome in adult patients after traumatic brain injury.
The serum phosphorylated neurofilament heavy subunit (pNF-H) is a nervous system-specific protein that is released from damaged neural tissue after traumatic brain injury (TBI). The aim of this study was to elucidate the usefulness of serum pNF-H as a predictive marker for the outcome of patients after TBI. Patients with TBI (Glasgow Coma Scale score of 13 or less on admission) were included. ⋯ The optimal cutoff value was 240 pg/mL, and the area under the curve in the receiver operating characteristic analysis was 0.930. The serum pNF-H value at 72 h after injury was correlated with an unfavorable outcome (vegetative state or death) at 6 months (p < 0.01) with a cutoff value of 80 pg/mL. Collectively, the results of this study indicate that the serum pNF-H value is a useful predictive marker for patient outcome after TBI.
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Journal of neurotrauma · Oct 2016
Randomized Controlled TrialCortical Thickness in Mild Traumatic Brain Injury.
Magnetic resonance imaging data were acquired at ∼24 h and ∼3 months post-injury on mild traumatic brain injury (mTBI; n = 75) and orthopedic injury (n = 60) cohorts. The mTBI subjects were randomly assigned to a treatment group with atorvastatin or a non-treatment mTBI group. The treatment group was further divided into drug and placebo subgroups. ⋯ Further analysis revealed significant cortical thinning only in the non-treatment group relative to the control group. In the follow-up, small regions with significant but subtle cortical thinning and thickening were seen in the frontal, temporal, and parietal lobes in the left hemisphere in the non-treatment group only. Our results indicate that cortical thickness could serve as a useful measure in identifying subtle changes in mTBI patients.
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Journal of neurotrauma · Oct 2016
Probenecid and N-acetylcysteine Prevent Loss of Intracellular Glutathione and Inhibit Neuronal Death after Mechanical Stretch Injury In Vitro.
Probenecid and N-acetylcysteine (NAC) can preserve intracellular levels of the vital antioxidant glutathione (GSH) via two distinct biochemical pathways. Probenecid inhibits transporter-mediated GSH efflux and NAC serves as a cysteine donor for GSH synthesis. We hypothesized that probenecid and NAC alone would maintain intracellular GSH concentrations and inhibit neuronal death after traumatic stretch injury, and that the drugs in combination would produce additive effects. ⋯ Interestingly, caspase 3 activity 24 h after mechanical trauma was more prominent in XX-neurons, and treatment effects (probenecid, NAC, and Pro-NAC) were observed in XX- but not XY-neurons; however, XY-neurons were ultimately more vulnerable to mechanical stretch-induced injury than their XX counterparts, as was evidenced by more neuronal death detected by LDH release and PI uptake. In addition, after stretch injury in HT22 hippocampal cells, both NAC and probenecid were highly effective at reducing oxidative stress detected by dichlorofluorescein fluorescence. These in vitro data support further testing of this drug combination in models of traumatic neuronal injury in vivo.
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Journal of neurotrauma · Oct 2016
Three months follow-up of rat mild traumatic brain injury: a combined [18F]FDG and [11C]PK11195 PET study.
Mild traumatic brain injury (mTBI) is the most common cause of head trauma. The time course of functional pathology is not well defined, however. The purpose of this study was to evaluate the consequences of mTBI in rats over a period of 3 months by determining the presence of neuroinflammation ([11C]PK11195) and changes in brain metabolism ([18F]FDG) with positron emission tomography (PET) imaging. ⋯ Alterations in glucose metabolism were detected over the 3 month period, with increased uptake in the medulla (p < 0.04, d ≥ 1.2), and decreased uptake in the globus pallidus, striatum, and thalamus (p < 0.04, d ≤ 1.2). Similar findings were observed in the voxel-based analysis (p < 0.05 at corrected cluster level). As a consequence of the mTBI, and in the absence of apparent behavioral alterations, relative brain glucose metabolism was found altered in several brain regions, which mostly correspond with those presenting neuroinflammation in the subacute stage.
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Journal of neurotrauma · Oct 2016
Circulating MicroRNAs as Potential Biomarkers for Traumatic Brain Injury-Induced Hypopituitarism.
Traumatic brain injury (TBI), a worldwide public health problem, has recently been recognized as a common cause of pituitary dysfunction. Circulating microRNAs (miRNAs) present in the sera are characteristically altered in many pathological conditions and have been used as diagnostic markers for specific diseases. It is with this goal that we planned to study miRNA expression in patients with TBI-induced hypopituitarism. ⋯ Statistical analyses showed that miRNA-126-3p (miR-126-3p) and miRNA-3610 (miR-3610) were detected in the sera of patients who developed hypopituitarism on the 1st, 7th, and 28th days, and in the 5th year following TBI. In addition, miRNA-3907 showed statistically significant and constant dynamic changes on the 1st, 7th, and 28th days, and in the 5th year in the patients with TBI. Our results indicated that altered expression of miR-126-3p and miR-3610 may play an important role in the development of TBI-induced hypopituitarism.