Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
Minimal traumatic brain injury in mice - PAR-1 and thrombin related changes.
Minimal traumatic brain injury (mTBI) is partially defined by the existence of retrograde amnesia and is associated with microscopic bleeds containing activated coagulation factors. In a previous study, we have found that mTBI immediately releases thrombin-like activity in the brain, which induces amnesia by activating protease-activated receptor 1 (PAR-1) and blocking long-term potentiation (LTP). In the present study, we assessed the effects of mTBI on thrombin and PAR-1 levels in the brain using the same model. ⋯ Interestingly, the late elevation in thrombin-like activity was also associated with elevation of the major central nervous system thrombin inhibitor, protease nexin-1, 72 h post-mTBI (10%; p < 0.005). When thrombin was injected into brain ventricles, an increased sensitivity to seizure-like activity was detected at 72 h post-mTBI. The results are compatible with astrocyte activation post-mTBI resulting in increased thrombin secretion, PAR-1 expression, and seizure sensitivity.
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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.
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Journal of neurotrauma · Oct 2016
Underlying Cortical Dysplasia as Risk Factor for Traumatic Epilepsy: An Animal Study.
Traumatic brain injury (TBI) is a significant risk factor for development of epilepsy in humans. It is unclear, however, why some persons are at an increased risk of becoming epileptic, while others recover from the TBI seizure-free. We previously showed that the presence of a proepileptic pathology increases the risk of epilepsy in an animal model of cortical dysplasia (CD) after a secondary insult, which we described as the "second hit". ⋯ All of the CD animals exhibited interictal spiking after TBI, while only a portion of nondysplastic animals produced spikes. These results suggest that the presence of a proepileptic pathology may increase the risk for the development of epilepsy after TBI. Diagnosis and treatment of TBI may depend on underlying pathologies contributing to epilepsy after a brain injury.
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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
Primary blast exposure increases hippocampal vulnerability to subsequent exposure reducing long-term potentiation.
Up to 80% of injuries sustained by U. S. soldiers in Operation Enduring Freedom and Operation Iraqi Freedom were the result of blast exposure from improvised explosive devices. Some soldiers experience multiple blasts while on duty, and it has been suggested that symptoms of repetitive blast are similar to those that follow multiple non-blast concussions, such as sport-related concussion. ⋯ The repeated blast exposure with a 24 h interval increased microglia staining and activation significantly but did not significantly increase cell death or damage axons, dendrites, or principal cell layers. Lack of overt structural damage and change in basal stimulated neuron response suggest that injury from repetitive primary blast exposure may specifically affect long-term potentiation. Our studies suggest repetitive primary blasts can exacerbate injury dependent on the injury severity and interval between exposures.