Journal of neurotrauma
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Journal of neurotrauma · Apr 2017
Retracted PublicationSex And Age Differences In Epinephrine Mechanisms And Outcomes After Brain Injury.
Traumatic brain injury (TBI) is the leading cause of injury-related death in children, with boys and children <4 years of age having particularly poor outcomes. Cerebral autoregulation is often impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure can be normalized by use of vasoactive agents. ⋯ Phosphorylated JNK MAPK was quantified by enzyme-linked immunosorbent assay (ELISA). Results show that EPI preserves autoregulation, prevents histopathology, and blocks phosphorylated JNK upregulation in newborn males and females and juvenile females but not juvenile males after TBI. These data indicate that EPI preserves cerebral autoregulation and limits histopathology after TBI through blockade of JNK in an age- and sex-dependent manner.
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Journal of neurotrauma · Apr 2017
Observational StudyVitamin D deficiency in traumatic brain injury and its relationship with severity of injury and quality of life: a prospective, observational study.
This single-center prospective observational study aims to describe the prevalence of vitamin D deficiency (VDD) in the traumatic brain injury (TBI) population and identify any relationship between vitamin D and severity of head injury or quality of life. One hundred twenty-four TBI patients had serum vitamin D (25-OHD) levels measured at the local post-TBI endocrine screening clinic over 20 months. Quality of Life after Brain Injury questionnaires were completed by the patient concurrently. ⋯ This is the first study to identify a significant relationship between vitamin D levels and severity of head injury. Clinicians should actively screen for and treat VDD in head-injured patients to reduce the risk of further morbidity, such as osteomalacia and cardiovascular disease. Future research should establish the natural history of vitamin D levels following TBI to identify at which stage VDD develops and whether vitamin D replacement could have a beneficial effect on recovery and quality of life.
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Journal of neurotrauma · Apr 2017
REGULATION OF MITOCHONDRIAL FUNCTION AND GLUTAMATERGIC SYSTEM ARE THE TARGET OF GUANOSINE EFFECT IN TRAUMATIC BRAIN INJURY.
Traumatic brain injury (TBI) is a highly complex multi-factorial disorder. Experimental trauma involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death. Mitochondrial dysfunction and glutamatergic excitotoxicity are the hallmark mechanisms of damage. ⋯ Our results showed that mitochondrial dysfunction contributed to decreased glutamate uptake and levels of glial glutamate transporters (glutamate transporter 1 and glutamate aspartate transporter), which leads to excitotoxicity. GUO treatment ameliorated mitochondrial damage and glutamatergic dyshomeostasis. Thus, GUO might provide a new efficacious strategy for the treatment acute physiological alterations secondary to TBI.
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Journal of neurotrauma · Apr 2017
SYNAPTIC MITOCHONDRIA SUSTAIN MORE DAMAGE THAN NON-SYNAPTIC MITOCHONDRIA FOLLOWING TRAUMATIC BRAIN INJURY AND ARE PROTECTED BY CYCLOSPORINE A.
Currently, there are no Food and Drug Administration (FDA)-approved pharmacotherapies for the treatment of those with traumatic brain injury (TBI). As central mediators of the secondary injury cascade, mitochondria are promising therapeutic targets for prevention of cellular death and dysfunction after TBI. One of the most promising and extensively studied mitochondrial targeted TBI therapies is inhibition of the mitochondrial permeability transition pore (mPTP) by the FDA-approved drug, cyclosporine A (CsA). ⋯ This is the first study to examine the effects of CsA on isolated synaptic and non-synaptic mitochondria after experimental TBI. We conclude that synaptic mitochondria sustain more damage than non-synaptic mitochondria 24 h after severe controlled cortical impact injury (CCI), and that intraperitoneal administration of CsA (20 mg/kg) 15 min after injury improves synaptic and non-synaptic respiration, with a significant improvement being seen in the more severely impaired synaptic population. As such, CsA remains a promising neuroprotective candidate for the treatment of those with TBI.
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Journal of neurotrauma · Apr 2017
Structural and Functional Integrity of the Intraparietal Sulcus in Moderate and Severe Traumatic Brain Injury.
Severe and moderate traumatic brain injury (sTBI) often results in long-term cognitive deficits such as reduced processing speed and attention. The intraparietal sulcus (IPS) is a neocortical structure that plays a crucial role in the deeply interrelated processes of multi-sensory processing and top down attention. Therefore, we hypothesized that disruptions in the functional and structural connections of the IPS may play a role in the development of such deficits. ⋯ The patients also showed reduced structural integrity of the superior longitudinal fasciculus (SLF), a key white matter tract connecting the IPS to anterior frontal areas, as measured by reduced mean kurtosis (MK) and fractional anisotropy (FA) and increased mean diffusivity (MD). Further, this reduced structural integrity of the SLF was associated with a reduction in overall cognitive performance. These findings suggest that disruptions in the structural and functional connectivity of the IPS may contribute to chronic cognitive deficits experienced by these patients.