Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Jun 2016
CONTRECOUP TRAUMATIC INTRACEREBRAL HEMORRHAGE: A GEOMETRIC STUDY OF THE IMPACT SITE AND ASSOCIATION WITH HEMORRHAGIC PROGRESSION.
Traumatic intracerebral hemorrhage (TICH) represents 13-48% of the lesions after a traumatic brain injury (TBI). The frequency of TICH-hemorrhagic progression (TICH-HP) is estimated to be approximately 38-63%. The relationship between the impact site and TICH location has been described in many autopsy-based series. ⋯ Factors independently associated with TICH-HP obtained through logistic regression included an initial volume of <1 cc, cisternal compression, falls, acute subdural hematoma, multiple TICHs, and contrecoup TICHs. We demonstrated a significant association between the TICH location and impact site. The contrecoup represents a risk factor independently associated with hemorrhagic progression.
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This 3-year prospective study examined the association between red blood cell transfusion (RBCT) and 1-year neurocognitive and disability levels in 309 patients with traumatic brain injury (TBI) admitted to the neurological intensive care unit (NICU). ⋯ Our results strongly suggest an independent association between RBCT and unfavorable long-term functional outcomes of patients with TBI.
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Journal of neurosurgery · Jun 2016
Neuron-derived orphan receptor 1 transduces survival signals in neuronal cells in response to hypoxia-induced apoptotic insults.
OBJECT Hypoxia can induce cell death or trigger adaptive mechanisms to guarantee cell survival. Neuron-derived orphan receptor 1 (NOR-1) works as an early-response protein in response to a variety of environmental stresses. In this study, the authors evaluated the roles of NOR-1 in hypoxia-induced neuronal insults. ⋯ After reducing cIAP2 translation, OGD-induced cell death was reduced. Sequentially, application of NOR-1 small interfering RNA to neuro-2a cells significantly inhibited OGD-induced cIAP2 mRNA expression and concurrently alleviated hypoxia-induced alterations in cell viability, caspase-3 activation, DNA damage, and cell apoptosis. CONCLUSIONS This study shows that NOR-1 can transduce survival signals in neuronal cells responsible for hypoxiainduced apoptotic insults through activation of a CREB/cIAP2-dependent mechanism.
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Journal of neurotrauma · Jun 2016
Neuropsychological, metabolic, and GABAA receptor studies in subjects with repetitive traumatic brain injury.
Repetitive traumatic brain injury (rTBI) occurs as a result of mild and accumulative brain damage. A prototype of rTBI is chronic traumatic encephalopathy (CTE), which is a degenerative disease that occurs in patients with histories of multiple concussions or head injuries. Boxers have been the most commonly studied patient group because they may experience thousands of subconcussive hits over the course of a career. ⋯ Glucose metabolism was impaired in frontal areas associated with cognitive dysfunction, similar to findings in Alzheimer's disease. Low binding potential (BP) of (18)F-flumazenil (FMZ) was found in the angular gyrus and temporal cortical regions, revealing neuronal deficits. These results suggested that cognitive impairment and motor dysfunction reflect chronic damage to neurons in professional boxers with rTBI.
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Journal of neurotrauma · Jun 2016
Neuroprotective effects of the glutamate transporter activator, MS-153, following traumatic brain injury in the adult rat.
Traumatic brain injury (TBI) in humans and in animals leads to an acute and sustained increase in tissue glutamate concentrations within the brain, triggering glutamate-mediated excitotoxicity. Excitatory amino acid transporters (EAATs) are responsible for maintaining extracellular central nervous system glutamate concentrations below neurotoxic levels. Our results demonstrate that as early as 5 min and up to 2 h following brain trauma in brain-injured rats, the activity (Vmax) of EAAT2 in the cortex and the hippocampus was significantly decreased, compared with sham-injured animals. ⋯ Administration of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a GLT-1 activator, beginning immediately after injury and continuing for 24 h, significantly decreased neurodegeneration, loss of microtubule-associated protein 2 and NeuN (+) immunoreactivities, and attenuated calpain activation in both the cortex and the hippocampus at 24 h after the injury; the reduction in neurodegeneration remained evident up to 14 days post-injury. In synaptosomal uptake assays, MS-153 up-regulated GLT-1 activity in the naïve rat brain but did not reverse the reduced activity of GLT-1 in traumatically-injured brains. This study demonstrates that administration of MS-153 in the acute post-traumatic period provides acute and long-term neuroprotection for TBI and suggests that the neuroprotective effects of MS-153 are related to mechanisms other than GLT-1 activation, such as the inhibition of voltage-gated calcium channels.