Articles: traumatic-brain-injuries.
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The purpose of this study was to retrospectively evaluate patients treated for traumatic brain injuries (TBI) to determine how multiple organ trauma (MOT) and lung injuries sustained at the time of initial injury affect outcome. ⋯ Age, GCS, Injury Severity Score, and critical head injuries (AIS ≥5) were significant tools in predicting outcome in this patient cohort. MOT and traumatic lung injury may cause significant damage to a patient suffering from a severe TBI, but these injuries do not predict mortality in this patient population.
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J Trauma Acute Care Surg · Jun 2016
Observational StudyThe acute respiratory distress syndrome following isolated severe traumatic brain injury.
Acute respiratory distress syndrome (ARDS) is common after traumatic brain injury (TBI) and is associated with worse neurologic outcomes and longer hospitalization. However, the incidence and associated causes of ARDS in isolated TBI have not been well studied. ⋯ Prognostic/epidemiologic study, level III.
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Evaluate the extent and severity of headache following deployment-related TBI (D-TBI) in veterans of the Iraq (OIF) and Afghanistan (OEF) wars over a follow-up period of 4-11 years with comparison to age, sex, race, and time of deployment matched controls. ⋯ At 4-11 years after D-TBI for TBIS, or after deployment for CS, the TBIS as compared to CS suffered much more frequent and severe headaches. For TBIS, there was no relation of headache intensity or phenotype to severity or cause of the TBI, and the Headache Burden has not improved over time up to 11 years after D-TBI. The process initiated by the D-TBI that relates to the headache has a prolonged effect up to and beyond 11 years.
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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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Adenosine kinase facilitated astrogliosis-induced cortical neuronal death in traumatic brain injury.
Adenosine kinase (ADK) plays a pivotal role in regulating brain function by regulating adenosine level, and ADK inhibition protects against neuronal damage in cerebral ischemia and epilepsy; however, the effects of ADK in traumatic brain injury (TBI) have not been investigated. For exploring its effects, we generated a blade-induced rat focal brain injury model. Western blot analysis, immunohistochemistry and immunofluorescent staining suggested that ADK was up-regulated after TBI, and it was temporally and spatially associated with astrogliosis. ⋯ Additionally, ADK knock-down didn't ameliorate LPS-induced astrocyte proliferation, but it protected against neuronal death by reducing iNOS expression, tumor necrosis factor α and interleukin 1β secretion of reactive astrocytes. Taken together, ADK was associated with astrogliosis after TBI, its inhibition in reactive astrocytes ameliorated astrogliosis-induced neuronal death. Our findings extended the current knowledge on the role of ADK in astrogliosis, and also provided new evidence for the TBI treatment.