Articles: traumatic-brain-injuries.
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The aim of present study was to elucidate the role of Interleukin-10 (IL-10) in the neuroprotection of hyperbaric oxygen (HBO) against traumatic brain injury (TBI) in mice. The TBI in mice was induced by controlled cortical impact (CCI). HBO was given for 1h at 2.0 absolute atmosphere (ATA) in 100% O2. ⋯ IL-10 deficiency aggravated TBI-induced damage in the brain and abrogated the beneficial effects of HBO on neuroinflammation, apoptosis, and edema after TBI. IL-10 deficiency itself had no significant effect on brain water content and neurological status. In conclusion, IL-10 played an important role in the neuroprotection of HBO therapy against TBI in mice.
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We investigated the effect of taurine on inflammatory cytokine expression, on astrocyte activity and cerebral edema and functional outcomes, following traumatic brain injury (TBI) in rats. 72 rats were randomly divided into sham, TBI and Taurine groups. Rats subjected to moderate lateral fluid percussion injury were injected intravenously with taurine (200mg/kg) or saline immediately after injury or daily for 7days. Functional outcome was evaluated using Modified Neurological Severity Score (mNSS). ⋯ Compared with the TBI group, taurine significantly suppressed growth-related oncogene (GRO/KC) and interleukin (IL)-1β levels while elevating the levels of regulated on activation, normal T cell expressed and secreted (RANTES) at 1day. And taurine markedly decreased the level of 17 cytokine: eotaxin, Granulocyte colony-stimulating factor (G-CSF), Granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-gamma (IFN-γ), IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-13, IL-17, leptin, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and only increased the level of MIP-1α in a week. The results suggest that taurine effectively mitigates the severity of brain damage in TBI by attenuating the increase of astrocyte activity and edema as well as pro-inflammatory cytokines.
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J. Neurosci. Methods · Apr 2014
Mechanical alloydnia induced by traumatic brain injury is independent of restraint stress.
This study identifies the relationship between a test for post-traumatic headache and a marker for acute stress in rodent models of traumatic brain injury. ⋯ Mechanical allodynia occurs independent of evoked restraint stress, while hypothalamic pituitary adrenal axis activity is dependent on head trauma and species.
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J Emerg Trauma Shock · Apr 2014
Use of recombinant factor VIIa (rFVIIa) as pre-hospital treatment in a swine model of fluid percussion traumatic brain injury.
Recombinant factor VIIa (rFVIIa) has been used as an adjunctive therapy for acute post-traumatic hemorrhage and reversal of iatrogenic coagulopathy in trauma patients in the hospital setting. However, investigations regarding its potential use in pre-hospital management of traumatic brain injury (TBI) have not been conducted extensively. ⋯ Early pre-hospital administration of rFVIIa in this swine TBI model reduced neuronal necrosis and intracranial hemorrhage (ICH). These results merit further investigation of this approach in pre-hospital trauma care.
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Journal of critical care · Apr 2014
Review Meta Analysis Comparative StudyComparison of the safety and efficacy of propofol with midazolam for sedation of patients with severe traumatic brain injury: A meta-analysis.
To perform a meta-analysis to compare the safety and efficacy of propofol with midazolam for sedation of patients with severe traumatic brain injury. ⋯ Our meta-analysis of 4 studies showed that there are no important differences between propofol and midazolam when administered to provide sedation for patients with severe traumatic brain injury. Further randomized, controlled trials comparing propofol with midazolam for sedation of such patients are needed.