Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Mar 2024
Experimental study on intracranial pressure and biomechanical response in rats under the blast wave.
Explosion overpressure propagates extracranially and causes craniocerebral injury after being transmitted into the brain. Studies on the extent of skull to reduce impact overpressure are still lacking. Therefore, it is necessary to study the relationship between intracranial pressure (ICP) and external field pressure and the situation of craniocerebral injury under the blast wave. ⋯ The fitting curve of air overpressure and ICP can be used to predict the changes of ICP under different external blast overpressure. Analysis of cranial injury showed that the area of cranial hemorrhage with extremely severe injury increased by 107.9% compared with mild injury, increased by 53.3% compared with moderate injury, and increased by 21.6% compared with severe injury. This work may provide references for the dynamic response of biological cranial and brain injury mechanism under the effect of blast wave.
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Systemic inflammation following traumatic brain injury (TBI) has been extensively studied over the past decades, as it contributes significantly to the pathophysiological injury mechanisms and subsequent poor outcomes. Systemic immune-inflammation (SII) index is a novel biomarker of systemic inflammatory response. However, its predictive value regarding TBI prognosis in clinical practice remains insufficiently investigated. ⋯ Our findings suggested that increased SII index during the early stages of TBI was an independent risk factor for poor prognosis with satisfactory predictive value. The SII index provides a reliable, convenient, and cost-effective prognostic model to evaluate systemic inflammation after TBI and identify patients at risk of poor outcomes, thereby offering valuable guidance for clinical practice.
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Long thought to be immune privileged, the central nervous system is far from being devoid of local immunity. Subarachnoid hemorrhage (SAH) and traumatic brain injury represent 2 distinct central nervous system injury situations which, while both exposed to external ventricular drains, present different incidences of ventriculostomy-related infection (VRI). We sought to compare VRI incidence and initial cerebrospinal fluid (CSF) inflammatory profiles in these 2 clinical situations. ⋯ Local inflammatory markers were markedly higher in SAH than in traumatic brain injury. However, positive events were more frequent in SAH. Furthermore, SAH may be a risk factor for VRI. Hypothesis that a primary injury to the subarachnoid space could impair central nervous system immune functions should be explored.
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This study aims to identify risk factors for central nervous system (CNS) infection in elderly patients hospitalized with traumatic brain injury (TBI) and to develop a reliable predictive tool for assessing the likelihood of CNS infection in this population. ⋯ A nomogram constructed based on several key predictors reasonably predicts the risk of CNS infection in elderly TBI patients upon hospital admission. The model of the nanogram may contribute to timely interventions and improve health outcomes among affected individuals.
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Journal of neurotrauma · Mar 2024
Protective effects of Hinokitiol on neuronal ferroptosis by activating the KEAP1/NRF-2/HO-1 pathway in traumatic brain injury.
In this study, we investigated the effects of hinokitiol, a small-molecule natural compound, against neuronal ferroptosis after traumatic brain injury (TBI). A controlled cortical impact (CCI) mouse model and excess glutamate-treated HT-22 cells were used to study the effects of hinokitiol on TBI. Hinokitiol mitigated TBI brain tissue lesions and significantly improved neurological function. ⋯ Mechanistically, hinokitiol upregulated heme oxygenase-1 (HO-1) expression, promoted nuclear factor-erythroid factor 2-related factor 2 (Nrf2) nuclear translocation, and inhibited the activation of microglia and astrocyte after TBI. These results suggest that hinokitiol has neuroprotective effects on rescuing cells from TBI-induced neuronal ferroptosis. In summary, hinokitiol is a potential therapeutic candidate for TBI by activating the Nrf2/Keap1/HO-1 signaling pathway.