Articles: brain-injuries.
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Increasing evidence suggests that endoplasmic reticulum stress (ER stress) and neuroinflammation are involved in the complex pathological process of traumatic brain injury (TBI). However, the pathological mechanisms of their interactions in TBI remain incompletely elucidated. Therefore, investigating and ameliorating neuroinflammation and ER stress post-TBI may represent effective strategies for treating secondary brain injury. ⋯ Changes in microglial/macrophage M1/M2 polarization were observed. Additionally, the PERK activator CCT020312 intervention eliminated the impact of AS-IV on post-TBI inflammation and ER stress-related proteins p-PERK, p-eIF2a, and ATF4. These results indicate that AS-IV alleviates neuroinflammation and brain damage post-TBI through the PERK pathway, offering new directions and theoretical insights for TBI treatment.
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Traumatic brain injury (TBI) significantly contributes to morbidity rates. While computed tomography (CT) scoring systems have been recognized as predictive factors for TBI outcomes, their association with shunt dependency in patients undergoing decompressive craniectomy (DC) has not been investigated. This study aimed to evaluate the predictive utility of CT scoring systems concerning shunt-dependent hydrocephalus in patients post-DC for TBI. ⋯ The CT scoring systems proved insufficient for predicting shunt-dependent hydrocephalus following DC for TBI. However, our observations underscore a significant correlation between post-traumatic shunt dependency after DC and an increased incidence of unfavorable outcomes during long-term follow-up.
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Early posttraumatic brain injury (TBI) tranexamic acid (TXA) may reduce blood-brain barrier (BBB) permeability, but it is unclear if this effect is fixed regardless of dose. We hypothesized that post-TBI TXA demonstrates a dose-dependent reduction of in vivo penumbral leukocyte mobilization, BBB microvascular permeability, and enhancement of neuroclinical recovery. ⋯ Only higher TXA dosing definitively abrogates penumbral leukocyte mobilization, preserving BBB integrity post TBI. Some neuroclinical recovery is observed, even with lower TXA dosing. Better outcomes with higher dose TXA after TBI may occur secondary to blunting of leukocyte-mediated penumbral cerebrovascular inflammation.