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Following traumatic brain injury (TBI), inhibition of the Na-K-Cl cotransporter1 (NKCC1) has been observed to alleviate damage to the blood-brain barrier (BBB). However, the underlying mechanism for this effect remains unclear. This study aimed to investigate the mechanisms by which inhibiting the NKCC1 attenuates disruption of BBB integrity in TBI.

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Secondary brain damageafter traumatic brain injury (TBI) involves oxidative stress, neuroinflammation, apoptosis, and necroptosis and can be reversed by understanding these molecular pathways. The objective of this study was to examine the impact of tasimelteon (Tasi) administration on brain injury through the nuclear factor erythroid 2-related factor 2 (NRF-2)/heme oxygenase-1 (HO-1) and receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like (MLKL) pathways in rats with TBI. Thirty-two male Wistar albino rats weighing 300-350 g were randomly divided into four groups: the control group, trauma group, Tasi-1 group (trauma + 1 mg/kg Tasi intraperitoneally), and Tasi-10 group (trauma + 10 mg/kg Tasi intraperitoneally).

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Objectives: Balancing oxygen requirements, neurologic outcomes, and systemic complications from transfusions in traumatic brain injury (TBI) patients is challenging. This review compares liberal and restrictive transfusion strategies in TBI patients.

Data Sources: Electronic databases were searched from inception to October 2024.

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Purpose: Mental health conditions after mild traumatic brain injury (mTBI) are common and can complicate injury outcomes, but are under-treated. According to the Common Sense Model of Self-Regulation, the way patients perceive their health conditions can influence the way they manage them, including if, when, and how they seek treatment. This study explored how individuals perceive persistent symptoms after mTBI, in order to develop a grounded theory about what motivates and demotivates them to seek mental health treatment after their injury.

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