Articles: traumatic-brain-injuries.
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Randomized Controlled Trial
An initial assessment of an opinion leader-informed intervention to improve concussion-related outcomes among middle school parents: a randomized controlled trial.
There is a need for evidence-based prevention programming that can reduce head impacts and increase reporting and disclosure of concussion. This study assessed an intervention to decrease concussion risk and improve concussion management through improving concussion-related knowledge, attitudes, intentions, and self-efficacy among parents in the middle school (MS) sport setting. ⋯ Although study arms did not differ in change scores from pre- to post-intervention, beneficial increases were nonetheless found across both knowledge and self-efficacy. Additional research is needed to further examine the beneficial manners in which concussion education can be best delivered and the most effective.
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Endoplasmic reticulum (ER) stress is recognized as a crucial contributor to the progression of traumatic brain injury (TBI) and represents a potential target for therapeutic intervention. This study aimed to assess the potential of J147, a novel neurotrophic compound, in alleviating ER stress by modulating related signaling pathways, thereby promoting functional recovery in TBI. To this end, adult mice underwent controlled cortical impact (CCI) injury to induce TBI, followed by oral administration of J147 one-hour post-injury, with daily dosing for 3 to 7 days. ⋯ At the molecular level, TBIinduced AMP-activated protein kinase (AMPK) dephosphorylation, sterol regulatory element binding protein-1 (SREBP-1) activation, and upregulation of ER stress marker proteins, including phosphorylated eukaryotic initiation factor-2α (p-eIF2a), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP) in perilesional cortex neurons at three days post-injury. Notably, the J147 treatment significantly attenuated AMPK dephosphorylation, SERBP-1 activation, and expression of the ER stress markers. In summary, this study reveals the therapeutic promise of J147 in mitigating secondary brain damage associated with TBI and improving long-term functional recovery by modulating ER stress pathways.
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The neuroinflammatory response promotes secondary brain injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation. However, the role of TREM1 in TBI is poorly studied. ⋯ Moreover, after TREM1 was inhibited, the secretion of the proinflammatory factors TNF-α and IL-1β was significantly reduced, while the secretion of the anti-inflammatory factors IL-4 and IL-10 was significantly increased. Additionally, inhibition of TREM1 by LP17 significantly reduced neuronal apoptosis and ameliorated nerve dysfunction in TBI model rats. In conclusion, our findings suggest that TREM1 enhances neuroinflammation and promotes neuronal apoptosis after TBI, and these effects may be partly mediated via the ERK/cPLA2 signalling pathway.
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Meta Analysis
Impact of fever on the outcome non-anoxic acute brain injury patients: a systematic review and meta-analysis.
Fever is a common condition in intensive care unit (ICU) patients, with an incidence between 30 and 50% in non-neurological ICU patients and up to 70-90% in neurological ICU patients. We aim to perform systematic review and meta-analysis of current literature to assess impact of fever on neurological outcomes and mortality of acute brain injury patients. ⋯ Fever was associated with poor neurological outcomes and mortality in patients with acute brain injury. Whether normothermia should be targeted in the management of all neuro critically ill patients warrants specific research.
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Mild traumatic brain injury (mTBI) is known to result in chronic somatic, cognitive, and emotional symptoms. Depression is commonly reported among individuals suffering from persistent concussion symptoms; however, the underlying mechanisms are not understood. The glutamatergic system has recently been linked with mTBI and depression due to reports of similar changes in expression of glutamatergic proteins. ⋯ Linear regression was performed to evaluate relationships between behavioral and molecular variables; the results suggested that injury affects these relationships in a region-dependent manner. Together, these results suggest that the development of chronic depression-like behavior was associated with changes in glutamatergic protein expression. Deeper investigations into how injury influences glutamatergic synaptic protein expression are needed, as this has the potential to affect circuit-level neurotransmission that drives depression-like behavior following mTBI.