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Description
TLVs and BEIs Based on the Documentation for Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices, ACGIH Cincinnati, Ohio (2023)

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We sought further evidence of the neuroinflammatory response to rmTBI and ALC treatment by examining the expression of CCL11, a chemokine that has received increased attention in TBI (Villeda et al., 2011), while elevated levels in the cortex of former American football players with CTE correlated with tau pathology and the number of years playing football ( Another important secondary injury mechanism following mTBI is excitotoxicity, involving impaired neuronal calcium regulation and glutamate release resulting in dendrite damage (S et al., 2008), and in the present study rmTBI mice displayed significant hippocampal excitotoxicity at 48 h, with increased GRIA1 expression indicating the attempts to clear excess glutamate

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