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The results of open field anxiety testing showed no difference in exploratory behavior in mice pre-MT-II treatment (185 13 crossings) compared to post-MT-II treatment (173 12 crossings)

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Fernandez-Lafuente R Strategies for the one-step immobilizationpurification of enzymes as industrial biocatalysts

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

Liu Y, Jin X, Li C, Bu J, Wang B, Bai M, et al

Although both acetyl-l-carnitine and gabapentin provided significant pain relief, acetyl-l-carnitine (100 mg/kg, i.p., 14 days), but not gabapentin (70 mg/kg, i.p., 14 days), significantly prevented nerve fibre and myelin thickness loss and increased axonal neurofilament immunoreactivity [16]