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The pathogenesis of epilepsy is complex, and clinical data and experimental studies suggest that free radicals generated by oxidative reactions in mitochondria during disease onset may be the most critical cause of epilepsy pathogenesis

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During our follow-up experiments with PenB, we discovered that knocking down bla AmpC strongly induced -lactamase activity and bla PenB expression in K56-2 (Fig

[31] but contradicts Thomas et al.s finding that increased LPCs and SM corresponded to more favorable outcomes at 6 months [31]