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the lifespan was significantly prolonged by counteracting oxidative stress, possibly through the epigenetic downregulation of histone H3 acetylation, thereby suppressing oxidative damage and necrosis

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The clinical sites, sample sources (CENTER TBI [31, 41] and the CanTBI bank [30]), severity of TBI, health status of controls, time points and methods for characterizing lipid metabolism varied between trials and contributed to the observed differences

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