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Pharmacological inhibition of mitochondrial -oxidation (e.g., with 4-bromocrotonic acid) or peroxisomal -oxidation (e.g., with thioridazine) under glucose-deprived conditions markedly compromises oligodendrocytes survival and optic nerve conduction, underscoring the central role of this catabolic pathway in white matter energy homeostasis

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The combination produced greater weight loss than either compound alone at sub-maximal doses

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Also, it is now discovered that inflammation and the accompanying generation of free radicals of oxygen (ROS) can trigger tissue plasticity by reverting cells to pluripotency [ 10 ]