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Frontiers | The epigenetic modification of DNA methylation in neurological diseases
Similarly, the effect of BPC 157 therapy in rats with myotendinous junction defect was recovery, along with counteraction of the increased MDA values and the increased NO values in the myotendinous junction [80]
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Therefore, in combination endothelial dysfunction, the expression of proinflammatory cytokines and monocyte and macrophage recruitment to the vascular walls, it can be concluded that arsenic exposure is a strong factor predisposing to the development of atherosclerosis
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