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Systematic integration of quantitative and qualitative information into the framework of an adverse outcome pathway revealed the causal involvement of oxidative stress in liver pathologies such as drug-induced liver injury, alcoholic liver disease, cholestatic liver injury, and nonalcoholic fatty liver disease (Kuijper et al
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The hypothesis that B12 could modulate CCL11 expression during persistent VCD via methyl-dependent epigenetic mechanisms was confirmed by the hypermethylation of DML a and c in leukocytes from cultures of impaired individuals incubated with the vitamin
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