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By enrolling patients with known baseline creatinine levels, we also reduced misclassification of early AKI status

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(D) GliT confers gliotoxin resistance on S

Melatonin administration reversed this phenotype by adopting a compensatory mechanism aimed at increasing Bcl-2 protein expression, blocking Bax proapoptotic activity via the SIRT1/NF-kB axis with a consequent and significant inhibition of Cyt C release and the lack of apoptosome formation and caspase 3 activation 37 (Fig