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Collectively, these results confirm that ATT-I exerts its protective effects against DSS-induced colitis through inhibition of ferroptosis, as the ferroptosis activator Erastin effectively reverses all the beneficial phenotypes conferred by ATT-I

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Prior studies have underscored persistent inequities and deviations from guideline-based recommendations, but they have not leveraged Explainable artificial intelligence (XAI) approaches to disentangle the relative impact of cardiorenal risk versus demographic factors