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While in many mammalian species UA is further degraded to allantoin, in humans and certain other primates the uricase activity responsible for this metabolic removal has been lost

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Iron overload following ischemia may be mediated through two primary pathways: IL-6JAK/STAT3hepcidin axis: Ischemia-induced IL-6 activates the JAK/STAT3 signaling pathway, which enhances hepcidin expression

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