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An integrated therapeutic approach to diabetes would target both the underlying cause of glucose intolerance as well as activate repair systems to prevent or reverse end organ damage, that is, a disease modifying therapeutic

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Contrary to our initial hypothesis that resistance-associated molecular programs would be broadly acquired under the selective pressure of NAC, we found that treatment-associated transcriptomic changes after NAC were relatively limited, whereas molecular features associated with recurrencemost notably those related to GSH metabolismwere frequently detectable prior to treatment

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