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The 4-N-substituted fluoroethyltriazole derivative significantly modulated KOR-dependent immune responses by decreasing IFN-γ and increasing IL-10 levels in human and mouse PBMCs, suggesting induction of tolerogenic immune pathways, and reduced EAE severity and CNS T-cell infiltration, albeit less effectively than U-50488
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Disturbances in mitochondrial genesis, morphology, and function are increasingly recognized as components of insulin resistance and the metabolic syndrome (1–3)
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