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MicroRNA 146a is believed to interact with intracellular mediators such as interleukin 1 receptor-associated kinase 1 and mammal-affiliated tumor necrosis factor receptor-associated factor 6, both of which are involved in cytokine-related signal transduction

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The lack of statistically significant reduction in infarct volume, despite a numerical decrease, suggests that DSIPs primary benefit in this model might be more related to functional neurorecovery and neural network plasticity rather than a direct, massive reduction of necrotic tissue [1]