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doi: 10.25259/IJPP_172_2025 Abstract Objectives: Traumatic brain injury (TBI) and hypoxic-ischemic encephalopathy (HIE) participate in a mutual pathophysiological connection of oxidative stress, neuroinflammatory response and mitochondrial damage which leads to the development of long-term neurologic deficits

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Moreover, this glucose control intervention increased the risk of hypoglycemic episodes (73)