https://www.selleckchem.com/products/sb290157-tfa.html SIGNIFICANCE Hypoxic ischemic events due to intrapartum complications represent the second cause of neonatal mortality and initiates an acute brain disorder known as hypoxic ischemic encephalopathy (HIE). In HIE, the brain undergoes primary and secondary energy failure phases separated by a latent phase in which partial neuronal recovery is observed. A hypoxic ischemic event leads to oxygen restriction causing ATP depletion, neuronal oxidative stress and cell death. Mitochondrial dysfunction and enhanced oxidant formation in brain cells are characteristic phenomena associated with energy failure. Recent advances Mitochondrial sources of oxidants in neurons include complex I of the mitochondrial respiratory chain, as a key contributor to ONO) yields peroxynitrite, a mitochondrial and cellular toxin. Quantitation of the redox state of cytochrome c oxidase, through broadband near infrared spectroscopy, represents a promising monitoring approach to evaluate mitochondrial dysfunction in vivo in humans, in conjunction with the determination of cerebral oxygenation and their correlation with the severity of brain injury. CRITICAL ISSUES Being the energetic failure a key phenomenon in HIE connected with the severity of the encephalopathy, measurement of mitochondrial dysfunction in vivo provides an approach to assess evolution, prognosis and adequate therapies. Restoration of mitochondrial redox homeostasis constitutes a key therapeutic goal. FUTURE DIRECTIONS While hypothermia is the only current accepted therapy in clinical management to preserve mitochondrial function, other mitochondrial-targeted and/or redox-based treatments are likely to synergize to ensure further efficacy.Anucleate platelets, long viewed as merely cell fragments with a limited repertoire of rapid-acting hemostatic functions, are now recognized to have a complex and dynamic transcriptome mirroring that of many nucleated cells. The field of megaka