Rapidly Increased Neuronal Mitochondrial Biogenesis After Hypoxic-Ischemic Brain Injury

Rapidly increased neuronal mitochondrial biogenesis after hypoxic-ischemic brain injury.

BACKGROUND AND PURPOSE Mitochondrial biogenesis is regulated through the coordinated actions of both nuclear and mitochondrial genomes to ensure that the organelles are replenished on a regular basis. This highly regulated process has been well defined in skeletal and heart muscle, but its role in neuronal cells, particularly when under stress or injury, is not well understood. In this study, w...

Multimodality Somatosensory Neuronal Responses in Hypoxic- Ischemic Brain Injury

Osteopontin enhances endogenous repair after neonatal hypoxic-ischemic brain injury.

BACKGROUND AND PURPOSE Hypoxic-ischemic (HI) brain injury is a frequent cause of perinatal morbidity and mortality with limited therapeutic options. To identify molecules important for cerebral damage and repair, we investigated the growth factor-related gene expression profile after neonatal cerebral HI. We identified osteopontin (OPN) as the most highly upregulated factor early after HI. We t...

Neuroprotection after infection-sensitized neonatal hypoxic-ischemic brain injury

s of the 51st Workshop for Pediatric Research 51st Workshop for Pediatric Research

Pharmacological Neuroprotection after Perinatal Hypoxic-Ischemic Brain Injury

Perinatal hypoxia-ischemia (HI) is an important cause of neonatal brain injury. Recent progress in the search for neuroprotective compounds has provided us with several promising drugs to reduce perinatal HI-induced brain injury. In the early stage (first 6 hours after birth) therapies are concentrated on prevention of the production of reactive oxygen species or free radicals (xanthine-oxidase...