English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Pro

Presents the zaia usage as premium feature

ZAIA

Presents AI Discovery search usage as a premium feature

AI Discovery

Presents AI Discovery explain and summary usage as a premium feature

Content Analysis

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Presents the pdf analysis as premium feature

PDF Analysis

1500 Top-up

3000 Top-up

Zendy Basic

2500 Top-up

Zendy Unlimited

Presents the access of premium content as premium feature

Premium Content

The brain injury associated with neonatal hypoxia ischemia (HI) is a major contributor to neonatal mortality and neurodevelopment retardation. Approximately 30–40% of infants with brain injury will die and 20–40% of survivors will develop significant neurological disorders and lifelong disability, such as cerebral palsy, seizures, visual impairment, mental retardation, learning impairment and epilepsy. Preterm birth is a high risk factor for neonatal brain injury. In the U.S., nearly 12% of babies are born preterm, and care of preterm infants accounts for more than half of pediatric health care dollars spent (Juul and Ferriero, 2014). A greater understanding of the complex mechanisms that result in neonatal hypoxia ischemic brain injury is the key to developing new protective therapeutics.

Iron metabolism, oxidative stress, and neonatal brain injury