Background: Neonatal hypoxia ischemia (HI) related brain injury is one of the major causes of life-long neurological morbidities that result in learning and memory impairments. Evidence suggests that male neonates are more susceptible to the detrimental effects of HI, yet the mechanisms mediating these sex-specific responses to neural injury in neonates remain poorly understood. We previously tested the effects of treatment with a small molecule agonist of the tyrosine kinase B receptor (TrkB), 7,8-dihydroxyflavone (DHF) following neonatal HI and determined that females, but not males exhibit increased phosphorylation of TrkB and reduced apoptosis in their hippocampi.
View Article and Find Full Text PDFObjectives: The nature and frequency of pediatric sedation adverse events (AEs) have been well described. However, the timing of specific AEs in induction, procedure, and recovery phase of sedation remains unknown. The objective was to describe the nature, frequency, and timing of AEs.
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