No abstract

Neonatal encephalopathy due to hypoxia-ischemia (HI) leads to severe, life-long morbidities in thousands of neonates born in the USA and worldwide each year. Varying capacities of long-term episodic memory, verbal working memory, and learning can present without cerebral palsy and have been associated with the severity of neonatal encephalopathy sustained at birth. Among children who sustain a moderate degree of HI at birth, girls have larger hippocampal volumes compared to boys. Clinical studies indicate that female neonatal brains are more resistant to the effects of neonatal HI, resulting in better long-term cognitive outcomes compared to males with comparable brain injury. Our most recent mechanistic studies have addressed the origins and cellular basis of sex differences in hippocampal neuroprotection following neonatal HI-related brain injury and implicate estrogen receptor-α (ERα) in the neurotrophin receptor-mediated hippocampal neuroprotection in female mice. This review summarizes the recent findings on ERα-dependent, neurotrophin-mediated hippocampal neuroprotection and weighs the evidence that this mechanism plays an important role in preservation of long-term memory and learning following HI in females.

The brachial plexus is a network of nerves formed by the ventral rami of the four lower cervical nerves (C5, C6, C7, C8) and the first thoracic nerve (T1), with some variability amongst different species.Brachial plexus injury (BPI) is a nerve injury defined by loss of function in one or both upper limbs resulting from partial or complete denervation of muscles. A BPI may occur when this network of nerves is compressed, stretched, or, in more serious cases, avulsed.Approximately 1.2% of multi-trauma patients suffer from some form

No abstract