机构:[1]Affiliated Bayi Children's Hospital, Beijing Military Region General Hospital, No 5, Nan Mencang, Dongcheng District, Beijing 100700, China首都医科大学附属北京儿童医院
Neonatal hypoxic-ischemic(H/I) brain damage is a serious complication of intrauterine asphyxia during perinatal period, eventually leading to severe long-term neurodevelopmental disability or even death. Survival babies would experience cerebral palsy, epilepsy, mental retardation, cognitive, sensory and motor dysfunctions. However, there has no proven effective treatment available to protect the brain against injury after H/I occurs, because the exact timing of the hypoxic-ischemic event is unknown and we hardly identify the phase of injury or recovery in an individual patient precisely. In recent years, much effort has been made on the understandings of the H/I damages in the brain and underlying mechanisms of neural dysfunction, expecting the intervention of targeted neuroprotection in the newborn stage. We briefly summarize recent findings of the pathogenesis of hypoxic-ischemic injury with an emphasis on the disturbed neurogenesis process in the brain; the potential role of neural regeneration in basic and clinical research, including the endogenous stem cells mobilization and cell transplantation aiming to enhance the brain function.
语种:
外文
中科院(CAS)分区:
出版当年[2013]版:
大类|4 区医学
小类|4 区医学:内科
最新[2023]版:
大类|4 区医学
小类|4 区医学:内科
第一作者:
第一作者机构:[1]Affiliated Bayi Children's Hospital, Beijing Military Region General Hospital, No 5, Nan Mencang, Dongcheng District, Beijing 100700, China
推荐引用方式(GB/T 7714):
Chai Y,Yin X.Neural dysfunction and neural regeneration, a new window into the neonatal hypoxic-ischemic brain damage[J].ACTA MEDICA MEDITERRANEA.2014,30(1):
APA:
Chai, Y&Yin, X.(2014).Neural dysfunction and neural regeneration, a new window into the neonatal hypoxic-ischemic brain damage.ACTA MEDICA MEDITERRANEA,30,(1)
MLA:
Chai, Y,et al."Neural dysfunction and neural regeneration, a new window into the neonatal hypoxic-ischemic brain damage".ACTA MEDICA MEDITERRANEA 30..1(2014)