Neuroprotective effects of geneticin (G418) via apoptosis in perinatal hypoxic-ischemic brain injury
نویسندگان
چکیده
접수 : 2007년 12월 4일, 승인 : 2008년 1월 9일 이 연구는 2002년도 대구가톨릭대학교 의과학연구소 연구비의 지원으로 이루어졌음 책임저자 : 김우택, 대구가톨릭대학병원 소아과청소년과 Correspondence : Woo Taek Kim, M.D. Tel : 053)650-4250 Fax : 053)622-4240 E-mail : [email protected] xia at birth is estimates to be 0.2-0.4% in full-term newborn infants and approaches 60% in preterm infants. About 20-50% of infants suffering from H-I encephalopathy expire during the neonatal period, and 25-30% of the survivors exhibit permanent neurodevelopmental abnormalities such as mental retardation, learning disability, epilepsy, and cerebral palsy 2, 3) . H-I brain injury can also result in attention deficit disorders and minimal brain disorder syndromes, and may in addition form the basis for psychiatric and neurodegenerative diseases later in life 4) . H-I brain injury triggers biochemical events such as energy failure, membrane depolarization, Neuroprotective effects of geneticin (G418) via apoptosis in perinatal hypoxic-ischemic brain injury
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Using the endocannabinoid system as a neuroprotective strategy in perinatal hypoxic-ischemic brain injury
One of the most important causes of brain injury in the neonatal period is a perinatal hypoxic-ischemic event. This devastating condition can lead to long-term neurological deficits or even death. After hypoxic-ischemic brain injury, a variety of specific cellular mechanisms are set in motion, triggering cell damage and finally producing cell death. Effective therapeutic treatments against this...
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Hypoxic-ischemic cerebral injury that occurs during the perinatal period is one of the most commonly recognized causes of severe, long-term neurologic deficits in children; it is often referred to as cerebral palsy. Despite improvements in perinatal practice during the past several decades, the incidence of cerebral palsy attributed to intrapartum asphyxia has remained essentially unchanged, pr...
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Apoptosis signal-regulating kinase 1 (ASK1) is a ubiquitously expressed protein kinase, which regulates cell fate in numerous injury conditions. Therefore, ASK1 may be a promising novel therapeutic target for injury. However, the expression and distribution of ASK1 in the perinatal brain following hypoxia-ischemia (HI) remains to be elucidated. In the present study, western blotting and immunof...
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BACKGROUND AND PURPOSE Brain injury after hypoxic-ischemic insults evolves via an apoptotic/necrotic cascade. Glutamate over release and N-methyl-d-aspartate (NMDA) receptor over activation (excitotoxicity) are believed to trigger this process. Xenon is a nontoxic anesthetic gas that reduces neurotransmitter release and functionally antagonizes NMDA receptors. Administering xenon to hypoxic-isc...
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Perinatal hypoxic-ischemic encephalopathy can be a devastating complication of childbirth. Herein, the authors review the pathophysiology of hypoxic-ischemic encephalopathy and the current status of neuroprotective strategies to ameliorate the injury centering on four themes: (1) monitoring in the perinatal period, (2) rapid identification of affected neonates to allow timely institution of the...
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