目的对足月新生儿缺氧缺血性脑病(HIE)生后6 h 内振幅整合脑电图(aEEG)的变化及其在 HIE 早期诊断和神经学预后评估的价值进行初步探讨。方法对2003年5月至2005年2月间在我院新生儿病房住院的33例足月 HIE 患儿在生后6 h 内进行 aEEG 描...目的对足月新生儿缺氧缺血性脑病(HIE)生后6 h 内振幅整合脑电图(aEEG)的变化及其在 HIE 早期诊断和神经学预后评估的价值进行初步探讨。方法对2003年5月至2005年2月间在我院新生儿病房住院的33例足月 HIE 患儿在生后6 h 内进行 aEEG 描记,并将 aEEG 监测结果与 HIE 患儿临床分度及18个月时的神经学预后进行相关性分析,分析其在 HIE 早期诊断和神经学预后预测中的价值。结果 33例 HIE 患儿中,aEEG 正常20例(60.6%),轻度异常5例(15.2%),重度异常8例(24.2%)。33例 HIE 患儿中,轻度 HIE 17例(51.5%),中度 HIE 9例(27.3%),重度HIE 7例(21.2%)。25例进行神经预后分析,其中19例神经学预后正常,1例伤残(智力缺陷),5例死亡。aEEG 分类结果与 HIE 临床分度及其神经学预后均相关性强。aEEG 异常预测新生儿中重度HIE 的敏感性为100%,特异性为81.3%,阳性预测值为85.0%,阴性预测值为100%;预测 HIE 异常神经学预后的敏感性为100%、特异性为90.9%、阳性预测值为93.3%和阴性预测值为100%。结论对足月 HIE 新生儿生后6 h 内 aEEG 监测能早期预测 HIE 病情轻重程度并预测其神经学预后。展开更多
Objective: To explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injur...Objective: To explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injury. Methods: Hippocampal neurons were obtained from rat embryo and were cultured in vitro. The ischemia and reperfusion of cultured rat hippocampal neurons were simulated by oxygen-glucose deprivation (OGD) and recovery. OGD at different time points ((0.25) h to (3.0) h) and then the same recovery (24 h) were prepared. Annexin (V-PI) staining and flow cytometry examined neuron death and apoptosis at different time after injury. Results: After OGD and recovery, both necrosis and apoptosis were observed. At different times after OGD, there were statistically significant differences in neuron necrosis rate (P<(0.05)), but not in apoptosis rate (P>(0.05)). At recovery, survival rate of hippocampal neurons further decreased while apoptosis rate increased. Furthermore, apoptosis rates of different time differed greatly (P<(0.05)). Apoptosis rate gradually increased with significant difference among those of different time points (P<(0.05)). However, 2 h after ischemia, apoptosis rate decreased markedly. Conclusions: Apoptosis is an important pathway of delayed neuron death. The therapeutic time window should be within 2 h after cerebral ischemia and hypoxia.展开更多
文摘目的对足月新生儿缺氧缺血性脑病(HIE)生后6 h 内振幅整合脑电图(aEEG)的变化及其在 HIE 早期诊断和神经学预后评估的价值进行初步探讨。方法对2003年5月至2005年2月间在我院新生儿病房住院的33例足月 HIE 患儿在生后6 h 内进行 aEEG 描记,并将 aEEG 监测结果与 HIE 患儿临床分度及18个月时的神经学预后进行相关性分析,分析其在 HIE 早期诊断和神经学预后预测中的价值。结果 33例 HIE 患儿中,aEEG 正常20例(60.6%),轻度异常5例(15.2%),重度异常8例(24.2%)。33例 HIE 患儿中,轻度 HIE 17例(51.5%),中度 HIE 9例(27.3%),重度HIE 7例(21.2%)。25例进行神经预后分析,其中19例神经学预后正常,1例伤残(智力缺陷),5例死亡。aEEG 分类结果与 HIE 临床分度及其神经学预后均相关性强。aEEG 异常预测新生儿中重度HIE 的敏感性为100%,特异性为81.3%,阳性预测值为85.0%,阴性预测值为100%;预测 HIE 异常神经学预后的敏感性为100%、特异性为90.9%、阳性预测值为93.3%和阴性预测值为100%。结论对足月 HIE 新生儿生后6 h 内 aEEG 监测能早期预测 HIE 病情轻重程度并预测其神经学预后。
文摘Objective: To explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injury. Methods: Hippocampal neurons were obtained from rat embryo and were cultured in vitro. The ischemia and reperfusion of cultured rat hippocampal neurons were simulated by oxygen-glucose deprivation (OGD) and recovery. OGD at different time points ((0.25) h to (3.0) h) and then the same recovery (24 h) were prepared. Annexin (V-PI) staining and flow cytometry examined neuron death and apoptosis at different time after injury. Results: After OGD and recovery, both necrosis and apoptosis were observed. At different times after OGD, there were statistically significant differences in neuron necrosis rate (P<(0.05)), but not in apoptosis rate (P>(0.05)). At recovery, survival rate of hippocampal neurons further decreased while apoptosis rate increased. Furthermore, apoptosis rates of different time differed greatly (P<(0.05)). Apoptosis rate gradually increased with significant difference among those of different time points (P<(0.05)). However, 2 h after ischemia, apoptosis rate decreased markedly. Conclusions: Apoptosis is an important pathway of delayed neuron death. The therapeutic time window should be within 2 h after cerebral ischemia and hypoxia.
