Regulation and Release of Vasoactive Endoglin by Brain Endothelium in Response to Hypoxia/Reoxygenation in Stroke

In large vessel occlusion stroke, recanalization to restore cerebral perfusion is essential but not necessarily sufficient for a favorable outcome. Paradoxically, in some patients, reperfusion carries the risk of increased tissue damage and cerebral hemorrhage. Experimental and clinical data suggest that endothelial cells, representing the interface for detrimental platelet and leukocyte responses, likely play a crucial role in the phenomenon referred to as ischemia/reperfusion (I/R)-injury, but the mechanisms are unknown. We aimed to determine the role of endoglin in cerebral I/R-injury; endoglin is a membrane-bound protein abundantly expressed by endothelial cells that has previously been shown to be involved in the maintenance of vascular homeostasis. We investigated the expression of membranous endoglin (using Western blotting and RT-PCR) and the generation of soluble endoglin (using an enzyme-linked immunosorbent assay of cell culture supernatants) after hypoxia and subsequent reoxygenation in human non-immortalized brain endothelial cells. To validate these in vitro data, we additionally examined endoglin expression in an intraluminal monofilament model of permanent and transient middle cerebral artery occlusion in mice. Subsequently, the effects of recombinant human soluble endoglin were assessed by label-free impedance-based measurement of endothelial monolayer integrity (using the xCELLigence DP system) and immunocytochemistry. Endoglin expression is highly inducible by hypoxia in human brain endothelial monolayers in vitro, and subsequent reoxygenation induced its shedding. These findings were corroborated in mice during MCAO; an upregulation of endoglin was displayed in the infarcted hemispheres under occlusion, whereas endoglin expression was significantly diminished after transient MCAO, which is indicative of shedding. Of note is the finding that soluble endoglin induced an inflammatory phenotype in endothelial monolayers. The treatment of HBMEC with endoglin resulted in a decrease in transendothelial resistance and the downregulation of VE-cadherin. Our data establish a novel mechanism in which hypoxia triggers the initial endothelial upregulation of endoglin and subsequent reoxygenation triggers its release as a vasoactive mediator that, when rinsed into adjacent vascular beds after recanalization, can contribute to cerebral reperfusion injury.     

Postischemic Neuroprotection of Aminoethoxydiphenyl Borate Associates Shortening of Peri-Infarct Depolarizations

Brain stroke is a highly prevalent pathology and a main cause of disability among older adults. If not promptly treated with recanalization therapies, primary and secondary mechanisms of injury contribute to an increase in the lesion, enhancing neurological deficits. Targeting excitotoxicity and oxidative stress are very promising approaches, but only a few compounds have reached the clinic with relatively good positive outcomes. The exploration of novel targets might overcome the lack of clinical translation of previous efficient preclinical neuroprotective treatments. In this study, we examined the neuroprotective properties of 2-aminoethoxydiphenyl borate (2-APB), a molecule that interferes with intracellular calcium dynamics by the antagonization of several channels and receptors. In a permanent model of cerebral ischemia, we showed that 2-APB reduces the extent of the damage and preserves the functionality of the cortical territory, as evaluated by somatosensory evoked potentials (SSEPs). While in this permanent ischemia model, the neuroprotective effect exerted by the antioxidant scavenger cholesteronitrone F2 was associated with a reduction in reactive oxygen species (ROS) and better neuronal survival in the penumbra, 2-APB did not modify the inflammatory response or decrease the content of ROS and was mostly associated with a shortening of peri-infarct depolarizations, which translated into better cerebral blood perfusion in the penumbra. Our study highlights the potential of 2-APB to target spreading depolarization events and their associated inverse hemodynamic changes, which mainly contribute to extension of the area of lesion in cerebrovascular pathologies.     

增城变电站500 kV增横甲线避雷器故障分析

2007年8月21日,广州供电局增城变电站500kV增横甲线遭受雷击而跳闸,L2相避雷器受损。介绍了这次故障的过程,通过电气试验分析和解体检查分析,找出L2相避雷器损坏的原因是内部绝缘击穿。通过分析三相避雷器的历史测试数据,发现L1相避雷器有阻陛电流增大的趋势,于是对L1相和L3相避雷器也进行了试验分析和解体检查分析,得出XAP 55081／444型避雷器内部存在共性绝缘缺陷的结论。最后,针对该批次XAP 55081型避雷器的共性缺陷提出处理意见。     

牛免疫球蛋白G的体外人源唾液酸化及Fc片段的制备

建立将牛免疫球蛋白G (bovine immunoglobulin G,bIgG)糖链末端N-羟乙酰神经氨酸酶切并连接人源N-乙酰神经氨酸(N-acetylneuraminic acid,Neu5Ac)的方法,在实现bIgG转化为人源IgG (human IgG,hIgG)的基础上,研究hIgG可结晶(Fc)片段的制备...     

炸药驱动预制破片轴向抛掷速度规律研究

为解决爆轰产物对轴向预制破片的作用压力从柱状装药中心沿径向逐渐降低,从而导致轴向预制破片抛掷速度沿径向逐渐变小的问题,研究了柱状装药长径比与装药壳体厚度等装药结构参数对轴向预制破片抛掷速度沿径向分布规律的影响,针对某种轴向前置预制破片战斗部,进行了破片轴向抛掷速度沿径向分布规律的试验.结果表明,装药长径比以及装药壳体等装药结构参数对轴向预制破片抛掷速度影响较大,通过装药尺寸、壳体厚度等参数匹配,可以调整轴向预制破片的抛掷速度.     

基于深度信任网络模型的乌东选煤厂铁路车号图像识别方法

精准识别铁路车号可以为煤厂装车提供依据,从而保证装车环节高效顺利地完成。为此,提出了基于深度信任网络模型的乌东选煤厂铁路车号图像识别方法。首先,利用高速摄像机设备采集原始的车号图像,并利用索贝尔算子检测图像边界;然后,根据列车车号的字体笔画宽度特点,采笔画宽度变换算法定位确定图像中的车号区域,并利用LBP算法提取车号区域内的特征;最后,将提取的特征输入到深度信任网络模型中,在训练网络模型并不断更新参数后,准确识别车号图像。实验表明：该方法能够精准识别乌东选煤厂铁路列车车号图像。在深度信任网络模型中,当受限玻尔兹曼机网络为4层、隐含层节点个数为128个时,该模型的分类识别能力最强,训练损失最小,性能最佳。     

雷击时10～35 kV电压互感器多相熔丝熔断的原因分析

本以110kV淤溪变电站为例，论述了中性点不接地系统中电压互感器一次侧熔丝在雷击时熔断的各种原因和处理方法，重点阐明了安装在电压互感器一次绕组中性点的消谐电阻不能限制电压互感器入口电容冲击电流的原理，并用此理论解释了1998年3月江苏省沿江地区变电站数百相次10～35kV电压互感器熔丝熔断这一典型现象。     

输电线路杆塔模型与防雷性能计算研究

输电线路防雷性能的评估主要是耐雷水平和雷击跳闸率的计算.近年来随着同杆并架技术的应用越来越多,双回线路的同时跳闸率也成为考核线路防雷性能的一项重要指标,但目前国内对同杆并架线路的防雷性能计算方法争论较多、分歧较大.文章在传输线杆塔模型、计算基本原理、计算过程、计算准确度以及适应性几方面,对目前国内比较常用的两种输电线路防雷性能的计算方法(即波阻抗模型计算方法和电感模型计算方法)进行了比较.发现电感模型计算方法在实际工程应用中可操作性强,且适应范围广.采用电感模型计算出的耐雷水平偏低、跳闸率偏高不是由计算方法本身所引起的,而是由计算过程中引入的导线感应电压过高造成的.此外,文中还指出,这两种方法的共同缺点是未明确给出同时跳闸率的计算.     

500kV同塔双回输电线路雷电反击仿真模型的建立与分析

雷击是造成输电线路跳闸的主要原因。做好500kV同塔双回输电线路防雷设计,是保证电力系统安全运行的重要环节之一。以某500kV线路为研究背景,用ATP-EMTP软件分别建立雷电流双指数波模型、杆塔分段传输线模型、输电线路Jmarti模型、绝缘子闪络和冲击接地电阻模型,搭建仿真电路,分析了接地电阻和线路档距对500kV同塔双回线路的反击耐雷水平的影响,以期为我国500kV同塔双回线路防雷分析提供参考。     

云广直流"6o5"行波保护动作RTDS仿真分析

针对2011年6月5日因行波保护动作发生的云广直流双极相继闭锁事故,运用RTDS故障仿真和录波回放等手段进行了分析。结果表明,在该事故中极Ⅱ因直流线路雷击短路故障,穗东、楚雄两站极Ⅱ行波保护正确动作;电磁耦合致极Ⅰ的直流电压、直流电流出现较大波动,逆变站极Ⅰ行波保护达到定值而动作。RTDS仿真测试得出结论,行波保护逆变站ΔIInv定值由-0.05改为-0.3能避免"6o5"情况下的逆变站极Ⅰ行波保护动作