非圆切削中双通道控制技术的研究

针对非圆活塞的特殊复杂型线,提出一种基于双通道控制技术的非圆活塞异型截面复合加工的方法。构建双通道系统控制模型,基于Turo PMAC开放伺服算法特性,设计模糊自整定PID算法,提高系统的动态响应特性。建立两通道间信号通讯,运用脉冲同步控制原理,实现双通道系统中主次系统协调控制。最后基于双通道高频往复直线进给实验平台,设计完成两通道间的同步跟随实验。结果表明:跟随实验验证了基于双通道控制技术的非圆活塞异型截面复合加工方法的可行性;在主轴转速范围为0~1 000 r/min内,跟随误差随主轴转速升高而增加。     

原料乳中药物残留和掺假物质检测方法的研究进展

原料乳中药物残留或掺假物质的存在造成的安全事件屡屡发生,这使我国乳品行业面临着巨大的挑战。本文主要综述了常规检测法、免疫分析法、仪器检测分析法、生物传感器和蛋白质芯片技术等对原料乳中常见聚醚类抗生素、类固醇激素、苯二氮卓类药物、苯基脲类除草剂、四环素类抗生素和青霉素类抗生素等药物残留、物理性质与原料乳相近的物质、常见电解质、非电解质、防腐剂等掺假物质的检测方法,以及对单一成分掺假物和多种成分掺假物的检测方法,并比较了不同检测方法的准确度、灵敏度、成本等优缺点,以期为相关检测部门进行质量监测或生产厂家牛乳收购提供技术参考。     

基于故障树的系统可靠性仿真分析

如何推断系统的寿命分布,是目前可靠性工程领域的一个重要问题.文章应用改进的故障树分析法建立系统的仿真模型,利用蒙特卡洛法在计算机上产生等价于基本部件寿命实现值的随机数,将其代入到系统的仿真模型中,经过逻辑运算得到等价于系统寿命实现值的随机数.这个过程重复多次,便得到足够多的代表系统寿命的实现值的随机序列.在概率图中对随机序列进行统计推断,从而得到系统的寿命分布.此方法简单易行,计算结果精度高,对系统的可靠性分析有重要意义.     

直流输电线路行波测距的误差机理及改进策略

针对目前直流输电线路行波测距精确度较低的问题,对测距误差的产生机理和典型的直流行波测距原理进行分析,指出波头到达时间的标定和行波波速的选取是影响直流行波测距精确度的两个关键因素;通过行波测距的误差计算公式的推导,明确了波头到达时间的标定误差和行波波速选取误差对测距精度的影响规律。以天广直流线路工程为例,分别探讨了波头到达时间的标定和波速选取中存在的问题,并提出了相应的改进策略,仿真结果验证了分析结论和改进策略的有效性。     

一种单相双输入九电平逆变器及其调制策略

由于传统多电平逆变器存在电路结构复杂、功率器件多、控制复杂等缺点,提出一种单相双输入九电平逆变器,通过2个直流输入电源与电容的串并联实现九电平输出,拓扑结构简单,能够以较少的功率器件和电容数量产生更多的输出电平,谐波含量低,并且其多输入结构适用于分布式发电和微电网等领域。首先给出逆变器的电路结构和工作原理,然后设计逆变器调制策略,并分析电容充放电过程及其对电压波动的影响,实验结果验证了所提九电平逆变器及其调制策略的有效性和可行性。     

直流串电引起的直流接地信号误报分析

随着高电压等级继电保护双重化的不断深入实施,保护电源与操作电源分开,由于各种原因,极有可能出现直流正负不对应混用现象。详细分析了两起实例,指出了由其导致的严重后果及危害,为保护双重化两组直流电源改造以及保护直流电源与操作直流电源分开的工作提供了实例警戒。     

基于网格聚类的热点路径探测

针对现有热点路径探测算法需要路网拓扑结构的支持,以及难以准确识别热点路径的复杂耦合现象的问题,提出了一种基于网格聚类的热点路径探测算法。算法将移动轨迹映射为网格序列,以邻接网格间的共有轨迹量来定义网格间的密度可达性,并据此将网格分划抽象为图模型。然后以图论中的相关理论为基础提出了网格聚类算法Grid Growth,即热点路径探测算法。实验结果表明:本文算法能有效探测热点路径,且能准确识别热点路径的复杂耦合现象。     

嵌入式NHD系统I/O性能分析及优化

嵌入式NHD（Network Hard Disk）系统是一种动态连接计算资源和存储资源的装置,它以硬件的方式对ATA存储控制器的访问接口进行功能模拟,即将对标准磁盘访问的ATA协议转化为对网络存储设备访问的NBD协议,从而为计算子系统提供虚拟的存储空间.文章对NHD系统的I/O性能进行分析,并针对性采用了DMA流水、零拷贝和TCP校验和卸载等优化技术.实验数据表明,在不改变硬件配置条件下,优化后NHD系统的I/O性能由原来的1.05MB/s提升为3.45MB/s,基本达到实用化需求.     

Prostacyclin formation elicited by endothelin-1 in rat aorta is mediated via phospholipase D activation and not phospholipase C or A2

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that also stimulates production of prostacyclin (PGI2) from arachidonic acid. The purpose of this study was to determine the contribution of phospholipases (PLs) A2, C, and/or D in ET-1-induced PGI2 formation in the rat aorta, measured as immunoreactive 6-ketoprostaglandin (PG) F1 alpha. ET-1 increased 6-keto-PGF1 alpha formation, which was not affected by a PLA2 inhibitor, 7,7-dimethyl eicosadienoic acid (DEDA). Furthermore, ET-1 failed to stimulate PLA2 activity measured in the cytosol (cPLA2), using phosphatidylcholine, L-a-1-palmitoyl-2-arachidonyl[14C] as a substrate. However, the adrenergic agonist norepinephrine increased 6-keto-PGF1 alpha formation, which was attenuated by DEDA, and enhanced PLA2 activity. ET-1 enhanced PLC activity, as indicated by increased inositol phosphate production, which was prevented by a PLC inhibitor, U-73122. However, ET-1-induced 6-keto-PGF1 alpha production was not altered by U-73122. An inhibitor of PLD activation, C2-ceramide, attenuated ET-1-induced PLD activity, as indicated by the production of phosphatidylethanol. Furthermore, ET-1-induced 6-keto-PGF1 alpha formation was inhibited by C2-ceramide as well as by ethanol treatment. Moreover, inhibitors of phosphatidate phosphohydrolase (propranolol) and diacylglycerol lipase (RHC-80267), attenuated ET-1-induced 6-keto-PGF1 alpha formation. Finally, ET-1-induced activation of PLD was not attenuated by a selective PKC inhibitor, bisindolylmaleimide I. These data suggest a novel pathway for ET-1-induced PGI2 formation in the rat aorta involving activation of PLD but not cPLA2 and independent of PLC or PKC activation.     

Optimization of an assay for baculovirus titer and design of regimens for the synchronous infection of insect cells

Electrochemical treatment (ECT) of cancer utilizes direct current to produce chemical changes in tumors. ECT has been suggested as an effective alternative local cancer therapy. However, a methodology is not established, and mechanisms are not well studied. In vivo studies were conducted to evaluate the effectiveness of ECT on animal tumor models. Radiation-induced fibrosarcomas were implanted subcutaneously in 157 female C3H/HeJ mice. Larger rat fibrosarcomas were implanted on 34 female Fisher 344 rats. When the spheroidal tumors reached 10 mm in the mice, two to five platinum electrodes were inserted into the tumors at various spacings and orientations. Ten rats in a pilot group were treated when their ellipsoidal tumors were about 25 mm long; electrode insertion was similar to the later part of the mouse study, i.e., two at the base and two at the center. A second group of 24 rats was treated with six or seven electrodes when their tumors were about 20 mm long; all electrodes were inserted at the tumor base. Of the 24 rats, 12 of these were treated once, 10 were treated twice. and 2 were treated thrice. All treated tumors showed necrosis and regression for both mice and rats; however, later tumor recurrence reduced long-term survival. When multiple treatments were implemented, the best 3 month mouse tumor cure rate was 59.3%, and the best 6 month rat tumor cure rate was 75.0%. These preliminary results indicate that ECT is effective on the radiation-induced fibrosarcoma (RIF-1) mouse tumor and rat fibrosarcoma. The effectiveness is dependent on electrode placement and dosage.