OPTO 22控制系统热备技术研究

为使OPTO 22控制系统实现控制器热备份,需要解决主控制器与备份控制器之间的连接组织、数据交换、故障识别和自动切换等一系列问题.根据实践提出解决方案,对OPTO22控制系统的热备过程应注意的几个问题提出了解决方法并进行了分析.     

Improved D-IDS using the federated peer-to-peer architecture

A number of IDSs have been proposed for a networked or distributed environment. A modified D-IDS using federated peer-to-peer architecture, MCR (Multicast Reflector) and modified shaker protocol were proposed. The suggested scheme can be implemented easily and performs the information sharing between low-level IDS agents. As all users within a group monitor each other's, the common control server can perform detect intrusions with less cost and support the detection of the inside intruders.     

On-line Cutting Quality Recognition in Milling Using a Radical Basis Function Neural Network

Tool wear, chatter vibration, chip breaking and built-up edge are main phenomena to be monitored in modern manufacturing processes, which are considered as important factors to the quality of products.They are closely related to the cutting parameters, which are to be selected in manufacturing process.However, it is very difficult to measure directly the cutting quality based on on-line monitoring.In this study, the relationship between the cutting parameters and cutting quality is analyzed.A Radical Basis Function (RBF) neural network based on-line quality recognition scheme is also presented, which monitors the level of surface roughness.The experimental results reveal that the RBF neural network has a high prediction success rate.     

一个现代综合银行业务处理系统的设计与实现

介绍了一个现代的综合银行业务处理系统的设计思想和实现技术．该系统采用目前国内外银行系统业务处理先进思想，以ＩＢＭＡＳ／４００计算机为主机，以ＷＩＮＤＯＷＳＮＴ网络为前台工作站，利用目前国内较为流行的计算机软件技术开发完成．整个系统在综合帐务处理、综合客户信息管理和综合柜员制模式下，完成对公、对私、国际业务、金融卡、同业往来、内部核算等银行业务的集中处理；提供柜台业务、电话银行、网点客户终端、企业／家庭银行、ＡＴＭ存取款、ＰＯＳ等服务手段；实现了辖内资金实时清算、异地私人储蓄通存通兑、异地对公资金实时到帐的电子联行     

载体对金属卟啉催化分解NO的影响

本文讨论了ZnO、TiO_2、Cr_2O_3、CuO、SiO_2和Ni_2O_3等金属氧化物作为NiTPP的载体对分解NO活性的影响.除比表面因素的影响以外,发现了NiTPP吸附在n型半导体类型的载体(ZnO、TiO_2、Cr_2O_3)上,其催化分解NO的活性比吸附在其它类型的载体上的催化活性高.实验是在GD-05型高压釜中进行的,反应温度250℃,反应压力为2×10~5Pa.     

Cardiac angiogenic imbalance leads to peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is an often fatal disease that affects pregnant women who are near delivery, and it occurs more frequently in women with pre-eclampsia and/or multiple gestation. The aetiology of PPCM, and why it is associated with pre-eclampsia, remain unknown. Here we show that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1α, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble FLT1 (sFLT1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with circulating levels of sFLT1. Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1α. Finally, plasma samples from women with PPCM contained abnormally high levels of sFLT1. These data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.     

Editing-defective tRNA synthetase causes protein misfolding and neurodegeneration

Misfolded proteins are associated with several pathological conditions including neurodegeneration. Although some of these abnormally folded proteins result from mutations in genes encoding disease-associated proteins (for example, repeat-expansion diseases), more general mechanisms that lead to misfolded proteins in neurons remain largely unknown. Here we demonstrate that low levels of mischarged transfer RNAs (tRNAs) can lead to an intracellular accumulation of misfolded proteins in neurons. These accumulations are accompanied by upregulation of cytoplasmic protein chaperones and by induction of the unfolded protein response. We report that the mouse sticky mutation, which causes cerebellar Purkinje cell loss and ataxia, is a missense mutation in the editing domain of the alanyl-tRNA synthetase gene that compromises the proofreading activity of this enzyme during aminoacylation of tRNAs. These findings demonstrate that disruption of translational fidelity in terminally differentiated neurons leads to the accumulation of misfolded proteins and cell death, and provide a novel mechanism underlying neurodegeneration.     

利用杀菌剂防治松萎蔫病

松萎蔫病是一种非常复杂的病害。据报道,松材线虫(Bursaphelenchus xylophilus)及其携带的细菌诱导了该病,但是对于细菌的的作用尚存争议。笔者筛选出杀细菌剂进行了温室和林间防治松萎蔫病的实验。利用每株3年生赤松(Pinus densiflora)注射3 mg的恶喹酸,松萎蔫病防效达到71 %。利用恶喹酸或阿维菌素及两者混合物对大约20年生赤松的试验表明,3种处理均显示了很高的防效。以上结果证明伴生细菌是诱导松萎蔫病的必要因素,对松萎蔫病可利用杀细菌剂或杀细菌剂与杀线剂混合物进行防控。     

60万千瓦汽轮发电机模拟机组弹性阻尼支承理论分析及计算

对60万千瓦汽轮发电机模拟组弹性阻尼支承进行了研究,开发研制了计算机程序,计算分析表明,该程序可应用于多质量多支承变截面的大挠性转子系统的计算.     

Evaluation and control of miRNA-like off-target repression for RNA interference

RNA interference (RNAi) has been widely adopted to repress specific gene expression and is easily achieved by designing small interfering RNAs (siRNAs) with perfect sequence complementarity to the intended target mRNAs. Although siRNAs direct Argonaute (Ago), a core component of the RNA-induced silencing complex (RISC), to recognize and silence target mRNAs, they also inevitably function as microRNAs (miRNAs) and suppress hundreds of off-targets. Such miRNA-like off-target repression is potentially detrimental, resulting in unwanted toxicity and phenotypes. Despite early recognition of the severity of miRNA-like off-target repression, this effect has often been overlooked because of difficulties in recognizing and avoiding off-targets. However, recent advances in genome-wide methods and knowledge of Ago–miRNA target interactions have set the stage for properly evaluating and controlling miRNA-like off-target repression. Here, we describe the intrinsic problems of miRNA-like off-target effects caused by canonical and noncanonical interactions. We particularly focus on various genome-wide approaches and chemical modifications for the evaluation and prevention of off-target repression to facilitate the use of RNAi with secured specificity.