从高放废液中去除超铀元素的TRPO流程热实验

阐述了从高放废液中去除超铀元素的ＴＲＰＯ流程热实验。热实验是用真实动力堆的 高放液进行的，取得了很好的效果。超铀元素镅、镎、钚和铀的去污系数分别大于 ３ ０００，４ ０００， ９５０和 ７ ０００。 ＴＲＰＯ流程在去除超铀元素的同时，还能去除对放射性废物长期危害起决定作用 的９９Ｔｃ。实验结果表明ＴＲＰＯ流程具有去污效率高，反萃效果好，锕系组分之间交叉污染小和试 剂成本低等诸多优点。ＴＲＰＯ流程是一个有效的从高放废液中去除超铀元素的流程。     

可调直立叶片潮流发电系统研究

以5kW潮流发电装置为背景,提出了可调叶片水轮机潮流发电控制方案.对水轮机及系统进行了数学建模,并在计算机上对所设计的系统进行了数字仿真.仿真结果表明该方案是可行的.     

QSL炼铅过程的热力学分析

根据已提出的直接炼铅过程的计算机模型，分析了ＱＳＬ炼铅法在工业上得不到弃渣而失败的根本原因，同时对精矿成分、熔炼温度、重油量和风量等操作条件进行了模拟，发现提高温度不能得到弃渣，而还原性的气氛却可极大地降低炉渣中铅含量，从而提出降低渣含铅的具体改进措施与方案，为在实际生产中解决这一问题提供可靠的依据．     

工作流网WRI WF-net的验证方法研究及实现

WF-net是一种工作流模型,合理性是衡量WF-net模型正确性的一个标准,不合理的工作流模型会导致运行错误.但是合理性验证问题是NP-complete问题,妨碍了WF-net的广泛应用.工作流模型WRI WF-net是WF-net的子集,能够直接保证工作流模型的合理性,这样只需确保用户建立的工作流模型符合WRI WF-net的约束,而不需要进行合理性验证.提出一个WRI WF-net的验证方法,能够在结构上验证模型是否满足WRI WF-net的约束,并且阐述了方法的实现.     

数字通信系统 第三版

本书全面介绍了数字通信系统的理论和实际应用方法，并且包含了在数字信号传输中需要运用的关于设计、实现和测试的最新方法和技术。此书介绍的基本技术有：纠错码、多路复用、数字调制、数字用户线路、电缆调制、移动无线网络、城域网和光纤网络。新的工业标准有：声音／视频编码、SONET/SDH、DWDM、ATM、宽带无线网、网络同步和网络管理。每一章节后都有评述和参考文献和大量习题（无答案）。     

New structure of Kalman filter for radar networking

1.INTRODUCTION Inpractice,radarsoftenoperateasynchronouslyandpro videdataatdifferentrateswithdifferentcommunication timedelays,thustheproblemofdatafusioninradarnet workingsystemisasynchronousinsteadofsynchronous. However,theresearchinthefieldofdatafusionfocuses onthesynchronousproblems,andthemeasurementsof differentsensorsarealwayspredictedatthesametimefor updatingKalmanfiltersynchronously.Thisapproachis complicatedforengineering,anditwillreducethedata ratesofthesystem,atthesametimethee…     

RESEARCH ON REUSE OF PAPERMAKING LIGNIN-CONVERSION OF LIGNIN TO BTX BY CATALYTIC PYROLYSIS IN A POWDER PARTICLE FLUIDIZED BED

INTRODUCTIONPlant consists essentially of three main polymers:lignin, cellulose, and hemicellulose, which are themost abundant and renewable hydrocarbon resourceson the earth. The annual yield of rice straw, wheatstraw, bagasse, reed, and bamboo in our country hasexceeded 1 billion tons. 30% of the yield of ricestraw and wheat straw are used for papermaking, which occupy 70-80% of the raw material. However, it is the difficulty in papermaking waste liquid treatment as well as the lack of c…     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.