可用带宽度量系统中的若干基本问题

结合过去3年中设计、开发和部署BNeck系统的经验，分析了13个可用带宽度量系统的工作原理及软件实现，并在此基础上总结了可用带宽度量系统中存在的若干基本问题，对这些问题的研究，不仅有利设计和开发出高效、准确的度量系统，也有利于推动网络管理和视频通信等多个相关领域的共同发展。

A Lagrangian for von Karman Equations of Large Deflection Problem of Thin Circular Plate

By the semi-inverse method proposed by He, a Lagrangian is established for the large deflection problem of thin circular plate. Ritz method is used to obtain an approximate analytical solution of the problem. First order approximate solution is obtained, which is similar to those in open literature. By Mathematica a more accurate solution can be deduced.

U19/Eaf2 Binds to and Stabilizes von Hippel-Lindau Protein

Studies have firmly established a key regulatory role for the tumor suppressor pVHL in the regulation of the vascular system and normal spermatogenesis. Here, we report that knockout of the newly identified tumor suppressor U19/Eaf2 also caused vascular system abnormalities and aspermatogenesis, suggesting a potential link between U19/Eaf2 and pVHL. Coimmunoprecipitation and in vitro binding assays showed an association between U19/Eaf2 and pVHL, whereas deletion mutagenesis revealed the requirement of the NH2 terminus of U19/Eaf2 and both the alpha and beta domains of pVHL for this binding. U19/Eaf2 stabilizes pVHL, as shown by protein stability and pulse-chase studies. Testes and mouse embryonic fibroblasts (MEF) derived from U19/Eaf2 knockout mice expressed reduced levels of pVHL, indicating that full in vivo expression of pVHL indeed requires U19/Eaf2. As expected, U19/Eaf2 knockout MEF cells exhibited an increased level and activity of hypoxia-inducible factor 1 alpha (HIF1 alpha), a protein typically regulated via a pVHL-mediated degradation pathway. Furthermore, angiogenesis in a Matrigel plug assay was significantly increased in U19/Eaf2 knockout mice. The above observations argue that U19/Eaf2 can modulate HIF1 alpha and angiogenesis, possibly via direct binding and stabilization of pVHL. [Cancer Res 2009;69(6):2599-606]

基于最大不动点模型的描述逻辑系统FL��的有穷基

研究了描述逻辑的有穷基问题,分析了有穷基在描述逻辑中的重要意义及其研究现状,并研究了形式概念分析中的属性蕴含和Duguenne-Guigues基问题.利用形式概念分析中Duguenne-Guigues基存在的证明结果,在F.Baader工作基础上设置了描述逻辑的描述背景,重新定义了描述背景下的属性蕴含,证明了带循环术语的描述逻辑系统FLε存在最大不动点语义(greatest fixed-points,gfp)模型,给出了带循环术语的描述逻辑系统FLε在最大不动点模型下的有穷基的存在性定理,并证明有穷基的可靠性和完备性.描述逻辑有穷基可以帮助知识工程师构建一个更适用于推理的描述逻辑知识库.

Endothelial microparticles released in thrombotic thrombocytopenic purpura express von Willebrand factor and markers of endothelial activation

It has been suggested that endothelial apoptosis is a primary lesion in the pathogenesis of thrombotic thrombocytopenic purpura (TTP). We tested this hypothesis by examining the phenotypic signatures of endothelial microparticles (EMP) in TTP patients. In addition, the effect of TTP plasma on microvascular endothelial cells (MVEC) in culture was further delineated. EMP released by endothelial cells (EC) express markers of the parent EC; EMP released in activation carry predominantly CD54 and CD62E, while those in apoptosis CD31 and CD105. We investigated EMP release in vitro and in TTP patients. Following incubation of MVEC with TTP plasma, EMP and EC were analysed by flow cytometry for the expression of CD31, CD51, CD54, CD62E, CD105, CD106 and von Willebrand factor (VWF) antigen. EMP were also analysed in 12 TTP patients. In both EC and EMP, CD62E and CD54 expression were increased 3- to 10-fold and 8- to 10-fold respectively. However, CD31 and CD105 were reduced 40-60% in EC but increased twofold in EMP. VWF expression was found in 55 +/- 15% of CD62E(+) EMP. Markers of apoptosis were negative. In TTP patients, CD62E(+) and CD31(+)/CD42b(-) EMP were markedly elevated, and preceded and correlated well with a rise in platelet counts and a fall in lactate dehydrogenase. CD62E(+) EMP (60 +/- 20%) co-expressed VWF and CD62E. The ratio of CD31(+)/42b(-) to CD62E(+) EMP exhibited a pattern consistent with activation. In conclusion, our studies indicate endothelial activation in TTP. EMP that co-express VWF and CD62E could play a role in the pathogenesis of TTP.