灰铸铁的应力屈服曲面及其三维热弹塑性应力解析

对原有的灰铸铁件应力屈服曲面进行了合理的简化,使其在理论上合理,工程应用上更为方便。建立了灰铸铁件三维非稳态热弹塑性应力场的有限元方法。以灰铸铁哑铃件为对象,用新屈服曲面对其应力发展过程进行了模拟,且比较了用新旧屈服面计算得到的结果。     

生长调节剂对大叶白蜡幼苗生长的影响

对一年生大叶白蜡实生苗用3种不同浓度的赤霉素（GA3）、ABT生根粉7号（ABT7）、萘乙酸（NAA）进行处理。结果表明，3种生长调节剂对大叶白蜡幼苗生长有明显的促进作用。处理后的苗木提高，生长加快，茎干增粗，叶片增大，抗性增强，其中以50mg/L的GA3作用最为显著。     

提高大型仪器设备利用率的新途径

大型仪器设备是高校开展教学、科研的物质保证,是高校实验室的主要技术装备,衡量一所高校办学实力和水平的重要指标之一.……     

Activation of a C. elegans Antennapedia homologue in migrating cells controls their direction of migration.

Anterior-posterior patterning in insects, vertebrates and nematodes involves members of conserved Antennapedia-class homeobox gene clusters (HOM-C) that are thought to give specific body regions their identities. The effects of these genes on region-specific body structures have been described extensively, particularly in Drosophila, but little is known about how HOM-C genes affect the behaviours of cells that migrate into their domains of function. In Caenorhabditis elegans, the Antennapedia-like HOM-C gene mab-5 not only specifies postembryonic fates of cells in a posterior body region, but also influences the migration of mesodermal and neural cells that move through this region. Here we show that as one neuroblast migrates into this posterior region, it switches on mab-5 gene expression; mab-5 then acts as a developmental switch to control the migratory behaviour of the neuroblast descendants. HOM-C genes can therefore not only direct region-specific patterns of cell division and differentiation, but can also act within migrating cells to programme region-specific migratory behaviour.     

多变量自校正控制计算机辅助设计软件系统

本文介绍了一个可帮助用户进行多变量自校正控制系统设计,而使用户不必了解算法细节的计算机辅助设计(CAD)软件系统;它既包括一些经典的自校正控制算法,又引入了一些近年来新研究的成果。使用情况表明,该系统算法先进,使用方便,控制效果较好,是一个实用的软件工具。     

协商理论简介

本文对协商问题的研究,特别对其与经济理论的联系作了一个简要的说明,重点按照公理形式探讨了协商理论的发展及其成果,并对协商问题在多人情形下的推广和关于协商问题风险性分析等都作了一些介绍。本文还对策略形式探索协商理论的主要发展“轮廓”作了描述。对有关协商理论各分支的研究现状和动态亦作了些评述。     

Resistant orthogonal procrustes analysis

In this paper two alternative loss criteria for the least squares Procrustes problem are studied. These alternative criteria are based on the Huber function and on the more radical biweight function, which are designed to be resistant to outliers. Using iterative majorization it is shown how a convergent reweighted least squares algorithm can be developed. In asimulation study it turns out that the proposed methods perform well over a specific range of contamination. When a uniform dilation factor is included, mixed results are obtained. The methods also yield a set of weights that can be used for diagnostic purposes.     

Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.     

Retrograde transport of endocytosed Shiga toxin to the endoplasmic reticulum.

Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol.