基于SIMULINK的Fuzzy-PID控制器设计

设计了一种Fuzzy-PID控制算法，利用MATLAB的SIMULINK进行仿真研究，结果表明，该控制器具有较强的抗干扰能力和鲁棒性，有较好的动、静态控制精度．     

双曲型叶片的数控加工模型研究

给出双曲型点构成的叶片工作面的解析方程,并用主曲率方法给出了刀具参数、数控加工中的步长和行距的定量计算模型,最后用等螺距叶片工作面算例验证本文所供方法不但确保了叶片工作面造型精度,而且大大地提高了加工效率．     

数位时代图书馆馆员专业知能发展之研究——以逢甲大学为例

受到资讯媒体新科技影响 ,图书馆读者使用行为已从单一的馆藏利用 ,转为期望图书馆提供更多元化的服务 ;另外在财政紧缩 资源扩增 人力不足等因素下 ,图书馆提供各类型服务的运作模式也受到相当的冲击 ,图书馆为提供以读者为道向的服务 ,必需付出许多努力并改变服务哲学 ,因而图书馆馆员的专业知能发展要不断提升才能因应数位时代的环境改变 ,并提供读者一个优质的资讯服务 ,发挥图书馆LearningResourceCenter学习资源中心的角色 .本研究主要探讨图书馆如何在有限资源下 ,有系统地规划发展馆员专业知能 ,并且利用那一种方法可以最有效率、花费最少成本达到最大的馆员能力提升效果 ,根据文献探讨以及学习行为方法理论 ,提出一个适合发展馆员专业知能的模式 (Approachmodel) ,通过探讨逢甲大学图书馆的两个专案其馆员专业知能转变的历程 ,检视了此发展模式的成效 ,并提出未来该模式可再改进的方向及建议     

For whom the bell tolls? DING proteins in health and disease

DING proteins, identified mainly by their eponymous N-terminal sequences, are ubiquitous in living organisms. Amongst bacteria, they are common in pseudomonads, and have been characterised with respect to genetics and structure. They form part of a wider family of phosphate-binding proteins, with emerging roles in phosphate acquisition and pathogenicity. Many DING proteins have been isolated in eukaryotes, in which they have been associated with very diverse biological activities, often in the context of possible signalling roles. Disease states in which DING proteins have been implicated include rheumatoid arthritis, lithiasis, atherosclerosis, some tumours and tumour-associated cachexia, and bacterial and viral adherence. Complete genetic and structural characterisation of eukaryotic DING genes and proteins is still lacking, though the phosphate-binding site seems to be conserved. Whether as bacterial proteins related to bacterial pathogenicity, or as eukaryotic components of biochemical signalling systems, DING proteins require further study. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

The Rab8 GTPase regulates apical protein localization in intestinal cells

A number of proteins are known to be involved in apical/basolateral transport of proteins in polarized epithelial cells. The small GTP-binding protein Rab8 was thought to regulate basolateral transport in polarized kidney epithelial cells through the AP1B-complex-mediated pathway. However, the role of Rab8 (Rab8A) in cell polarity in vivo remains unknown. Here we show that Rab8 is responsible for the localization of apical proteins in intestinal epithelial cells. We found that apical peptidases and transporters localized to lysosomes in the small intestine of Rab8-deficient mice. Their mislocalization and degradation in lysosomes led to a marked reduction in the absorption rate of nutrients in the small intestine, and ultimately to death. Ultrastructurally, a shortening of apical microvilli, an increased number of enlarged lysosomes, and microvillus inclusions in the enterocytes were also observed. One microvillus inclusion disease patient who shows an identical phenotype to Rab8-deficient mice expresses a reduced amount of RAB8 (RAB8A; NM_005370). Our results demonstrate that Rab8 is necessary for the proper localization of apical proteins and the absorption and digestion of various nutrients in the small intestine.     

一种新型高速码垛机械手的设计与实现

针对包装袋规格和码垛技术要求,提出一种新型的高速码垛机械手的设计方案.该方案采用气压驱动,并通过手指开合机构、侧板夹紧机构和压袋机构,实现包装袋的可靠抓包、搬运和码放等动作.在此基础上,通过详细分析与计算,完成了该机械手的结构设计,并在Pro/E平台中建立了该机械手的三维CAD模型.对该机械手的动作规划、动力学计算以及气动系统等问题进行了分析与研究.仿真结果表明,该机械手能够在规定的时间内完成规定动作.     

Local charge of the ν = 5/2 fractional quantum Hall state

Electrons moving in two dimensions under the influence of strong magnetic fields effectively lose their kinetic energy and display exotic behaviour dominated by Coulomb forces. When the ratio of electrons to magnetic flux quanta in the system (ν) is near 5/2, the electrons are predicted to condense into a correlated phase with fractionally charged quasiparticles and a ground-state degeneracy that grows exponentially as these quasiparticles are introduced. The only way for electrons to transform between the many ground states would be to braid the fractional excitations around each other. This property has been proposed as the basis of a fault-tolerant quantum computer. Here we present observations of localized quasiparticles at ν = 5/2, confined to puddles by disorder. Using a local electrometer to compare how quasiparticles at ν = 5/2 and ν = 7/3 charge these puddles, we were able to extract the ratio of local charges for these states. Averaged over several disorder configurations and samples, we found the ratio to be 4/3, suggesting that the local charges are = e/3 and = e/4, where e is the charge of an electron. This is in agreement with theoretical predictions for a paired state at ν = 5/2. Confirming the existence of localized e/4 quasiparticles shows that proposed interferometry experiments to test statistics and computational ability of the state at ν = 5/2 would be possible.     

New Sclerocactus (Cactaceae) from Nevada

Named as new is Sclerocactus schlesseri Heil & Welsh. The taxon is described and its relationships discussed.     

Fbxw7/Cdc4 is a p53-dependent, haploinsufficient tumour suppressor gene

The FBXW7/hCDC4 gene encodes a ubiquitin ligase implicated in the control of chromosome stability. Here we identify the mouse Fbxw7 gene as a p53-dependent tumour suppressor gene by using a mammalian genetic screen for p53-dependent genes involved in tumorigenesis. Radiation-induced lymphomas from p53+/- mice, but not those from p53-/- mice, show frequent loss of heterozygosity and a 10% mutation rate of the Fbxw7 gene. Fbxw7+/- mice have greater susceptibility to radiation-induced tumorigenesis, but most tumours retain and express the wild-type allele, indicating that Fbxw7 is a haploinsufficient tumour suppressor gene. Loss of Fbxw7 alters the spectrum of tumours that develop in p53 deficient mice to include a range of tumours in epithelial tissues such as the lung, liver and ovary. Mouse embryo fibroblasts from Fbxw7-deficient mice, or wild-type mouse cells expressing Fbxw7 small interfering RNA, have higher levels of Aurora-A kinase, c-Jun and Notch4, but not of cyclin E. We propose that p53-dependent loss of Fbxw7 leads to genetic instability by mechanisms that might involve the activation of Aurora-A, providing a rationale for the early occurrence of these mutations in human cancers.