WAVE技术及其在导弹总体结构研制上的应用

本文研究了UG/WAVE技术及其内涵,探讨了利用该技术建立产品模型的方法。以某弹体的开发过程为例,说明了采用WAVE技术,可以通过改变产品的整体参数控制整个产品及其零部件的自动更新,探讨了利用UG/WAVE技术建立自顶向下的产品设计模型的方法,及并行设计开发过程。     

UGNX／WAVE在FA702并纱机设计中的应用

介绍了FA702并纱机的结构和特点,对UGNX／WAVE技术的主要内容及其技术内涵进行了简要的阐述,并以FA702并纱机数字化样机设计为例,介绍了如何利用WAVE技术实现产品模型设计过程中的参数化设计方法。     

UG/WAVE技术及其应用

UG/WAVE技术可实现产品的控制结构与装配的并行设计，动态操纵复杂产品设计，自动更新零部件设计，防止重复设计，极大地提高了产品的设计效率，有利于企业效益的最大化。     

实现产品快速变型设计的关键技术研究

针对中小企业创新能力不足、设计效率低下的问题,面向产品快速变型设计需求,结合产品数字化快速设计系统研究、开发和应用经验,本文对数字化产品变型快速设计的关键技术——建立快速设计模板的QFD技术、模块化设计技术、GT技术、设计知识的表达技术、多驱动的设计实现的机制及相关的管理技术进行了总结、研究和探讨。     

相关参数化技术在组合机床总体设计中的研究和应用

为了提高组合机床总体设计的设计效率和质量,通过讨论WAVE技术的主要功能和应用范围,研究了WAVE技术在组合机床总体设计的实现过程和关键技术。并以孔加工组合机床为实例,提出了组合机床总体设计控制结构的建立和各功能模块的并行设计,实现了数据关联性的同时也保证了装配的准确性。     

基于NX的挖掘机斗杆参数化建模与强度仿真分析

为缩短挖掘机的设计周期,满足用户在设计中时常更新关键参数的需求,基于Siemens NX的PTS模块和WAVE功能,构建了大型挖掘机斗杆的可重用参数化设计模型;利用PTS和WAVE强大的交互操作功能实现了无代码的可重用系统的编制;最后通过动态强度的仿真验证了模型的可靠性。     

基于UG的冷冲模造型设计系统

针对冷冲压模具CAD系统的标准化程度较低、专用性不强、开发手段落后等问题,研究了参数化造型与特征建模基本理论及基于UG的标准件建库方法.构建了基于UG的冷冲模造型设计系统,应用UG二次开发技术建立了冷冲模标准件库和标准模具库,运用"自底向上"的方法进行冷冲模的装配设计.在模具零件设计造型过程中采用了UG WAVE技术.通过某汽车零件落料模的设计实例,验证了应用此冷冲模造型设计系统对提高模具设计效率、加强模具设计标准化具有重要意义.     

基于UG参数化和WAVE技术在变速器设计中的应用

本文通过变速器设计说明UG的参数化和WAVE相关性设计的应用。介绍参数化和WAVE相关性设计在提高设计速度和避免重复性修改中的作用。     

基于VC++的旋风分离器CAD系统开发

综合应用可视化技术、面向对象技术、ODBC教据库技术和三维绘图技术开发出旋风分离器CAD系统。建立了产品介绍、设计参数和设计结果数据库;阐述了产品介绍和参数化快速设计的设计方法;在SolidWorks平台下,建立三维参数化模型,利用设计结果数据库的数据建立系列零件列表,实现了旋风分离器的三维参数化快速绘图。     

反求与快速成型技术在模具制造中的应用

快速成型技术问世以来,已实现了相当大的市场。该技术通过与数控加工、铸造、金属冷喷涂、硅胶模等制造手段结合,已成为现代模型、模具和零件制造的强有力手段,在航空航天、汽车摩托车、家电等领域得到了广泛应用。本文从快速成型技术的基本原理出发,简述了产品快速设计与制造系统的基本结构、主要功能和构建方法,并通过实例探讨了产品快速设计与制造集成系统的上程应用。     

用多媒体技术实现随机信号的原理与实践

随机信号是宽频带随机激振方式的基础。在缺少宽频带随机信号发生器的情况下，本文将论述如何用软件方法实现随机信号发生器在Windows环境下，根据MicrosoftMultimediaKit提供的接口，用BorlandC ObjectWindowsLibrary[1]设计声音WAVE文件，并由EM88美王声卡输出随机信号。     

WAVE2 is required for directed cell migration and cardiovascular development

WAVE2, a protein related to Wiskott-Aldrich syndrome protein, is crucial for Rac-induced membrane ruffling, which is important in cell motility. Cell movement is essential for morphogenesis, but it is unclear how cell movement is regulated or related to morphogenesis. Here we show the physiological functions of WAVE2 by disruption of the WAVE2 gene in mice. WAVE2 was expressed predominantly in vascular endothelial cells during embryogenesis. WAVE2-/- embryos showed haemorrhages and died at about embryonic day 10. Deficiency in WAVE2 had no significant effect on vasculogenesis, but it decreased sprouting and branching of endothelial cells from existing vessels during angiogenesis. In WAVE2-/- endothelial cells, cell polarity formed in response to vascular endothelial growth factor, but the formation of lamellipodia at leading edges and capillaries was severely impaired. These findings indicate that WAVE2-regulated actin reorganization might be required for proper cell movement and that a lack of functional WAVE2 impairs angiogenesis in vivo.     

Phosphorylation of WAVE1 regulates actin polymerization and dendritic spine morphology

WAVE1--the Wiskott-Aldrich syndrome protein (WASP)--family verprolin homologous protein 1--is a key regulator of actin-dependent morphological processes in mammals, through its ability to activate the actin-related protein (Arp2/3) complex. Here we show that WAVE1 is phosphorylated at multiple sites by cyclin-dependent kinase 5 (Cdk5) both in vitro and in intact mouse neurons. Phosphorylation of WAVE1 by Cdk5 inhibits its ability to regulate Arp2/3 complex-dependent actin polymerization. Loss of WAVE1 function in vivo or in cultured neurons results in a decrease in mature dendritic spines. Expression of a dephosphorylation-mimic mutant of WAVE1 reverses this loss of WAVE1 function in spine morphology, but expression of a phosphorylation-mimic mutant does not. Cyclic AMP (cAMP) signalling reduces phosphorylation of the Cdk5 sites in WAVE1, and increases spine density in a WAVE1-dependent manner. Our data suggest that phosphorylation/dephosphorylation of WAVE1 in neurons has an important role in the formation of the filamentous actin cytoskeleton, and thus in the regulation of dendritic spine morphology.     

UG／WAVE技术在叠压夹具设计上的应用

介绍了UG／WAVE的基本功能和叠压央具的设计特点。探讨了运用系统工程和自顶向下的设计原则建立叠压夹具模型的步骤和方法，实现了叠压夹具的高效设计。     

Mechanism of regulation of WAVE1-induced actin nucleation by Rac1 and Nck

Rac signalling to actin -- a pathway that is thought to be mediated by the protein Scar/WAVE (WASP (Wiskott-Aldrich syndrome protein)-family verprolin homologous protein -- has a principal role in cell motility. In an analogous pathway, direct interaction of Cdc42 with the related protein N-WASP stimulates actin polymerization. For the Rac-WAVE pathway, no such direct interaction has been identified. Here we report a mechanism by which Rac and the adapter protein Nck activate actin nucleation through WAVE1. WAVE1 exists in a heterotetrameric complex that includes orthologues of human PIR121 (p53-inducible messenger RNA with a relative molecular mass (M(r)) of 140,000), Nap125 (NCK-associated protein with an M(r) of 125,000) and HSPC300. Whereas recombinant WAVE1 is constitutively active, the WAVE1 complex is inactive. We therefore propose that Rac1 and Nck cause dissociation of the WAVE1 complex, which releases active WAVE1-HSPC300 and leads to actin nucleation.     

IRSp53 is an essential intermediate between Rac and WAVE in the regulation of membrane ruffling

Neural Wiskott-Aldrich syndrome protein (N-WASP) functions in several intracellular events including filopodium formation, vesicle transport and movement of Shigella frexneri and vaccinia virus, by stimulating rapid actin polymerization through the Arp2/3 complex. N-WASP is regulated by the direct binding of Cdc42 (refs 7, 8), which exposes the domain in N-WASP that activates the Arp2/3 complex. A WASP-related protein, WAVE/Scar, functions in Rac-induced membrane ruffling; however, Rac does not bind directly to WAVE, raising the question of how WAVE is regulated by Rac. Here we demonstrate that IRSp53, a substrate for insulin receptor with unknown function, is the 'missing link' between Rac and WAVE. Activated Rac binds to the amino terminus of IRSp53, and carboxy-terminal Src-homology-3 domain of IRSp53 binds to WAVE to form a trimolecular complex. From studies of ectopic expression, we found that IRSp53 is essential for Rac to induce membrane ruffling, probably because it recruits WAVE, which stimulates actin polymerization mediated by the Arp2/3 complex.     

Structure and control of the actin regulatory WAVE complex

Members of the Wiskott-Aldrich syndrome protein (WASP) family control cytoskeletal dynamics by promoting actin filament nucleation with the Arp2/3 complex. The WASP relative WAVE regulates lamellipodia formation within a 400-kilodalton, hetero-pentameric WAVE regulatory complex (WRC). The WRC is inactive towards the Arp2/3 complex, but can be stimulated by the Rac GTPase, kinases and phosphatidylinositols. Here we report the 2.3-?ngstrom crystal structure of the WRC and complementary mechanistic analyses. The structure shows that the activity-bearing VCA motif of WAVE is sequestered by a combination of intramolecular and intermolecular contacts within the WRC. Rac and kinases appear to destabilize a WRC element that is necessary for VCA sequestration, suggesting the way in which these signals stimulate WRC activity towards the Arp2/3 complex. The spatial proximity of the Rac binding site and the large basic surface of the WRC suggests how the GTPase and phospholipids could cooperatively recruit the complex to membranes.