排序方式: 共有46条查询结果,搜索用时 109 毫秒
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提出了基于预埋压力传感器的量化测试方法,研究了螺栓松动边界对纤维增强复合薄板振动特性的影响。首先,自主设计并开发了带有预埋压力传感器的螺栓松动边界下复合薄板的振动测试系统,并详细介绍了系统各个部件的组成和功能;然后,归纳出一套合理、规范的松动边界下复合薄板的振动测试流程,并对HF10碳纤维/树脂复合薄板进行了实际测试。结果表明:随着螺栓松动程度的不断增加,复合薄板的固有频率逐渐降低,模态振型的节线位置也发生了不同程度的变化,但其阻尼结果呈现先增大后减小的趋势;而共振和非共振响应呈现先减小后增大的趋势。 相似文献
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宽厚板厂房的行车轨道在行车运行时承受来自行车水平导向轮的水平推力,该水平推力可能导致压轨器破坏,为确保压轨器的安全设计,采用平面光弹性、三维光弹性进行实验测试,分析在最不利工况下,各种压轨器所承担的水平推力份额,压轨器的变形和应力分布,给出强度分析评估,确定系统中各个压轨器以及固定螺栓的关键部位的应力水平。 相似文献
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针对精细化模型与Abaqus摩擦模型所存在问题, 提出一种基于螺纹几何特征的螺旋线螺纹模型, 采用脚本语言实现了螺旋线螺纹模型生成自动化, 并应用到某发动机机体主轴承盖螺栓螺孔的强度分析. 分析结果表明, 仿真计算得到的螺栓及机体螺孔处的应力很好地表征了螺栓连接结构螺纹处的实际应力分布, 与螺纹精细模型相近, 比Abaqus摩擦模型精度更高, 且计算方便、实用、高效, 验证了本文方法的准确、可行. 相似文献
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提出了一种基于几何特征的正六边形检测方法。在简述Hough变换原理和正六边形特点的基础上,把正六边形的检测分解成直线和圆的检测,以及线段长度和直线夹角的计算。利用检测到的直线,在图像平面内建立直线方程,依据直线方程,计算相邻两条直线的夹角和交点,求出每条边的长度,同时检测6个交点是否均匀分布在同一圆周上。在螺栓头部正六边形检测实验中,角度测量误差为0.38%,边长测量误差为0.85%。结果表明,该方法是有效的,能准确地检测出图像中的正六边形。 相似文献
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Josef Malík 《Applications of Mathematics》1998,43(6):413-438
The main goal of the paper is to give a variational formulation of the behaviour of bolt systems in rock mass. The problem arises in geomechanics where bolt systems are applied to reinforce underground openings by inserting steel bars or cables. After giving a variational formulation, we prove the existence and uniqueness and some other properties. 相似文献
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Ozawa E 《Proceedings of the Japan Academy. Series B, Physical and biological sciences》2010,86(8):798-821
In 1987, about 150 years after the discovery of Duchenne muscular dystrophy (DMD), its responsible gene, the dystrophin gene, was cloned by Kunkel. This was a new substance. During these 20 odd years after the cloning, our understanding on dystrophin as a component of the subsarcolemmal cytoskeleton networks and on the pathomechanisms of and experimental therapeutics for DMD has been greatly enhanced. During this paradigm change, I was fortunately able to work as an active researcher on its frontiers for 12 years. After we discovered that dystrophin is located on the cell membrane in 1988, we studied the architecture of dystrophin and dystrophin-associated proteins (DAPs) complex in order to investigate the function of dystrophin and pathomechanism of DMD. During the conduct of these studies, we came to consider that the dystrophin-DAP complex serves to transmembranously connect the subsarcolemmal cytoskeleton networks and basal lamina to protect the lipid bilayer. It then became our working hypothesis that injury of the lipid bilayer upon muscle contraction is the cause of DMD. During this process, we predicted that subunits of the sarcoglycan (SG) complex are responsible for respective types of DMD-like muscular dystrophy with autosomal recessive inheritance. Our prediction was confirmed to be true by many researchers including ourselves. In this review, I will try to explain what we observed and how we considered concerning the architecture and function of the dystrophin-DAP complex, and the pathomechanisms of DMD and related muscular dystrophies. 相似文献
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