水泥砂浆的率型损伤演化

实验结果表明,水泥砂浆在受力变形中的损伤演化是率相关的,因此,类似于位错运动的热激活机制;给出了水泥砂浆的率型损伤演化律．     

夹杂物问题应力场的数值计算

等效夹杂物方法是细观力学中的一种重要方法，文中编制的数值计算程序能在考虑多个夹杂物相互响应的情况下计算材料应力、应变场，并实现了计算结果的三维显示．计算结果与文献中的计算结果非常吻合．本文编制的数值计算程序不仅可以用于研究复合材料的损伤演化及失效，而且利用特殊构型的椭球空洞来模拟裂纹，可以计算裂纹群的应力、应变场。     

产品易碎性的评定—理论和试验方法

本文以冲击谱为基础探讨了评定产品易损性的理论及其试验方法,给出了产品损坏边界曲线的形成理论,从而为进行产品的运输缓冲包装设计提供了基础。     

基于溶剂热反应快速沉积ZrO_2-基激光光学薄膜

基于丙醇锆-乙酸-乙醇混合体系的溶剂热反应（423 K,10 h）合成了稳定的ZrO2-基溶胶,采用旋转镀膜技术在K9玻璃基片上制备了ZrO2-基光学薄膜。借助动态光散射、傅里叶变换红外光谱、原子力显微镜、紫外/可见/近红外透射光谱、FilmTMTek 3000型薄膜分析仪以及强激光辐照实验对溶胶与薄膜的微观结构及光学性能进行表征。研究发现,通过与溶剂乙醇的酯化反应和与丙醇锆的配合反应,乙酸具有温和地提供反应水和降低丙醇锆水解活性的双重作用。在各工艺参数适当配置的情况下,采用该方法可以快速合成颗粒流体力学直径为10 nm~15 nm的溶胶,由此沉积的薄膜具有平整的表面、较高的折射率1.633（测试波长为632 nm）和高的激光损伤阈值34.7 J/cm2（激光波长为1 064 nm,脉冲宽度为3 ns,＂R/1＂测试模式）。     

世界核电设备与结构将长期面临的一个问题--微动损伤

核电设备至仍面临许多不易解决的问题,经过对核电和结构部件多例事故的分析可知,核电设备中微动是不可避免的现象,核能工程中的相当一部分结构损伤事故与和微动损伤有着直接的关系;在反应力集中,腐蚀部位,微动又是许多核电设备提前损伤失效的直接原因。     

碾压混凝土拱坝诱导缝损伤开裂准则研究

混凝土宏观裂缝失稳扩展前 ,裂缝前缘存在较大范围的损伤区 ,使得线弹性断裂判据失效。本文采用虚拟裂缝模型和连续损伤力学方法 ,计算了断裂过程区的长度和损伤度。根据碾压混凝土拱坝诱导缝构造特点 ,分别将诱导缝简化为穿透形裂缝和椭圆形裂缝 ,应用双K断裂准则 ,计算了诱导缝起始扩展和失稳扩展时的等效损伤度和等效应变 ,建立了碾压混凝土拱坝诱导缝的损伤开裂准则     

GaN中质子辐照损伤的分子动力学模拟研究

本文利用分子动力学方法研究了GaN在质子辐照下的损伤。对不同能量（1~10 keV）初级离位原子（PKA）引起的级联碰撞进行了研究,分析了点缺陷与PKA能量的关系、点缺陷随时间的演化规律、点缺陷的空间分布及点缺陷团簇的尺寸特征。研究结果表明,点缺陷的产生与PKA能量呈线性关系,不同类型的点缺陷随时间演化规律相似,点缺陷多产生在PKA径迹旁,点缺陷团簇多为孤立的点缺陷和小团簇。     

振动功率流方法诊断梁的损伤

利用振动功率流方法对无限直梁在集中力作用下的损伤进行了诊断研究。损伤部位模拟为转动弹簧,利用断裂力学的有关理论得到其转动刚度。研究了梁在集中载荷作用下的弯曲波运动以及振动功率流的输入和传播,分析了振动功率流与破损位置及其特征尺寸的关系。首先从理论上研究了破损诊断的具体步骤,然后进行了实验研究,结果证明了理论分析的准确性和可靠性。     

Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases MUTYH and hOGG1 in Colorectal Cancer Patients

Oxidative stress, oxidative DNA damage and resulting mutations play a role in colorectal carcinogenesis. Impaired equilibrium between DNA damage formation, antioxidant status, and DNA repair capacity is responsible for the accumulation of genetic mutations and genomic instability. The lesion-specific DNA glycosylases, e.g., hOGG1 and MUTYH, initiate the repair of oxidative DNA damage. Hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome) with germline mutations causing a loss-of-function in base excision repair glycosylases, serve as straight forward evidence on the role of oxidative DNA damage and its repair. Altered or inhibited function of above glycosylases result in an accumulation of oxidative DNA damage and contribute to the adenoma-adenocarcinoma transition. Oxidative DNA damage, unless repaired, often gives rise G:C > T:A mutations in tumor suppressor genes and proto-oncogenes with subsequent occurrence of chromosomal copy-neutral loss of heterozygosity. For instance, G>T transversions in position c.34 of a KRAS gene serves as a pre-screening tool for MUTYH-associated polyposis diagnosis. Since sporadic colorectal cancer represents more complex and heterogenous disease, the situation is more complicated. In the present study we focused on the roles of base excision repair glycosylases (hOGG1, MUTYH) in colorectal cancer patients by investigating tumor and adjacent mucosa tissues. Although we found downregulation of both glycosylases and significantly lower expression of hOGG1 in tumor tissues, accompanied with G>T mutations in KRAS gene, oxidative DNA damage and its repair cannot solely explain the onset of sporadic colorectal cancer. In this respect, other factors (especially microenvironment) per se or in combination with oxidative DNA damage warrant further attention. Base excision repair characteristics determined in colorectal cancer tissues and their association with disease prognosis have been discussed as well.     

Multiplexed-Based Assessment of DNA Damage Response to Chemotherapies Using Cell Imaging Cytometry

The current methods for measuring the DNA damage response (DDR) are relatively labor-intensive and usually based on Western blotting, flow cytometry, and/or confocal immunofluorescence analyses. They require many cells and are often limited to the assessment of a single or few proteins. Here, we used the Celigo^® image cytometer to evaluate the cell response to DNA-damaging agents based on a panel of biomarkers associated with the main DDR signaling pathways. We investigated the cytostatic or/and the cytotoxic effects of these drugs using simultaneous propidium iodide and calcein-AM staining. We also describe new dedicated multiplexed protocols to investigate the qualitative (phosphorylation) or the quantitative changes of eleven DDR markers (H2AX, DNA-PKcs, ATR, ATM, CHK1, CHK2, 53BP1, NBS1, RAD51, P53, P21). The results of our study clearly show the advantage of using this methodology because the multiplexed-based evaluation of these markers can be performed in a single experiment using the standard 384-well plate format. The analyses of multiple DDR markers together with the cell cycle status provide valuable insights into the mechanism of action of investigational drugs that induce DNA damage in a time- and cost-effective manner due to the low amounts of antibodies and reagents required.