原发性高血压病靶器官损害的预测仿真研究

研究原发性高血压病靶器官损害准确预测问题,由于原发性高血压病靶器官损害的影响因子之间存在着高度冗余和非线性,导致传统方法预测准确率低,为提高预测精度,构建了一种改进的基因表达式编程算法的原发性高血压病靶器官损害预测模型,首先设计了适合靶器官损害预测的适应度函数,然后为克服早熟现象提出了以平均适应度形式自适应的改变重组算子概率和变异算子概率,通过数据训练得到靶器官损害的2年预测模型。采用对山东中医药大学第二附属医院原发性高血压病历史数据进行验证性仿真,结果表明,方法的预测精度更高,在原发性高血压病靶器官损害的预测中有着广泛的应用前景。     

Surface characterization of 6H-SiC (0001) substrates in indentation and abrasive machining

Surface characterization of 6H-SiC (0001) substrates in indentation and abrasive machining was carried out to investigate microfracture, residual damage, and surface roughness associated with material removal and surface generation. Brittle versus plastic deformation was studied using Vickers indention and nano-indentation. To characterize the abrasive machining response, the 6H-SiC (0001) substrates were ground using diamond wheels with grit sizes of 25, 15 and 7 μm, and then polished with diamond suspensions of 3 and 0.05 μm. It is found that in indentation, there was a scale effect for brittle versus plastic deformation in 6H-SiC substrates. Also, in grinding, the scales of fracture and surface roughness of the substrates decreased with a decrease in diamond grit size. However, in polishing, a reduction in grit size of diamond suspensions gave no significant improvement in surface roughness. Furthermore, the results showed that fracture-free 6H-SiC (0001) surfaces were generated in polishing with the existence of the residual crystal defects, which were associated with the origin of defects in single crystal growth.     

长期高温服役的12%Cr耐热合金钢性能退化与恢复

X2 0CrMoV12 1耐热合金钢广泛应用于热电厂主蒸汽管线等主要部件。经长期高温负荷运行后 ,材料性能明显退化。观察显微组织发现 ,材料性能下降是和晶界碳化物的粗化密切相关的。文章着重研究了损伤材料重新热处理后的性能和组织结构的变化 ,初步探讨了材料长期服役后通过热处理恢复其原始性能的可能性     

金属板材成形中拉深损伤模拟的两种求解方法

讨论用数值模拟预测板材成形中发生拉深损伤破坏的两种不同的求解方法。第一种是采用完全耦合的弹塑性破坯模型的动力显式数值方法。基于状态参量的不可逆热力学过程 ,完全耦合的本构方程考虑各向同性强化和拉深。这些已引入有限元软件ABAQUS/E用于对金属成形的模拟。在数值技术方面 ,隐式积分方法被用来对本构方程的局部时间积分 ,动力显式技术用于求解总体平衡方程。第二种方案是采用简化的损伤模型的方法 ,被称为逆法 (InveseApprch)。I.A被限定在考虑各向同性强化和损伤的塑性全量理论基础上的简单的本构关系。做比例加载和临界损伤达到以后的损伤饱和假定 ,可以得到损伤演化方程的封闭解。这两种损伤模型在编程中的实施采用两种方式 :计算中考虑或不考虑损伤作用 ,也就是耦合的或非耦合的计算。文中给出一些算例来说明每种损伤模型的优点     

桥梁健康监测中损伤特征提取的小波包方法

针对桥梁健康监测中结构损伤识别的特点,从模式识别的角度提出和分析了损伤特征提取问题.阐述了基于小波包分析的两种节点能量特征提取的方法.为了研究小波包系数节点能量和小波包信号成分节点能量对损伤信息进行特征提取的差异,通过对随机荷载激励下的连续梁进行数值模拟,得到了结构未损和损伤状态下的加速度时程信号.应用小波包变换,对不同结构状态下的加速度信号分别提取了两种小波包节点能量特征,并对它们作为结构损伤特征指标的敏感性进行了比较.认为两种特征指标的敏感性相差很小,而小波包系数节点能量特征指标的计算效率更高,更适合桥梁健康监测中损伤特征提取的要求.     

Role of TRPA1 in Tissue Damage and Kidney Disease

TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation.     

高纯Fe中氢损伤规律的研究

本文采用正电子湮没技术研究了高纯Fe中的氢损伤规律,实验结果表明,在0.5mol/L H_2SO_4溶液中不加毒化剂电解充氢时,产生氢损伤的临界电流密度为20 mA/cm~2;而在0.5mol/L H_2SO_4溶液中加少量As_2O_3作为毒化剂电解充氢时,即使很小的电流密度也会产生氢损伤,配合慢拉伸试验,还发现试样内部产生氢损伤以后,它将控制随后的形变和断裂过程     

Grain-size effects in the quasi-static fracture resistance of a thermally embrittled RPV steel (quenched and tempered microstructures)

The elastic-plastic fracture toughness and crack extension behavior under the quasi-static loading regimen of several thermally embrittled conditions of a nuclear reactor pressure vessel (RPV) steel were assessed on the basis of microstructural parameters. It was discovered that the bainite packet size is the fracture properties controlling parameter of single-phase quenched and tempered microstructures. Results were found in close agreement to those obtained in a parallel study with dual-phase annealed microstructures derived from the same low alloy steel. Similarly, it was concluded that a Hall-Petch type relationship correlates J-fracture mechanics criteria to the grain size.     

辐照损伤对锆合金电化学性能的影响

综述了堆内辐照对锆合金电化学性能影响的概况，浅析了堆内辐照损伤的机理，并重点探讨了主要的堆内辐照源——中子辐照对锆合金微观结构与氧化性能的影响。进一步阐述了堆外离子轰击模拟堆内中子辐照研究方法的进展概况，并就离子轰击实验参量的选择进行了较为深入的分析。     

2—甲基—1，4—萘醌对DNA光敏损伤的诱导作用

选择波长337nm的激光作为激励光源，借助凝胶电泳研究了2－甲基－1，4－萘醌诱导的DNA光敏损伤。结果表明：在氧气饱和、脱氧条件下光敏损伤显著，DNA损伤主要与光子剂量、核酸与萘醌浓度比及DNA存在形式有关。