AR参数灵敏度及结构损伤控制图识别

推导了时间序列模型的自回归参数对结构单元刚度损伤系数的灵敏度方程,并对该方程的正确性进行了验证。分析了自回归参数的灵敏度特性,在此基础上采用控制图进行结构损伤识别。该方法首先以结构在随机作用下的时域响应进行主成分分析;然后以第一主元建立适用阶的时序模型;最后以自回归参数建立休哈特控制图,通过自回归参数的统计性变化判断结构是否发生损伤。针对一梁结构,试验验证了控制图用于损伤识别的有效性和可行性。     

微控制器静态时序分析方法研究

静态时序分析方法不依赖于激励,且可以穷尽所有路径,运行速度很快,占用内存很少,克服了动态时序验证的缺陷.我们探讨了时序路径、路径延迟、时序约束等问题,重点研究了多周期路径造成的时序异常排除方法,并用静态时序分析工具Primetime对微控制器软核HGD08R01进行了案例分析,获得了满意的效果.     

特大型零件热态成形制造技术基础研究

在中国国家自然科学基金重点项目《特大件成形制造技术基础研究》、国家科技支撑计划课题《大型轧机共性技术》、国家重点基础研究发展计划(973计划)前期研究专项《大型零件热态成形制造虚拟技术基础研究》,以及中国河北省科技攻关项目《大型轧机共性技术》和《特大件成形制造技术基础研究》共同资助下,以大型锻钢轧辊(辊身直径超过1 000 mm或质量大于100 t)为对象,通过宏观 微观强耦合建模,解决铸造缺陷信息遗传、孔洞锻合条件、形变焊合条件、材料断裂准则构建,以及热 力 微观组织耦合建模等关键技术问题,建立以淬硬层深度数值预测技术为核心的热处理工艺分析与优化系统,提出基于非均质轧辊辊间接触力学模型的轧辊强度设计方法,构建起大型锻钢轧辊热态成形制造与服役评估的多学科耦合决策支持理论体系,提出理论研究报告。针对缩孔和气孔等大型铸钢锭铸造中的孔洞缺陷控制,以大锻件内部孔洞锻造闭合过程为科学问题,以大锻件内部有效锻合区域数值预测为目标,将有限元方法与人工神经网络技术相结合,利用神经网络的非线性映射能力,描述材料变形抗力、温度、应力应变与孔洞闭合程度之间的复杂关系,将孔洞锻合过程有限元模拟结果作为神经网络训练样本,建立起温度、应力和变形等多场耦合作用下的孔洞锻合条件模型(VCCM)。针对孔洞形变焊合机理与物理模拟模型一致性问题,以消除大锻件心部残留微孔隙,实现物理闭合状态下的锻合孔洞缺陷的真正冶金结合为目标,基于临界闭合孔洞界面接触力学原型和原子高温扩散理论,以界面接触应变和高温环境作为孔洞焊合的驱动力,利用高温和大变形对闭合孔洞界面扩散焊合的有利影响,提出适用于大锻件在锻造成形阶段的内部孔洞缺陷形变的形变焊合方法,通过物理模拟实     

Experimental Investigation and Thermodynamic Description of the Cu-Zr System

The Cu-Zr binary system is re-investigated via experiment and thermodynamic modeling. Four alloys were prepared by arc melting in order to check the controversial phase equilibria reported in the literature. Both as-cast and annealed alloys were examined by optical microscopy, x-ray diffraction and electron probe microanalysis, and the phase transformation temperatures were measured by differential scanning calorimetry. The intermetallic compounds, Cu₂₄Zr₁₃, Cu₂Zr and Cu₅Zr₈, were demonstrated to be not the stable phases. Based on the literature information and present experimental data, the Cu-Zr system was critically evaluated by means of CALculation of PHAse Diagram approach. A set of self-consistent thermodynamic parameters was obtained, and the calculated phase diagram and thermodynamic properties are in a satisfactory agreement with the experimental data.     

Endometrial Epithelial ARID1A Is Required for Uterine Immune Homeostasis during Early Pregnancy

A growing body of work suggests epigenetic dysregulation contributes to endometriosis pathophysiology and female infertility. The chromatin remodeling complex subunit AT-rich interaction domain 1A (ARID1A) must be properly expressed to maintain normal uterine function. Endometrial epithelial ARID1A is indispensable for pregnancy establishment in mice through regulation of endometrial gland function; however, ARID1A expression is decreased in infertile women with endometriosis. We hypothesized that ARID1A performs critical operations in the endometrial epithelium necessary for fertility besides maintaining gland function. To identify alterations in uterine gene expression resulting from loss of epithelial ARID1A, we performed RNA-sequencing analysis on pre-implantation uteri from Ltf^iCre/+Arid1a^f/f and control mice. Differential expression analysis identified 4181 differentially expressed genes enriched for immune-related ingenuity canonical pathways including agranulocyte adhesion and diapedesis and natural killer cell signaling. RT-qPCR confirmed an increase in pro-inflammatory cytokine and macrophage-related gene expression but a decrease in natural killer cell signaling. Immunostaining confirmed a uterus-specific increase in macrophage infiltration. Flow cytometry delineated an increase in inflammatory macrophages and a decrease in uterine dendritic cells in Ltf^iCre/+Arid1a^f/f uteri. These findings demonstrate a role for endometrial epithelial ARID1A in suppressing inflammation and maintaining uterine immune homeostasis, which are required for successful pregnancy and gynecological health.     

Cytokinin Confers Brown Planthopper Resistance by Elevating Jasmonic Acid Pathway in Rice

Plants have evolved a sophisticated defense system that employs various hormone pathways to defend against attacks by insect pests. Cytokinin (CK) plays an important role in plant growth and stress tolerance, but the role of CKs in plant–insect interaction remains largely unclear. Here, we report that CKs act as a positive regulator in rice resistance against brown planthopper (BPH), a devastating insect pest of rice. We found that BPH feeding promotes CK biosynthesis and signaling in rice. Exogenous application of CKs significantly increased the rice resistance to BPH. Increasing endogenous CKs by knocking out cytokinin oxidase/dehydrogenase (OsCKXs) led to enhanced resistance to BPH. Moreover, the levels of the plant hormone jasmonic acid (JA) and the expression of JA-responsive genes were elevated by CK treatment and in OsCKXs knockout plants. Furthermore, JA-deficient mutant og1 was more susceptible to BPH, and CK-induced BPH resistance was suppressed in og1. These results indicate that CK-mediated BPH resistance is JA-dependent. Our findings provide the direct evidence for the novel role of CK in promoting insect resistance, and demonstrate that CK-induced insect resistance is JA-dependent. These results provide important guidance for effective pest management strategies in the future.     

Podocyte-Related Mechanisms Underlying Survival Benefit of Long-Term Angiotensin Receptor Blocker

We previously found that short-term treatment (week 8 to 12 after injury) with high-dose angiotensin receptor blocker (ARB) induced the regression of existing glomerulosclerosis in 5/6 nephrectomy rats. We therefore assessed the effects of long-term intervention with ARB vs. nonspecific antihypertensives in this study. Adult rats underwent 5/6 nephrectomy and renal biopsy 8 weeks later. The rats were then divided into three groups with equivalent renal function and glomerular sclerosis and treated with high-dose losartan (ARB), nonspecific antihypertensive triple-therapy (TRX), or left untreated (Control) until week 30. We found that blood pressure, serum creatinine levels, and glomerulosclerosis were lower at sacrifice in ARB and TRX vs. Control. Only ARB reduced proteinuria and maintained the density of WT-1-positive podocytes. Glomerular tufts showed more double-positive cells for CD44, a marker of activated parietal epithelial cells, and synaptopodin after ARB vs. TRX or Control. ARB treatment reduced aldosterone levels. ARB-treated rats had significantly improved survival when compared with TRX or Control. We conclude that both long-term ARB and triple-therapy ameliorate progression, but do not sustain the regression of glomerulosclerosis. ARB resulted in the superior preservation of podocyte integrity and decreased proteinuria and aldosterone, linked to increased survival in the uremic environment.