线性系统的H2/H-故障检测优化方法设计

针对一类具有未知扰动的线性系统的故障检测(FD)问题,通过对系统进行重构,设计出了系统的H2/H-优化FD观测器。利用构造的Lyapunov函数和线性矩阵不等式,证明并给出了FD观测器有解的充分条件和优化设计方法。所设计的观测器使系统具有渐近稳定性,抑制干扰能力强,满足所给的范数指标。仿真结果验证了所设计方法的有效性。     

锻造质量对冷挤压模具寿命的影响

通过改变锻造方法，观察金相组织及模具现场试用，探讨锻造质量对高速钢及基体钢模具寿命的影响，结果表明：控制碳化物不均匀性在三级以内及合理的纤维流线分布，可显著提高引进冷挤压设备上的模具寿命。     

Hesperidin Promotes Osteogenesis and Modulates Collagen Matrix Organization and Mineralization In Vitro and In Vivo

This study evaluated the direct effect of a phytochemical, hesperidin, on pre-osteoblast cell function as well as osteogenesis and collagen matrix quality, as there is little known about hesperidin’s influence in mineralized tissue formation and regeneration. Hesperidin was added to a culture of MC3T3-E1 cells at various concentrations. Cell proliferation, viability, osteogenic gene expression and deposited collagen matrix analyses were performed. Treatment with hesperidin showed significant upregulation of osteogenic markers, particularly with lower doses. Mature and compact collagen fibrils in hesperidin-treated cultures were observed by picrosirius red staining (PSR), although a thinner matrix layer was present for the higher dose of hesperidin compared to osteogenic media alone. Fourier-transform infrared spectroscopy indicated a better mineral-to-matrix ratio and matrix distribution in cultures exposed to hesperidin and confirmed less collagen deposited with the 100-µM dose of hesperidin. In vivo, hesperidin combined with a suboptimal dose of bone morphogenetic protein 2 (BMP2) (dose unable to promote healing of a rat mandible critical-sized bone defect) in a collagenous scaffold promoted a well-controlled (not ectopic) pattern of bone formation as compared to a large dose of BMP2 (previously defined as optimal in healing the critical-sized defect, although of ectopic nature). PSR staining of newly formed bone demonstrated that hesperidin can promote maturation of bone organic matrix. Our findings show, for the first time, that hesperidin has a modulatory role in mineralized tissue formation via not only osteoblast cell differentiation but also matrix organization and matrix-to-mineral ratio and could be a potential adjunct in regenerative bone therapies.     

Study on diffusion welding SiCp/ZL101 with Cu interlayer

Through the vacuum diffusion welding SiCp/ZL101 aluminum with Cu interlayer,the effect of welding parame-ter and the thickness of Cu on the welded joint property was investigated,and the optimal welding parameters were putforward at the same time.The microstructure of joint was analyzed by means of optical-microscope,scanning electron mi-croscope in order to study the relationship between the macro-properties of joint and the microstructure.The results showthat diffusion welding with Cu interlayer could be used for welding aluminum matrix composites SiCp/ZL101 successfully.     

Effect of pulse parameters on microstructure of joint in laser beam welding for SiC_p/6063 composite

1　INTRODUCTIONSiC particlesreinforcedcomposites ,thankstotheirlowcostsandhighlevelofstructuralproperties ,areshowingtheirpotentialincivilandmilitaryappli cation .SiC particlesreinforcedaluminummatrixcomposites wideapplicationinaerospaceandautomo tiveareattributedtotheirperformanceofhighspecif icstrength ,highspecificstiffness ,highelasticmodu lusandexcellentwearresistance .Thecoefficientofthermalexpansionandthermalconductivitycanberegulatedbychangingthecontentandsizeofrein forcingparticl…     

加权平均量的自收敛性与权的确定

在多因素综合评价决策中,合理确定各因素权重系数是评价决策的关键。文章引入了加权平均量的自收敛性来描绘被评价分数的随机变量的稳定性,以概率论理论为基础,得到了一般情况下权重系数确定的优化模型和协方差矩阵为正定矩阵的一系列的确定权的方法,建立了一套较完整的确定权重系数的理论。     

基于事件触发的电力系统H∞优化控制

针对大规模集中用电导致电力系统负荷端激增从而影响电力系统稳定性的问题,提出一种基于事件触发的H_∞优化控制方式。本文采用扇区法对单机无穷大电力系统进行线性化处理,之后通过模糊逻辑建立电力系统的T-S模糊模型。通过事件触发理论和模糊逻辑利用并行分布补偿(parallel distribution compensation,PDC)的方法设计系统控制器。H∞优化控制相比于传统的控制方法提高了系统的稳定性及抗干扰能力,因此本文根据李雅普诺夫稳定性理论和H∞优化控制理论,基于线性矩阵不等式(linear Matrix Inequality,LMI),给出了保证单机无穷大电力系统闭环渐进稳定的充分条件,并采用MATLAB仿真软件对系统进行仿真,从而证明稳定条件的存在。     

Collagen I Modifies Connexin-43 Hemichannel Activity via Integrin α2β1 Binding in TGFβ1-Evoked Renal Tubular Epithelial Cells

Chronic Kidney Disease (CKD) is associated with sustained inflammation and progressive fibrosis, changes that have been linked to altered connexin hemichannel-mediated release of adenosine triphosphate (ATP). Kidney fibrosis develops in response to increased deposition of extracellular matrix (ECM), and up-regulation of collagen I is an early marker of renal disease. With ECM remodeling known to promote a loss of epithelial stability, in the current study we used a clonal human kidney (HK2) model of proximal tubular epithelial cells to determine if collagen I modulates changes in cell function, via connexin-43 (Cx43) hemichannel ATP release. HK2 cells were cultured on collagen I and treated with the beta 1 isoform of the pro-fibrotic cytokine transforming growth factor (TGFβ1) ± the Cx43 mimetic Peptide 5 and/or an anti-integrin α2β1 neutralizing antibody. Phase microscopy and immunocytochemistry observed changes in cell morphology and cytoskeletal reorganization, whilst immunoblotting and ELISA identified changes in protein expression and secretion. Carboxyfluorescein dye uptake and biosensing measured hemichannel activity and ATP release. A Cytoselect extracellular matrix adhesion assay assessed changes in cell-substrate interactions. Collagen I and TGFβ1 synergistically evoked increased hemichannel activity and ATP release. This was paralleled by changes to markers of tubular injury, partly mediated by integrin α2β1/integrin-like kinase signaling. The co-incubation of the hemichannel blocker Peptide 5, reduced collagen I/TGFβ1 induced alterations and inhibited a positive feedforward loop between Cx43/ATP release/collagen I. This study highlights a role for collagen I in regulating connexin-mediated hemichannel activity through integrin α2β1 signaling, ahead of establishing Peptide 5 as a potential intervention.     

Inhalational Anesthetics Inhibit Neuroglioma Cell Proliferation and Migration via miR-138, -210 and -335

Inhalational anesthetics was previously reported to suppress glioma cell malignancy but underlying mechanisms remain unclear. The present study aims to investigate the effects of sevoflurane and desflurane on glioma cell malignancy changes via microRNA (miRNA) modulation. The cultured H4 cells were exposed to 3.6% sevoflurane or 10.3% desflurane for 2 h. The miR-138, -210 and -335 expression were determined with qRT-PCR. Cell proliferation and migration were assessed with wound healing assay, Ki67 staining and cell count kit 8 (CCK8) assay with/without miR-138/-210/-335 inhibitor transfections. The miRNA downstream proteins, hypoxia inducible factor-1α (HIF-1α) and matrix metalloproteinase 9 (MMP9), were also determined with immunofluorescent staining. Sevoflurane and desflurane exposure to glioma cells inhibited their proliferation and migration. Sevoflurane exposure increased miR-210 expression whereas desflurane exposure upregulated both miR-138 and miR-335 expressions. The administration of inhibitor of miR-138, -210 or -335 inhibited the suppressing effects of sevoflurane or desflurane on cell proliferation and migration, in line with the HIF-1α and MMP9 expression changes. These data indicated that inhalational anesthetics, sevoflurane and desflurane, inhibited glioma cell malignancy via miRNAs upregulation and their downstream effectors, HIF-1α and MMP9, downregulation. The implication of the current study warrants further study.