大城市次输电网优化潮流

随着电力市场的形成,要求电网以最低的成本,向用户连续地提供优质电能。以网损最低为目标,对大城市次电网潮流的优化,及其实现方法进行探讨和研究,并提出昼夜合理安排主变压器的运行方式。     

一类带积分边界奇异边值问题正解的存在性

通过构造一个适当的积分算子,并结合锥不动点理论和格林函数的性质,给出一类带有积分边界条件的二阶微分方程奇异边值问题正解和多个正解的存在性定理。     

光纤倏逝波生物传感器的结构研究

光纤倏逝波生物传感器的性能主要体现在探测能力和简便性两个方面,为了提高其探测极限和野外适应性,针对光纤探头的倏逝场激发能量和系统结构的整体性进行了较为系统的研究,分析了三种不同发展阶段的系统结构,设计和搭建了一种目前发展的基于光纤束的荧光光纤倏逝波生物传感器系统,以此系统为基础进行了实验检测并取得了较为满意的检测效果.最后给出了下一阶段的系统结构发展方向并分析了其优越性和可行性.     

高纯纳米HNS的制备与表征

采用溶液急冷重结晶和溶剂非溶剂重结晶相结合的方法得到了2,2′,4,4′,6,6′-六硝基茋(HNS)高纯纳米颗粒.经过纳米化后,HNS的颗粒形貌更为圆滑,粒度分布处于58.9～231.6nm之间,纯度由90.1％提高到99.44％,比表面积为19.27m2·g-1.撞击感度测试表明,纳米HNS的撞击感度较之原料HNS有所降低,冲击片感度提高.     

Semaphorin 7A promotes human vascular smooth muscle cell proliferation and migration through the β-catenin signaling pathway

Background: Vascular smooth muscle cells (VSMCs) undergo a conversion from a contractile phenotype to a proliferative synthetic phenotype, contributing to the pathogenesis of cardiovascular diseases. Semaphorin 7A (SEMA7A) is a glycosylphosphatidylinositol-anchored membrane protein that plays an important role in vascular homeostasis by regulating endothelial cell behaviors. However, the expression and role of SEMA7A in VSMCs remain unclear.Methods: In this study, we screened for VSMC-regulating genes in publicly available datasets and analyzed the expression of SEMA7A in human coronary artery smooth muscle cells (hCASMCs) treated with platelet-derived growth factor-BB (PDGF-BB). The effects of SEMA7A overexpression and knockdown on hCASMC proliferation and migration were examined. The signaling pathways involved in the action of SEMA7A in hCASMCs were determined.Results: Bioinformatic analysis showed that SEMA7A was significantly dysregulated in VSMCs treated with oxidized low-density lipoprotein or overexpressing progerin, a pro-atherogenic gene. The PDGF-BB stimulation led to a concentration- and time-dependent induction of SEMA7A. Depletion of SEMA7A attenuated PDGF-BB-induced hCASMC proliferation and migration. Conversely, overexpression of SEMA7A enhanced hCASMC proliferation and migration. Mechanistically, SEMA7A stimulated the activation of the β-catenin pathway and upregulated c-Myc, CCND1, and MMP7. Knockdown of β-catenin impaired SEMA7A-induced hCASMC proliferation and migration.Conclusions: SEMA7A triggers phenotype switching in VSMCs through the β-catenin signaling pathway and may serve as a potential therapeutic target for cardiovascular diseases.