[目的]接触网与受电弓的匹配性直接影响弓网系统的受流性能,随着架空刚性接触网适用的列车运行速度等级逐渐提高,有必要开展与架空刚性接触网匹配的高速受电弓选型研究。[方法]基于有限元分析法建立了架空刚性接触网-受电弓耦合仿真模型...[目的]接触网与受电弓的匹配性直接影响弓网系统的受流性能,随着架空刚性接触网适用的列车运行速度等级逐渐提高,有必要开展与架空刚性接触网匹配的高速受电弓选型研究。[方法]基于有限元分析法建立了架空刚性接触网-受电弓耦合仿真模型,对适用于列车运行速度为200 km/h架空刚性接触网的受电弓关键参数进行分析;利用正交试验设计法,研究了受电弓多结构参数同时变化对弓网动态性能的影响。[结果及结论]单一参数变化的相对最优取值为:弓头等效质量为6.4 kg,下框架等效质量为6.6 kg,下臂杆等效刚度为10 N/m,弓头等效阻尼为40~60 N s/m,下臂杆等效阻尼为130 N s/m。弓头等效质量变化对弓网动态响应的影响最大,弓头等效刚度、弓头及上框架等效阻尼次之,下臂杆等效质量的影响最小。所获得的适用于列车运行速度为200 km/h架空刚性接触网的受电弓优组合参数为:弓头等效质量为5.7 kg,下臂杆等效质量为4.6 kg,弓头等效刚度为10373 N/m、弓头等效阻尼为60 N s/m,上框架等效阻尼为40 N s/m。展开更多
Transcriptional factor Forkhead box M1(FOXM1)plays an important role in pancreatic ductal adenocarcinoma(PDAC)development and progression.The molecular mechanisms underlying its dysregulation remain unclear.We identif...Transcriptional factor Forkhead box M1(FOXM1)plays an important role in pancreatic ductal adenocarcinoma(PDAC)development and progression.The molecular mechanisms underlying its dysregulation remain unclear.We identified and functionally validated the microRNAs(miRNAs)that critically regulate FOXM1 expression in PDAC.The expression levels of miRNA-23a(miR-23a-3p and-5p)were altered in PDAC cell lines and their effects on FOXM1 signaling and cell proliferation and migration and tumorigenesis were examined in vitro and in vivo using mouse PDAC models.Compared with non-tumor pancreatic tissues,PDAC tissues and cell lines exhibited significantly reduced levels of miR-23a expression.Reduced miR-23a expression and concomitant increase in FOXM1 expression were also observed in acinar-toductal metaplasia and pancreatic intraepithelial neoplasia,the major premalignant lesions of PDAC.Transgenic expression of miR-23a reduced the expression of FOXM1 and suppressed cell proliferation and migration in PDAC cells,whereas the inhibitors of miR-23a did the opposite.Loss or reduced levels of miR-23a increased the levels of FOXM1 expression,while increased expression of FOXM1 down-regulated miR-23a expression,suggesting that miR-23a and FOXM1 were mutual negative regulators of their expression in PDAC cells.Therefore,the miR-23a/FOXM1 signaling axis is important in PDAC initiation and progression and could serve as an interventional or therapeutic target for patients with early or late stages of PDAC.展开更多
文摘[目的]接触网与受电弓的匹配性直接影响弓网系统的受流性能,随着架空刚性接触网适用的列车运行速度等级逐渐提高,有必要开展与架空刚性接触网匹配的高速受电弓选型研究。[方法]基于有限元分析法建立了架空刚性接触网-受电弓耦合仿真模型,对适用于列车运行速度为200 km/h架空刚性接触网的受电弓关键参数进行分析;利用正交试验设计法,研究了受电弓多结构参数同时变化对弓网动态性能的影响。[结果及结论]单一参数变化的相对最优取值为:弓头等效质量为6.4 kg,下框架等效质量为6.6 kg,下臂杆等效刚度为10 N/m,弓头等效阻尼为40~60 N s/m,下臂杆等效阻尼为130 N s/m。弓头等效质量变化对弓网动态响应的影响最大,弓头等效刚度、弓头及上框架等效阻尼次之,下臂杆等效质量的影响最小。所获得的适用于列车运行速度为200 km/h架空刚性接触网的受电弓优组合参数为:弓头等效质量为5.7 kg,下臂杆等效质量为4.6 kg,弓头等效刚度为10373 N/m、弓头等效阻尼为60 N s/m,上框架等效阻尼为40 N s/m。
基金Guangzhou Ruiqian Biotech Company(China)(No.20230330 to TJ)the National Natural Science Foundation of China(No.82072632)+1 种基金Guangzhou Municipality Bureau of Science and Technology,Guangzhou,China(No.202102010033)the Natural Science Foundation of Guangdong Province,China(No.2022A1515012585 to KX).
文摘Transcriptional factor Forkhead box M1(FOXM1)plays an important role in pancreatic ductal adenocarcinoma(PDAC)development and progression.The molecular mechanisms underlying its dysregulation remain unclear.We identified and functionally validated the microRNAs(miRNAs)that critically regulate FOXM1 expression in PDAC.The expression levels of miRNA-23a(miR-23a-3p and-5p)were altered in PDAC cell lines and their effects on FOXM1 signaling and cell proliferation and migration and tumorigenesis were examined in vitro and in vivo using mouse PDAC models.Compared with non-tumor pancreatic tissues,PDAC tissues and cell lines exhibited significantly reduced levels of miR-23a expression.Reduced miR-23a expression and concomitant increase in FOXM1 expression were also observed in acinar-toductal metaplasia and pancreatic intraepithelial neoplasia,the major premalignant lesions of PDAC.Transgenic expression of miR-23a reduced the expression of FOXM1 and suppressed cell proliferation and migration in PDAC cells,whereas the inhibitors of miR-23a did the opposite.Loss or reduced levels of miR-23a increased the levels of FOXM1 expression,while increased expression of FOXM1 down-regulated miR-23a expression,suggesting that miR-23a and FOXM1 were mutual negative regulators of their expression in PDAC cells.Therefore,the miR-23a/FOXM1 signaling axis is important in PDAC initiation and progression and could serve as an interventional or therapeutic target for patients with early or late stages of PDAC.
