针对高速永磁电机的充磁方式问题,对一台250 k W,67 000 r/min高速永磁电机的径向充磁、平行充磁和Halbach充磁3种永磁体充磁方式进行了研究,对不同充磁方式给高速永磁电机气隙磁场、齿槽转矩、损耗的影响进行了分析。利用有限元分析的...针对高速永磁电机的充磁方式问题,对一台250 k W,67 000 r/min高速永磁电机的径向充磁、平行充磁和Halbach充磁3种永磁体充磁方式进行了研究,对不同充磁方式给高速永磁电机气隙磁场、齿槽转矩、损耗的影响进行了分析。利用有限元分析的方法,根据实际的充磁方式,在有限元软件中建立了高速永磁电机模型,对高速永磁电机不同充磁方式下的性能进行了研究,对比分析了平行充磁、径向充磁及Halbach充磁这3种充磁方式对高速永磁电机气隙磁场、齿槽转矩、定子空载铁耗、转子涡流损耗、额定运行时总损耗等的影响,并且总结了高速永磁电机理想的充磁方式。研究结果表明:采用平行充磁方式时高速永磁电机的气隙磁密波形更趋于正弦、齿槽转矩更小,电机的总损耗最小,运行性能更优。展开更多
Mitochondria play an important role in pressure overload-induced cardiac hypertrophy.The present study aimed to investigate the role of mitochondrial transient receptor potential vanilloid 3(TRPV3)in myocardial hypert...Mitochondria play an important role in pressure overload-induced cardiac hypertrophy.The present study aimed to investigate the role of mitochondrial transient receptor potential vanilloid 3(TRPV3)in myocardial hypertrophy.A 0.7 mm diameter U-shaped silver clip was used to clamp the abdominal aorta of Sprague Dawley(SD)rats and establish an animal model of abdominal aortic constriction(AAC).Rat H9C2 myocardial cells were treated with angiotensin II(Ang II)to establish a hypertrophic myocardial cell model,and TRPV3 expression was knocked down using TRPV3 small interfering RNA(siRNA).JC-1 probe was used to detect mitochondrial membrane potential(MMP).DHE probe was used to detect ROS generation.Enzyme activities of mitochondrial respiratory chain complex I and III and ATP production were detected by assay kits.Immunofluorescence staining was used to detect TRPV3 expression in H9C2 cells.Western blot was used to detect the protein expression levels ofβ-myosin heavy chain(β-MHC),mitochondrial TRPV3 and mitochondrial NOX4.The results showed that,in the rat AAC model heart tissue and H9C2 cells treated with Ang II,the protein expression levels ofβ-MHC,mitochondrial TRPV3 and mitochondrial NOX4 were up-regulated,MMP was decreased,ROS generation was increased,mitochondrial respiratory chain complex I and III enzyme activities were decreased,and ATP production was reduced.After knocking down mitochondrial TRPV3 in H9C2 cells,the protein expression levels ofβ-MHC and mitochondrial NOX4 were down-regulated,MMP was increased,ROS generation was decreased,mitochondrial respiratory chain complex I and III enzyme activities were increased,and ATP production was increased.These results suggest that mitochondrial TRPV3 in cardiomyocytes exacerbates mitochondrial dysfunction by up-regulating NOX4,thereby participating in the process of pressure overload-induced myocardial hypertrophy.展开更多
文摘针对高速永磁电机的充磁方式问题,对一台250 k W,67 000 r/min高速永磁电机的径向充磁、平行充磁和Halbach充磁3种永磁体充磁方式进行了研究,对不同充磁方式给高速永磁电机气隙磁场、齿槽转矩、损耗的影响进行了分析。利用有限元分析的方法,根据实际的充磁方式,在有限元软件中建立了高速永磁电机模型,对高速永磁电机不同充磁方式下的性能进行了研究,对比分析了平行充磁、径向充磁及Halbach充磁这3种充磁方式对高速永磁电机气隙磁场、齿槽转矩、定子空载铁耗、转子涡流损耗、额定运行时总损耗等的影响,并且总结了高速永磁电机理想的充磁方式。研究结果表明:采用平行充磁方式时高速永磁电机的气隙磁密波形更趋于正弦、齿槽转矩更小,电机的总损耗最小,运行性能更优。
基金supported by the National Natural Science Foundation of China (No. 30872716)the Natural Science Foundation of Hubei Province,China (No. 2015CFB288)Open Foundation of Hubei Province Key Laboratory of Tumor Microenvironment and immunotherapy (No. 2023KZL06)。
文摘Mitochondria play an important role in pressure overload-induced cardiac hypertrophy.The present study aimed to investigate the role of mitochondrial transient receptor potential vanilloid 3(TRPV3)in myocardial hypertrophy.A 0.7 mm diameter U-shaped silver clip was used to clamp the abdominal aorta of Sprague Dawley(SD)rats and establish an animal model of abdominal aortic constriction(AAC).Rat H9C2 myocardial cells were treated with angiotensin II(Ang II)to establish a hypertrophic myocardial cell model,and TRPV3 expression was knocked down using TRPV3 small interfering RNA(siRNA).JC-1 probe was used to detect mitochondrial membrane potential(MMP).DHE probe was used to detect ROS generation.Enzyme activities of mitochondrial respiratory chain complex I and III and ATP production were detected by assay kits.Immunofluorescence staining was used to detect TRPV3 expression in H9C2 cells.Western blot was used to detect the protein expression levels ofβ-myosin heavy chain(β-MHC),mitochondrial TRPV3 and mitochondrial NOX4.The results showed that,in the rat AAC model heart tissue and H9C2 cells treated with Ang II,the protein expression levels ofβ-MHC,mitochondrial TRPV3 and mitochondrial NOX4 were up-regulated,MMP was decreased,ROS generation was increased,mitochondrial respiratory chain complex I and III enzyme activities were decreased,and ATP production was reduced.After knocking down mitochondrial TRPV3 in H9C2 cells,the protein expression levels ofβ-MHC and mitochondrial NOX4 were down-regulated,MMP was increased,ROS generation was decreased,mitochondrial respiratory chain complex I and III enzyme activities were increased,and ATP production was increased.These results suggest that mitochondrial TRPV3 in cardiomyocytes exacerbates mitochondrial dysfunction by up-regulating NOX4,thereby participating in the process of pressure overload-induced myocardial hypertrophy.
