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  • 简介:摘要: Motor-Cad是十分强大的电机设计分析工具。本论文基于Motor-Cad设计了某功率型号的外转子直驱式轮毂电机并对其性能进行了研究,电机采用永磁同步电动机,相对于传统的车用驱动电机,这种电机具有高效、高功率密度、结构简单紧凑等一系列优点,特别适合作为车用电机使用,对其性能的研究也表明,设计的电机能够完全满足电动车使用要求。

  • 标签: 外转子 直驱式 轮毂电机 永磁同步电动机
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  • 简介:AbstractBackground:Investigations of the pathogenic mechanisms in motor neurons (MNs) derived from amyotrophic lateral sclerosis (ALS) disease-specific induced pluripotent stem (iPS) cell lines could improve understanding of the issues affecting MNs. Therefore, in this study we explored mutant superoxide dismutase 1 (SOD1) protein expression in MNs derived from the iPS cell lines of ALS patients carrying different SOD1 mutations.Methods:We generated induced pluripotent stem cell (iPSC) lines from two familial ALS (FALS) patients with SOD1-V14M and SOD1-C111Y mutations, and then differentiated them into MNs. We investigated levels of the SOD1 protein in iPSCs and MNs, the intracellular Ca2+ levels in MNs, and the lactate dehydrogenase (LDH) activity in the process of differentiation into the MNs derived from the controls and ALS patients’ iPSCs.Results:The iPSCs from the two FALS patients were capable of differentiation into MNs carrying different SOD1 mutations and differentially expressed MN markers. We detected high SOD1 protein expression and high intracellular calcium levels in both the MN and iPSCs that were derived from the two SOD1 mutant patients. However, at no time did we observe stronger LDH activity in the patient lines compared with the control lines.Conclusions:MNs derived from patient-specific iPSC lines can recapitulate key aspects of ALS pathogenesis, providing a cell-based disease model to further elucidate disease pathogenesis and explore gene repair coupled with cell-replacement therapy. Incremental mutant expressions of SOD1 in MNs may have disrupted MN function, either causing or contributing to the intracellular calcium disturbances, which could lead to the occurrence and development of the disease.

  • 标签: Amyotrophic lateral sclerosis Induced pluripotent stem cell SOD1 gene mutation Motor neuron SOD1 aggregation