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Cutter design and multi-objective optimization of machine for cable peeling is proposed to use mechanical peeling instead of manual peeling in this paper. First, the design of the machine for cable peeling includes executive mechanism, driving part for cable, driving part for executive mechanism, and peeling mechanism. Then, the cutting experiment platform is set up to verify the actual effect of cutting, and different cutting depths, cutting speeds and fixing cables methods are discussed by the cutting experiment platform. A numerical simulation method is proposed, and different cutting methods, cutting depths and cutting speeds for cutting different materials are discussed by simulation method. The results show that simultaneous cutting is better than sequential cutting. The results show a good agreement between the results obtained from the finite element modelling and experimental investigations. A theoretical reference is provided for subsequent structural improvement. Finally, multi-objective optimization of machine for cable peeling is realized. The aim of the optimization was improving the dimensional accuracy after cutting and reducing the deformation of the cut surface. Cutter thickness, cutter angle, and cutter material are used as optimization variables, and the final optimal solution is obtained. The cutter is manufactured according to the final optimal solution, experiment of cutting is performed, and good agreements were achieved between optimal solution and experiments. Comparing the final results with the initial results shows a significant improvement.

Oxidative low-density lipoprotein (ox-LDL) is thought to induce vascular endothelial cell injury, which contributes to the aetiopathogenesis of atherosclerosis (AS). Several previous reports have identified that lncRNA ZEB1-AS1 participates in the regulatory mechanisms of endothelial cell injury, but the potential interaction mechanism between ZEB1-AS1 and miR-590-5p in ox-LDL-induced endothelial cell damage is not clear. ZEB1-AS1 and miR-590-5p expression were tested by quantitative real-time polymerase chain reaction (qRT-PCR) in ox-LDL-treated endothelial cells. The proliferation and apoptosis were determined by MTT and Annexin V/PI double-staining assay, respectively. The protein expression of HDAC9, tumor necrosis factor  (TNF-), cleaved caspase-3, and cleaved PARP were measured by western blot analysis. Dual-luciferase reporter and RIP assays affirmed the functional targets of ZEB1-AS1. ZEB1-AS1 expression was upregulated in ox-LDL-treated HUVECs, and miR-590-5p was lessened in a dose- or time-depended manner, respectively. Knockdown of ZEB1-AS1 facilitated ox-LDL-treated endothelial cell proliferation and inhibited cell apoptosis. Moreover, miR-590-5p was directly targeted via ZEB1-AS1 in ox-LDL-treated HUVECs. ZEB1-AS1 silencing attenuated ox-LDL-induced cell injury via regulation of miR-590-5p expression. Furthermore, HDAC9 reversed the influence of miR-590-5p on propagation and apoptosis of ox-LDL-induced endothelial cells. Knockdown of ZEB1-AS1 alleviates ox-LDL-induced endothelial cell injury by regulating the miR-590-5p/HDAC9 axis.