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Additive thin-walled parts have the characteristics of complex features and weak rigidity, which are prone to processing chatter vibration during the subsequent local feature milling and finishing. Therefore, this paper designed an electromagnetic magnetorheological damping fixture to semi-actively suppress processing vibration and improve processing quality. By simplifying the thin-walled part of the additive into a rectangular thin plate, considering the magneto-rheological fluid（MRF） excitation solidification damping characteristics, using the mode superposition method, the dynamic response model of the milling of the thin-walled part under the change of the magnetic induction intensity was obtained, and the fixture-workpiece system milling. The maximum error between the predicted value of dynamic response and the measured value is 21.4%. The feasibility and effectiveness of the method were verified through modal hammer percussion experiments and milling experiments, and the matching relationship between milling force, process parameters and magnetic induction intensity was fitted. Finally, the processing quality test of the typical samples was carried out. The processing flatness and roughness are increased by 80.0% and 80.3% respectively. The electromagnetic magneto-rheological damping fixture can effectively suppress the milling chatter, improve the processing stability of thin-walled parts, and improve the surface processing of the workpiece quality.

In order to explore the flow characteristics at tip clearance and the coupling deformation of the blade during running on the centrifugal air compressor, based on the fluid-structure coupling heat transfer theory, the hydrodynamic and structural mechanics numerical calculation models of the impeller were established. Considering centrifugal force, aerodynamic force and thermal stress, the stress and deformation distribution at the blade tip under different tip clearances were analyzed. The results show that tip clearance can generate inlet separation vortex and tip leakage flow, which together disturb the flow in the main flow zone and increase the flow loss. Under the combined action of centrifugal force, air pressure load and thermal load, the maximum deformation of the blade occurs at about 0. 3 chord length of the blade tip. The maximum deformation of the suction surface is 3. 7% larger than that of the pressure surface. With the decrease of the blade height, deformation decreases gradually. The stress value at the leading edge of blade tip is small, and the maximum stress value at the pressure surface and suction surface is not in the same axial position. With the increase of clearance value, the overall stress value at the top gradually decreases. Through the flow field and structure analysis, the optimum clearance size was determined, and the blade was optimized. The aerodynamic performance and safety of the blade were significantly improved after optimization. [ABSTRACT FROM AUTHOR]

This study investigates the mechanism by which microRNA (miR)-30e-3p reduces coronary microembolism (CME)-induced cardiomyocyte pyroptosis and inflammation. Cardiac function tests, histological staining, and transmission electron microscopy were performed on CME-model rats injected with adeno-associated viral vectors. Cardiomyocytes were transfected 24 h before a cellular model of pyroptosis was established via treatment with 1 μg/mL lipopolysaccharide (LPS) for 4 h and 5 mM ATP for 30 min. Pyroptosis, inflammation, and Wnt/β-catenin signaling in cardiomyocytes were detected. Dual-luciferase reporter assays and/or RNA pull-down assays were performed to verify the binding of miR-30e-3p to HDAC2 mRNA or HDAC2 to the SMAD7 promoter. Chromatin immunoprecipitation was used to assess the level of H3K27 acetylation at the SMAD7 promoter. miR-30e-3p and SMAD7 expression levels were downregulated and HDAC2 expression was upregulated with CME. The overexpression of miR-30e-3p restored cardiac functions in CME-model rats and reduced serum cTnI, IL-18, and IL-1β levels, microinfarcts, inflammatory cell infiltration, apoptosis, collagen content, and GSDMD-N, cleaved caspase-1, and NLRP3 expression in the myocardium, but these effects were reversed by SMAD7 knockdown. The overexpression of miR-30e-3p or knockdown of HDAC2 reduced LDH, IL-18, and IL-1β secretion, propidium iodide intake, and GSDMD-N, NLRP3, cleaved caspase-1, Wnt3a, Wnt5a, and β-catenin expression in the cardiomyocyte model. miR-30e-3p inhibited the expression of HDAC2 by binding HDAC2 mRNA. HDAC2 repressed the expression of SMAD7 by catalyzing H3K27 deacetylation at the SMAD7 promoter. miR-30e-3p, by binding HDAC2 to promote SMAD7 expression, reduces CME-induced cardiomyocyte pyroptosis and inflammation.