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        Design of cross-linked baffle and analysis of its wave suppression characteristics

        Minmin Shen,Baohong Tong,Chuanbin Sun,Hu Huang,Kun Zhang 대한기계학회 2022 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.36 No.12

        Under variable speed condition, oil in a fuel tank is shaken violently, thereby causing damage to the fuel tank structure and supply interruption, affecting the safe driving of the vehicle. A structural design scheme of a fuel tank with cross-linked baffle is proposed. Oil sloshing in the fuel tank under braking conditions is numerically simulated using a method verified by experiments. The characteristics of cross-linkage baffled fuel tanks to inhibit oil sloshing are analysed. The results show that the baffles can be linked when stiffeners are installed between baffles in the fuel tank. Applying the force opposite to the oil impact pressure improves the rigidity of the baffle and enables a reduction in fatigue damage. The cross-linked baffled has little influence on the baffle wall pressure but has a certain impact on the shape of oil sloshing. With the increase of braking acceleration, the jet velocity of the oil passing through the baffle pores increases, and the nonlinear phenomenon caused by the jet hitting the liquid surface is further aggravated. With the rise of the fuel tank filling rate, the jet velocity of the oil passing through the baffle pores decreases, and the intensity of sloshing is reduced. The vortex generated near the cross-linked baffle changes the flow field structure, reduces the oil climbing speed, and ultimately restrains sloshing.

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        SET8 suppression mediates high glucose-induced vascular endothelial inflammation via the upregulation of PTEN

        Shen Xuefang,Chen Xiangyuan,Wang Jing,Liu Jing,Wang Zhiyao,Hua Qing,Wu Qichao,Su Yanguang,He Huanzhong,Hu Yuqin,Meng Zhipeng,Xiong Wanxia,Zhu Minmin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        Hyperglycemia-mediated endothelial inflammation participates in the pathogenesis of cardiovascular complications in subjects with diabetes. Previous studies reported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) and SET8 participate in high glucose-mediated endothelial inflammation. In this study, we hypothesize that SET8 regulates PTEN expression, thus contributing to high glucose-mediated vascular endothelial inflammation. Our data indicated that plasma soluble intercellular adhesion molecule-1 (sICAM-1) and endothelial selectin (e-selectin) were increased in patients with diabetes and diabetic rats. PTEN expression was augmented in the peripheral blood mononuclear cells of patients with diabetes and in the aortic tissues of diabetic rats. Our in vitro study indicated that high glucose increased monocyte/endothelial adhesion, endothelial adhesion molecule expression and p65 phosphorylation in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose led to endothelial inflammation via upregulation of PTEN. Furthermore, high glucose inhibited SET8 expression and histone H4 lysine 20 methylation (H4K20me1), a downstream target of SET8. SET8 overexpression reversed the effects of high-glucose treatment. shSET8-mediated endothelial inflammation was counteracted by siPTEN. Furthermore, SET8 was found to interact with FOXO1. siFOXO1 attenuated high glucose-mediated endothelial inflammation. FOXO1 overexpression-mediated endothelial inflammation was counteracted by siPTEN. H4K20me1 and FOXO1 were enriched in the PTEN promoter region. shSET8 increased PTEN promoter activity and augmented the positive effect of FOXO1 overexpression on PTEN promoter activity. Our in vivo study indicated that SET8 was downregulated and FOXO1 was upregulated in the peripheral blood mononuclear cells of patients with diabetes and the aortic tissues of diabetic rats. In conclusion, SET8 interacted with FOXO1 to modulate PTEN expression in vascular endothelial cells, thus contributing to hyperglycemia-mediated endothelial inflammation.

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