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Compressive Behavior of Damaged Tubular T-joints Retrofitted with Collar Plate
Peng Deng,Jianxun Guo,Yan Liu,Zhongying Wang 대한토목학회 2019 KSCE JOURNAL OF CIVIL ENGINEERING Vol.23 No.9
The static bearing capacity and failure modes of damaged tubular T-joints retrofitted with collar plates under axial compression were investigated. Two-step loading was applied: First, the chord deformation was loaded to the pre-designed degree, followed by unloading and collar plate installation. Subsequently, the specimens were reloaded. The maximum capacity and corresponding displacement (Δ1,m) were determined, and the ratio of the chord deformation of the other joints to Δ1,m was utilized to define the damage degree. The maximum capacity of retrofitted tubular T-joints could be up to 13 – 77% in second step loading, compared with that of unreinforced T-joints; however, the capacity decreased by 2 – 10% compared to that of directly reinforced T-joints. Sixty-nine finite element models were generated. The effects of chord wall thickness, chord diameters and collar plate lengths on the bearing capacity under different damage degrees were analyzed. A satisfactory effect could be obtained by using a suitable size of expanded collar plates under a constant damage degree. Retrofitting with collar plates could mitigate the development of equivalent plastic strain in the joint intersection, even for considerably damaged tubular T-joints. A modified formula considering the damage degree was proposed for bearing capacity prediction of retrofitted tubular T-joints.
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JiSheng Hu,ShangJing Pi,MingRui Xiong,ZhongYing Liu,Xia Huang,Ran An,TongCun Zhang,BaiYin Yuan 한국분자세포생물학회 2020 Molecules and cells Vol.43 No.8
The migration, dedifferentiation, and proliferation of vascular smooth muscle cells (VSMCs) are responsible for intimal hyperplasia, but the mechanism of this process has not been elucidated. WD repeat domain 1 (WDR1) promotes actin-depolymerizing factor (ADF)/cofilin-mediated depolymerization of actin filaments (F-actin). The role of WDR1 in neointima formation and progression is still unknown. A model of intimal thickening was constructed by ligating the left common carotid artery in Wdr1 deletion mice, and H&E staining showed that Wdr1 deficiency significantly inhibits neointima formation. We also report that STAT3 promotes the proliferation and migration of VSMCs by directly promoting WDR1 transcription. Mechanistically, we clarified that WDR1 promotes the proliferation and migration of VSMCs and neointima formation is regulated by the activation of the JAK2/STAT3/WDR1 axis.
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