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- 저자 : Liu Caijun (검색결과 2 건)
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Static behavior of high strength friction-grip bolt shear connectors in composite beams
Ying Xing,Yanbin Liu,Caijun Shi,Zhipeng Wang,Qi Guo,Jin-feng Jiao 국제구조공학회 2022 Steel and Composite Structures, An International J Vol.42 No.3
Superior to traditional welded studs, high strength friction-grip bolted shear connectors facilitate the assembling and demounting of the composite members, which maximizes the potential for efficiency in the construction and retrofitting of new and old structures respectively. Hence, it is necessary to investigate the structural properties of high strength friction-grip bolts used in steel concrete composite beams. By means of push-out tests, an experimental study was conducted on post-installed high strength friction-grip bolts, considering the effects of different bolt size, concrete strength, bolt tensile strength and bolt pretension. The test results showed that bolt shear fracture was the dominant failure mode of all specimens. Based on the loadslip curves, uplifting curves and bolt tensile force curves between the precast concrete slab and steel beam obtained by push-out tests, the anti-slip performance of steel-concrete interface and shear behavior of bolt shank were studied, including the quantitative analysis of anti-slip load, and anti-slip stiffness, frictional coefficient, shear stiffness of bolt shank and ultimate shear capacity. Meanwhile, the interfacial anti-slip stiffness and shear stiffness of bolt shank were defined reasonably. In addition, a total of 56 push-out finite element models verified by the experimental results were also developed, and used to conduct parametric analyses for investigating the shear behavior of high-strength bolted shear connectors in steel-concrete composite beams. Finally, on ground of the test results and finite element simulation analysis, a new design formula for predicting shear capacity was proposed by nonlinear fitting, considering the bolt diameter, concrete strength and bolt tensile strength. Comparison of the calculated value from proposed formula and test results given in the relevant references indicated that the proposed formulas can give a reasonable prediction.
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Chen Shunlun,Lei Linchuan,Li Zemin,Chen Fan,Huang Yuming,Jiang Guowei,Guo Xingyu,Zhao Zhuoyang,Liu Hui,Wang Hua,Liu Caijun,Zheng Zhaomin,Wang Jianru 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Intervertebral disc degeneration (IVDD) is a main cause of low back pain, and inflammatory factors play key roles in its pathogenesis. Gremlin-1 (Grem1) was reported to induce an inflammatory response in other fields. This study aimed to investigate the mechanisms of Grem1 in the degenerative process of intervertebral discs. Dysregulated genes were determined by analyzing microarray profiles. The expression of Grem1 in 17 human disc samples (male:female = 9:8) and rat models (n = 5 each group) was measured by western blotting (WB), real-time quantitative PCR (RT-qPCR), and immunohistochemistry (IHC). The regulatory effects of Grem1 on apoptosis were examined using siRNAs, flow cytometry, immunofluorescence (IF), and WB. The therapeutic effect was evaluated by locally injecting specific Grem1 siRNA into IVDD rats. The expression of Grem1 was significantly increased in human degenerative intervertebral discs; furthermore, the expression of Grem1 positively correlated with the level of intervertebral disc degeneration. Grem1 was significantly overexpressed in tumor necrosis factor (TNF)-α-induced degenerative NP cells. Apoptosis in degenerative NP cells transfected with siRNA targeting Grem1 was significantly lower than that in the control group. Specific Grem1 siRNA markedly repressed the development of IVDD in surgery-induced IVDD rats. These results indicated that the expression of Grem1 was positively correlated with the severity of intervertebral disc degeneration, and Grem1 siRNA could inhibit Grem1-induced apoptosis and extracellular matrix alterations by mediating the TGF-β/Smad signaling pathway. This study may provide a therapeutic strategy for alleviating inflammation-induced apoptosis associated with intervertebral disc degeneration.
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