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Hydraulic fracture simulation of concrete using the SBFEM-FVM model
Peng Zhang,Chengbin Du,Wenhu Zhao,Deheng Zhang 국제구조공학회 2021 Structural Engineering and Mechanics, An Int'l Jou Vol.80 No.5
In this paper, a hybrid scaled boundary finite element and finite volume method (SBFEM-FVM) is proposed for simulating hydraulic-fracture propagation in brittle concrete materials. As a semi-analytical method, the scaled boundary finite element method is introduced for modelling concrete crack propagation under both an external force and water pressure. The finite volume method is employed to model the water within the crack and consider the relationship between the water pressure and the crack opening distance. The cohesive crack model is used to analyse the non-linear fracture process zone. The numerical results are compared with experimental data, indicating that the F-CMOD curves and water pressure changes under different loading conditions are approximately the same. Different types of water pressure distributions are also studied with the proposed coupled model, and the results show that the internal water pressure distribution has an important influence on crack propagation.
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Jianle Wang,Majid Nisar,Chongan Huang,Xiangxiang Pan,Dongdong Lin,Gang Zheng,Haiming Jin,Deheng Chen,Naifeng Tian,Qianyu Huang,Yue Duan,Yingzhao Yan,Ke Wang,Congcong Wu,Jianing Hu,Xiaolei Zhang,Xiangy 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Oxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of intervertebral disc degeneration (IVDD). Sirtuin 3 (SIRT3), a sirtuin family protein located in mitochondria, is essential for mitochondrial homeostasis; however, the role of SIRT3 in the process of IVDD has remained elusive. Here, we explored the expression of SIRT3 in IVDD in vivo and in vitro; we also explored the role of SIRT3 in senescence, apoptosis, and mitochondrial homeostasis under oxidative stress. We subsequently activated SIRT3 using honokiol to evaluate its therapeutic potential for IVDD. We assessed SIRT3 expression in degenerative nucleus pulposus (NP) tissues and oxidative stressinduced nucleus pulposus cells (NPCs). SIRT3 was knocked down by lentivirus and activated by honokiol to determine its role in oxidative stress-induced NPCs. The mechanism by which honokiol affected SIRT3 regulation was investigated in vitro, and the therapeutic potential of honokiol was assessed in vitro and in vivo. We found that the expression of SIRT3 decreased with IVDD, and SIRT3 knockdown reduced the tolerance of NPCs to oxidative stress. Honokiol (10 μM) improved the viability of NPCs under oxidative stress and promoted their properties of anti-oxidation, mitochondrial dynamics and mitophagy in a SIRT3-dependent manner. Furthermore, honokiol activated SIRT3 through the AMPKPGC- 1α signaling pathway. Moreover, honokiol treatment ameliorated IVDD in rats. Our study indicated that SIRT3 is involved in IVDD and showed the potential of the SIRT3 agonist honokiol for the treatment of IVDD.
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