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Vibration Control of Soil-structure Systems and Pile-soil-structure Systems
Lihua Zou,Leiqing Fang,Kai Huang,Liyuan Wang 대한토목학회 2012 KSCE JOURNAL OF CIVIL ENGINEERING Vol.16 No.5
The purpose of this paper is to investigate the influence of Soil-Structure Interaction (SSI) and Pile-Soil-Structure Interaction (PSSI) on vibration control effect. Assuming the ground as an isotropic elastic half space and the soil around the foundation as a horizontal and rotational spring-dashpot system, a SSI model for buildings with rigid shallow foundations is established. Based on Penzien model, a PSSI model for structures with pile-foundations is also set up. Then, after the motion and control equations of the SSI system and PSSI system are derived, the influences of SSI and PSSI on vibration control are investigated. Important parameters of soil and structures are studied. Numerical results show that the SSI and PSSI have an obvious influence on the control effect of structures. Parameters such as shear-wave velocity, embedded depth of soil and stiffness of superstructure and pile, play a significant role in vibration control. The influences of SSI and PSSI mainly depend on characteristics of the upper soil layer, hence, the SSI influence on buildings with rigid foundations is more obvious than that of PSSI on buildings with pile foundations.
Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy
( Jiang Zou ),( Qiang Ma ),( Ru Sun ),( Jiajing Cai ),( Hebin Liao ),( Lei Xu ),( Jingruo Xia ),( Guangcheng Huang ),( Lihua Yao ),( Yan Cai ),( Xiaowu Zhong ),( Xiaolan Guo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.8
Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, γ-H<sub>2</sub>AX, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy. [BMB Reports 2019; 52(8): 520-525]