Damage and failure of underground subway stations under different soil constraint conditions.

Investigations from past earthquakes have shown that underground subway stations can suffer excessive deformation under strong seismic loads, leading to the damage of critical components and the collapse of structures. This study presents the results of finite element analyses on the seismic damage of underground subway stations installed under different soil constraint conditions. The plastic hinge distribution and damage characteristics of cut and cover double-storey and three-storey subway stations are analyzed using the finite element method software ABAQUS. Combined with the static analysis results of the column sections, a discriminant method for bending plastic hinges is presented. The numerical results show that the collapse of the subway stations begins with the failure of the bottom columns' bottom sections, which leads to the bending of the plates and the destruction of the whole structure. The bending deformation at the end section of columns has an approximatively linear relationship with the inter-storey drift ratio, and the change in soil conditions shows no apparent influence. The sidewall deformation behavior varies significantly under different soil conditions, and the bending deformation at the bottom section of sidewalls increases along with an increase in the soil-structure stiffness ratio at the same inter-storey drift deformation level. The sidewall bending ductility ratio of the double-storey and three-storey stations at the elastic-plastic drift ratio limit increases by 61.6% and 26.7%, respectively. In addition, the fitting curves between the component bending ductility ratio and inter-storey drift ratio based on the analysis results are also presented. The findings may provide a helpful reference for the seismic performance evaluation and design of underground subway stations.

Gefitinib induces lung cancer cell autophagy and apoptosis via blockade of the PI3K/AKT/mTOR pathway.

Gefitinib is a selective inhibitor of the tyrosine kinase epidermal growth factor receptor, which inhibits tumor pathogenesis, metastasis and angiogenesis, as well as promoting apoptosis. Therefore, gefitinib presents an effective drug for the targeted therapy of lung cancer. However, the underlying mechanisms by which gefitinib induces lung cancer cell death remain unclear. To investigate the effects of gefitinib on lung cancer cells and the mechanism of such, the present study analyzed the effect of gefitinib on the autophagy, apoptosis and proliferation of the A549 and A549-gefitinib-resistant (GR) cell lines GR. The regulation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/ mammalian target of rapamycin (mTOR) pathway was also investigated. Acridine orange staining revealed that gefitinib induced autophagy of A549 cells but not A549-GR cells. In addition, gefitinib promoted apoptosis and inhibited proliferation of A549 cells but not A549-GR cells. Furthermore, western blot analysis demonstrated that gefitinib treatment led to the downregulation of PI3K, AKT, pAKT, mTOR and phosphorylated-mTOR protein expression in A549 cells but not A549-GR cells. LY294002 blocked the PI3K/AKT/mTOR pathway and induced autophagy and apoptosis of A549 cells, however, no synergistic effect was observed following combined treatment with gefitinib and LY294002. In conclusion, the results of the present study indicate that gefitinib promotes autophagy and apoptosis of lung cancer cells via blockade of the PI3K/AKT/mTOR pathway, which leads to lung cancer cell death.