Based on Zak's stress function, the eigen-equation of stress singularity of bi-materials with a V-notch was obtained. A new definition of stress intensity factor for a perpendicular interfacial V-notch of bi-material was put forward. The effects of shear modulus and Poisson's ratio of the matrix material and attaching material on eigen-values were analyzed. A generalized expression for calculating KI of the perpendicular V-notch of bi-materials was obtained by means of stress extrapolation. Effects of notch depth, notch angle and Poisson's ratio of materials on the singular stress field near the tip of the V-notch were analyzed systematically with numerical simulations. As an example, a finite plate with double edge notches under uniaxial uniform tension was calculated by the method presented and the influence of the notch angle and Poisson's ratio on the stress singularity near the tip of notch was obtained.KEY WORDS bi-material, V-notch, eigen-equation, stress intensity factor, finite element method
The occurrence of paclitaxel (PTX) resistance in nonsmall cell lung cancer (NSCLC) is a major challenge for NSCLC treatment. Circular RNAs (circRNAs) have been reported to associate with cancer resistance, but the role of circ_0010235 in PTX resistance of NSCLC is unclear. The expression of circ_0010235 and microRNA-512-5p (miR-512-5p) were determined by quantitative real-time PCR. Cell counting kit-8 assay, transwell assay and flow cytometry were performed to measure the PTX resistance, proliferation, migration, invasion and apoptosis of cells. All proteins were assessed via western blot analysis. The combination between miR-512-5p and circ_0010235 or FAM83F was predicted by the online database and confirmed by a dual-luciferase reporter assay. Angiogenesis assay was used to detect the ability of cells to form blood vessels. Animal experiments were employed to confirm the effect of circ_0010235 on NSCLC tumor growth in vivo. Circ_0010235 and FAM83F were upregulated in PTX-resistant NSCLC tissues and cells. Circ_0010235 knockdown suppressed the resistance to PTX, proliferation, angiogenesis and migration/invasion in A549/PTX and H1299/PTX cells but promoted apoptosis rate. MiR-512-5p could be sponged by circ_0010235, and its overexpression had an inhibition effect on the PTX resistance of NSCLC cells. FAM83F was a target of miR-512-5p and circ_0010235 could modulate FAM83F expression by sponging miR-512-5p. In vivo experiments revealed that silenced circ_0010235 could improve the sensitivity of the tumor to PTX. Therefore, these findings advocated targeting the circ_0010235/miR-512-5p/ FAM83F axis as a potential therapeutic option for patients with NSCLC who are resistant to PTX. Anti-Cancer Drugs 33: 1024
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