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The machined surface topography, surface roughness and surface location error are very important evaluation indexes for machining quality, which directly affect the performance characteristics of the machined workpiece. In this paper, a new model of the arbitrary point of the cutter edge with respect to the arbitrary frame of the machining feature point is built. The proposed model incorporates the surface location error into the relative motion of the cutter with respect to the workpiece using the harmonic balance methods. Further, a nonlinear programming problem is proposed to obtain the scallop value of an arbitrary point on the nominal machined surface. Since the obtained scallop value of each point can be used for constructing the topography of the machined surface as well as calculating the surface roughness, the proposed model can simultaneously predict the surface topography, surface roughness and surface location error.Simulations and experiments indicate that feed per tooth, runout and number of cutter teeth are vital factors influencing the topology of the machined surface. The surface location error of the cutter due to the number of cutter teeth is an essential factor that influences the parallelism or perpendicularity of the machining feature. The effectiveness and feasibility of the proposed method is verified by a machining example.

Tumor necrosis factor-α-inducing protein (Tipα) is a newly identified toxin, which promotes the inflammation and carcinogenesis caused by Helicobacter pylori (H. pylori). However, its mechanism of pathogenesis is still unclear. To investigate the carcinogenic mechanisms of Tipα, SGC7901 cells and SGC7901-derived cancer stem-like cells (CSCs) were stimulated by recombinant Tipα protein with or without Wnt/β-catenin signaling inhibitor XAV939. qRT-PCR and Western blotting were employed to detect expression of epithelial-mesenchymal transition (EMT), CSCs markers, and downstream target genes of this signaling pathway. The cell migration ability was measured by wound healing assay and transwell assay. Our results indicated that Tipα promoted CSC properties of SGC7901 spheroids, including increased expression of CSC specific surface markers CD44, Oct4, Nanog, and an increased capacity for self-renewal. Tipα activated Wnt/β-catenin signaling in both SGC7901 cells or CSCs. Furthermore, Tipα induced the EMT and increased the expressions of downstream target genes of this signaling, including c-myc, cyclin D1, and CD44. However, XAV939 pretreatment inhibited Tipα-induced EMT and CSC properties in SGC7901 cells or CSCs. These results suggest that Tipα promotes EMT and CSC-like properties in gastric cancer cells through activation of Wnt/β-catenin signaling pathway, thereby accelerating the progression of gastric cancer.