The pathogenesis of CRC remains to be further understood. This study was designed to elucidate the role of Foxp3+IL-17+ T cells in the pathogenesis of CRC. Surgically removed CRC tissue was collected from 12 patients with CRC. The frequency and cytokine profile of Foxp3+IL-17+ T cells in CRC were examined by flow cytometry. Chemokine CXCL11 was examined in CRC tissue by Western blotting. Treg chemotaxis was examined in a transwell system. The effect of Foxp3+IL-17+ T cells on induction of cancer-initiating cells was examined; the latter's Akt and MAPK activities and colony formation were examined afterward. Abundant Foxp3+IL-17+ T cells were detected in CRC tissue that expresses high levels of TGF-β, CXCR3, CCR6, and RORγt. High levels of CXCL11 were detected in CRC tissue-derived CD68+ cells, which had a strong chemotactic effect on Foxp3+ Tregs. Hypoxia induced the expression of IL-17 in Foxp3+ Tregs; Foxp3+IL-17+ T cells were capable of inducing CRC-associated cell markers in BMMo and drove the cells to be cancer-initiating cells. High levels of phosphorylated Akt and MAPK were detected in the induced cancer-initiation cells; the latter has the capability to form a colony. CRC tissue-derived Foxp3+IL-17+ cells have the capacity to induce cancer-initiating cells.
Experimental tests were conducted on the composite rock-concrete specimens with four roughness profiles to investigate the propagation process of interfacial cracks under three-point bending and four-point shear conditions. By measuring the initial fracture loads, various combinations of interfacial stress intensity factors (SIFs) of modes I and II corresponding to the initial fracture conditions were determined. Based on these results, an expression for classifying the initiation of interfacial cracks under the mixed mode I-II fracture was derived by normalization, which could eliminate the effect of interfacial roughness. Furthermore, a criterion for specifying the propagation of the interfacial crack by considering the nonlinear interfacial characteristics was proposed, which indicates that the crack would start to propagate along the interface when the SIFs caused by the external loads and the cohesive stresses satisfied this criterion. The numerical simulations on the interfacial fracture process were also conducted by introducing the crack propagation criterion to predict the load versus crack mouth opening displacement (P-CMOD) curves, and a fairly good agreement with the experimental results could be obtained. Finally, by combining the criterion for the maximum circumferential stress with the proposed criterion for crack propagation, the interfacial crack propagation mode was assessed. The results indicated that once the initial fracture toughnesses for the rock, concrete and interface from experimental work were obtained, the propagation process of the interfacial cracks and the corresponding fracture modes including nonlinear characteristics of the materials and interface could be predicted by using the method derived in this study.
Direct tension tests were conducted on plain concrete specimens in a stiff loading frame which allowed complete stress-deformation relations to be obtained. The suitability of the specimen shape and the testing apparatus was verified by finite-element analysis. The behaviours of notched and un-notched specimens with different water-cement ratios were examined and compared. Piecewise linear and exponential stress-deformation relations are proposed and interpreted physically. Relationships between fracture parameters fracture energy and brittleness indices) and basic strength properties are also presented.
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