Microstructure evolution of alloy 600MA was explored after surface mechanical attrition treatment (SMAT) with different durations via scanning electronic microscopy, electron backscattered ...diffraction, transmission electron microscopy and transmission Kikuchi diffraction. The grain refinement and coarsening occurred gradually as strain accumulated with increasing SMAT time. During grain refinement, the initiation and development of dislocation walls or cells came up at early stage. A strip of dislocation wall led to straight element concentration just prior to the formation of ultrafine-laminated (UFL) structures containing abundant twin boundaries (TB) and low angle grain boundaries (LAGB). The UFL structures with a texture orientation were subdivided by the development of dislocation arrays into ultrafine-grained (UFG) structures with random orientations. Meanwhile, the elements were dispersedly concentrated in a few grains. During grain coarsening, the dispersed element concentration still existed. The fraction of LAGB, TB and dislocation density was significantly reduced while the fraction of high angle grain boundary (HAGB) increased along with grain growth.
•The grain refinement and coarsening occurred gradually as strain accumulated with increasing SMAT time.•During grain refinement, the initiation and development of dislocation walls or cells came up at early stage.•A strip of dislocation wall led to straight element concentration just prior to the formation of UFL structures.•The UFL structures with a texture orientation were subdivided into UFG structures with random orientations.•LAGB, TB and dislocation density was significantly reduced while the fraction of high angle grain boundary increased.
The effect of displacement amplitude on fretting wear behavior and damage mechanisms of alloy 690 in air and nitrogen atmospheres was investigated in detail. The results showed that in air, the ...friction coefficient gradually increased with the increase in displacement amplitude which conformed to the universal law. In nitrogen, however, it had the highest point at the displacement amplitude of 60 μm due to very strong adhesion. Whether in air or nitrogen, the wear volume gradually increased with the increase in displacement amplitude. The wear volume in air was larger than that in nitrogen except at 30 μm. At 30 μm, the wear volume in air was slightly smaller. With an increase in displacement amplitude, a transformation of fretting running status between partial slip, mixed stick-slip, and final gross slip occurred along with the change of Ft-D curves from linear, to elliptic, to, finally, parallelogrammical. Correspondingly, the fretting regime changed from a partial slip regime to a mixed regime to a gross slip regime. With the increase in displacement amplitude, the transition from partial slip to gross slip in nitrogen was delayed as compared with in air due to the strong adhesion actuated by low oxygen content in a reducing environment. Whether in air or nitrogen, the competitive relation between fretting-induced fatigue and fretting-induced wear was prominent. The cracking velocity was more rapid than the wear. Fretting-induced fatigue dominated at 30 μm in air but at 30–60 μm in nitrogen. Fretting-induced wear won the competition at 45–90 μm in air but at 75–90 μm in nitrogen.
In the study, the protective effect of plasma protein from
(PPTT) on acute kidney injury (AKI) and the related molecular mechanisms were first investigated by Western blotting analyses, TdT-mediated ...dUTP Nick-End Labeling (TUNEL) assay, and immunohistochemistry. It was found that PPTT had an obviously inhibitory effect on Reactive oxygen species (ROS) in cyclophosphamide (CTX)-exposed mice. Furthermore, results demonstrated that the renal cell death mode is due to inducing apoptosis and autophagy inhibited by dose-dependent PPTT in mice treated with CTX by decreasing the protein expression of bax, beclin-1, and LC3 and increasing the expression of bcl-2. Moreover, the p38 MAPK and PI3K/Akt signaling pathways were observed to take part in the PPTT-induced renal cell growth effect by enhancing the upregulation of the expression of Akt and p-Akt as well as the downregulation of the expression of p38 and p-p38, which indicated a PPTT ameliorating effect on AKI CTX-induced in mice through p38 MAPK and PI3K/Akt signaling pathways. Briefly, this article preliminarily studies the mechanism of the PPTT ameliorating effect on AKI CTX-induced in mice, which helps to provide a reference for PPTT clinical application in AKI therapy.
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