Recrystallization Mechanism and Processing Map of 18CrNiMo7-6 Alloy Steel during Hot Deformation

In this study, isothermal single-pass forming doformation of forged 18CrNiMo7-6 alloy steel was carried out by Gleeble-3500 thermal simulation testing machine. The constitutive equations and processing maps with parameters of deformation temperature and strain rate were established. The results show that the optimum hot deformation parameters are temperature 1050 °C, strain rate 0.1 s–1 with the peak power efficiency being 0.432. The mechanism of grain refinement during hot compression was also characterized by electron backscatter diffraction (EBSD). The results show that continuous dynamic recrystallization (CDRX), discontinuous dynamic recrystallization (DDRX) and grain growth are the main microstructure evolution mechanisms during hot working. The rotation of sub-grains under CDRX mechanism is the main factor for the formation of new grains. In addition, the DDRX mechanism is formed by the bulging of HAGBs at the grain boundary triple junction of the original grains, and the CDRX mechanism forms finer grains. The study also found that temperature affected the organization evolution mechanism, the DDRX mechanism plays a leading role when the temperature is low. With the increase of deformation temperature, CDRX begins to play a leading role and forms finer grains. When the deformation temperature rises to 1150 °C, the grains continue to grow at a higher temperature

Pin1/YAP pathway mediates matrix stiffness‐induced epithelial–mesenchymal transition driving cervical cancer metastasis via a non‐Hippo mechanism

Abstract Cervical cancer metastasis is an important cause of death in cervical cancer. Previous studies have shown that epithelial–mesenchymal transition (EMT) of tumors promotes its invasive and metastatic capacity. Alterations in the extracellular matrix (ECM) and mechanical signaling are closely associated with cancer cell metastasis. However, it is unclear how matrix stiffness as an independent cue triggers EMT and promotes cervical cancer metastasis. Using collagen‐coated polyacrylamide hydrogel models and animal models, we investigated the effect of matrix stiffness on EMT and metastasis in cervical cancer. Our data showed that high matrix stiffness promotes EMT and migration of cervical cancer hela cell lines in vitro and in vivo. Notably, we found that matrix stiffness regulates yes‐associated protein (YAP) activity via PPIase non‐mitotic a‐interaction 1 (Pin1) with a non‐Hippo mechanism. These data indicate that matrix stiffness of the tumor microenvironment positively regulates EMT in cervical cancer through the Pin1/YAP pathway, and this study deepens our understanding of cervical cancer biomechanics and may provide new ideas for the treatment of cervical cancer