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        Additive/subtractive hybrid manufacturing of 316L stainless steel powder: Densification, microhardness and residual stress

        Yuying Yang,Yadong Gong,Shuoshuo Qu,Bo Xin,Yunchao Xu,Yang Qi 대한기계학회 2019 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.33 No.12

        316L stainless steel specimens were manufactured by additive/subtractive hybrid manufacturing (ASHM). The densification level, microstructure, microhardness and residual stress characterization in the different zones of the part were investigated. The density was determined by the Archimedes method, and the density measurement was divided into three regions, namely, the bottom, middle and top zones. The results show that the middle zone has a much smoother melting surface and that a relative density of nearly 100 % was achieved for the part in this study. The hardness profiles at room temperature, along the width and height directions of the cross-section of the top and bottom zones, were also studied. The residual stress was evaluated by X-ray diffraction (XRD) for the 316L SS specimen fabricated by the ASHM process, and it was compared with a specimen manufactured by the additive laser directed energy deposition (DED) process. The results show that the top and bottom zones exhibit tensile stress, and compressive stress occurs in the middle area. Moreover, the residual stress of ASHM shows a slightly smaller trend than that of the simplex DED due to the stress relaxation of the subsequent subtractive milling. These results may offer guidance for ASHM-fabricated 316L parts.

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        Gastrin stimulates pancreatic cancer cell directional migration by activating the Gα12/13–RhoA–ROCK signaling pathway

        Ganggang Mu,Qianshan Ding,Hongyan Li,Li Zhang,Lingli Zhang,Ke He,Lu Wu,Yunchao Deng,Dongmei Yang,Lianlian Wu,Ming Xu,Jie Zhou,Honggang Yu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-

        The mechanism by which gastrin promotes pancreatic cancer cell metastasis is unclear. The process of directing polarized cancer cells toward the extracellular matrix is principally required for invasion and distant metastasis; however, whether gastrin can induce this process and its underlying mechanism remain to be elucidated. In this study, we found that gastrin-induced phosphorylation of paxillin at tyrosine 31/118 and RhoA activation as well as promoted the metastasis of PANC-1 cancer cells. Depletion of Gα12 and Gα13 inhibited the phosphorylation of paxillin and downstream activation of GTP-RhoA, blocked the formation and aggregation of focal adhesions and facilitated polarization of actin filaments induced by gastrin. Suppression of RhoA and ROCK also exhibited identical results. Selective inhibition of the CCKBR–Gα12/13–RhoA–ROCK signaling pathway blocked the reoriented localization of the Golgi apparatus at the leading edge of migrated cancer cells. YM022 and Y-27632 significantly suppressed hepatic metastasis of orthotic pancreatic tumors induced by gastrin in vivo. Collectively, we demonstrate that gastrin promotes Golgi reorientation and directional polarization of pancreatic cancer cells by activation of paxillin via the CCKBR–Gα12/13–RhoA–ROCK signal pathway.

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