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Abstract Non-penetration laser welding of lap joints in austenitic stainless steel sheets is commonly preferred in fields where the surface quality is of utmost importance. However, the application of non-penetration welded austenitic stainless steel parts is limited owing to the micro bulging distortion that occurs on the back surface of the partial penetration side. In this paper, non-penetration lap laser welding experiments, were conducted on galvanized and SUS304 austenitic stainless steel plates using a fiber laser, to investigate the mechanism of bulging distortion. A comparative experiment of DC01 galvanized steel-Q235 carbon steel lap laser welding was carried out, and the deflection and distortion profile of partially penetrated side of the sheets were measured using a non-contact laser interferometer. In addition, the cold-rolled SUS304 was subjected to heat holding at different temperatures and water quenching after bending to characterize its microstructure under tensile and compressive stress. The results show that, during the heating stage of the thermal cycle of laser lap welding, the partial penetration side of the SUS304 steel sheet generates compressive stress, which extrudes the material in the heat-affected zone to the outside of the back of the SUS304 steel sheet, thereby forming a bulge. The findings of these experiments can be of great value for controlling the distortion of the partial penetrated side of austenitic stainless steel sheet during laser non-penetration lap welding.

In this paper, the combined effect of Sn addition and solution treatment temperature on natural aging (NA) hardness behavior and microstructure of Al-0.4Mg-1.0Si alloy were investigated by hardness test, scanning electron microscope (SEM) and scanning transmission electron microscope (STEM). The evolutions of clusters characterized by three-dimensional atom probe (3DAP) during initials stages of NA are also investigated based on the slow in formation of clusters due to Sn addition. The results shown that a Sn-rich particles with round shape retained in Al matrix after quenching treatment when the added Sn content exceeds it limit solubility, which will reduce the Mg content of the designed alloy. The suppression of NA can be enhanced with the increase in the adding Sn content and solution treatment temperature, which is strongly related to the delay of the segregation of Mg and Si to form clusters due to more trapping vacancies by Sn atoms. The addition of Sn also revealed that the segregation of Si during NA is earlier than that of Mg atoms. The Si-rich clusters are formed preferentially during initial stage of NA, and Mg–Si co-clusters are formed after long period of NA. The Mg/Si ratio and average size of Sn-containing clusters in the 0.04%Sn and 0.1%Sn alloy are obviously higher than that of Sn-free clusters regardless of the 1 day NA or 14 days NA as more Mg atoms are dragged into Sn-containing clusters due to strong interaction between Sn and Mg atoms.

Abstract Autophagy plays an important role in determining stem‐cell differentiation. During the osteogenic differentiation of mesenchymal stem cells (MSCs), autophagosome formation is upregulated but the reason is unknown. A long‐standing quest in the autophagy field is to find the membrane origin of autophagosomes. In this study, cytoplasmic coat protein complex II (COPII) vesicles, endoplasmic reticulum‐derived vesicles responsible for the transport of storage proteins to the Golgi, are demonstrated to be a critical source of osteoblastic autophagosomal membrane. A significant correlation between the number of COPII vesicle and the autophagy level is identified in the rat bone tissues. Disruption of COPII vesicles restrained osteogenesis and decreased the number and size of autophagosomes. SEC31a (an outer coat protein of COPII vesicle) is found to be vital to regulate COPII vesicle‐dependent autophagosome formation via interacting with ATG9a of autophagosomal seed vesicles. The interference of Sec31a inhibited autophagosome formation and osteogenesis in vitro and in vivo. These results identified a novel mechanism of autophagosome formation in osteogenic differentiation of stem cells and identified SEC31a as a critical protein that mediates the interplay between COPII and ATG9a vesicles. These findings broaden the understanding of the regulatory mechanism in the osteogenic differentiation of MSCs.