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The microstructure and tensile failure evolution of AA5754O aluminum alloy CMT joints were investigated in this study. First, the microstructure and properties of aluminum alloy were observed using a hardness test and metallographic test. The microstructure and tensile failure evolution of AA5754O aluminum alloy CMT joints were studied using in situ CT tests. The defects in the heat-affected zone were mainly composed of pores with large sphericity. The softening failure was mainly due to the decrease in the effective bearing area due to the increase in the number of defects. There were a large number of shrinkage pores with sphericity less than 0.6 in the fusion zone defects. The softening failure was mainly due to the continuous growth and combination of shrinkage pores, which led to a decrease in the effective bearing area. Meanwhile, the variation process of the mean radii of the meso-defects in the heat-affected zone and fusion zone were analyzed. The material constants αRT and αRTm were 1.87 and 6.20 in the heat-affected zone and 7.21 and 5.31 in the fusion zone, respectively, which were found using the Rich and Tracey model and the improved Rich and Tracey model. [ABSTRACT FROM AUTHOR]

Macrophages are key responders of inflammation and are closely related with oxidative stress. Activated macrophages can enhance oxygen depletion, which causes an overproduction of reactive oxygen species (ROS) and leads to further excessive inflammatory response and tissue damage. Agmatine, an endogenous metabolite of L-arginine, has recently been shown to have neuroprotective effects based on its antioxidant properties. However, the antioxidant effects of agmatine in peripheral tissues and cells, especially macrophages, remain unclear. In this study we explored the role of agmatine in mediating antioxidant effects in RAW 264.7 cells and studied its antioxidant mechanism. Our data demonstrate that agmatine is an activator of Nrf2 signaling that markedly enhances Nrf2 nuclear translocation, increases nuclear Nrf2 protein level, up-regulates the expression of the Nrf2 downstream effector HO-1, and attenuates ROS generation induced by Lipopolysaccharide (LPS). We further demonstrated that the agmatine-induced activation of Nrf2 is likely through the PI3K/Akt pathway. LY294002, a specific PI3K/Akt inhibitor, abolished agmatine-induced HO-1 up-regulation and ROS suppression significantly. Inhibiting HO-1 pathway significantly attenuated the antioxidant effect of agmatine which the products of HO-1 enzymatic activity contributed to. Furthermore, the common membrane receptors of agmatine were evaluated, revealing that α2-adrenoceptor, I1-imidazoline receptor or I2-imidazoline receptor are not required by the antioxidant properties of agmatine. Taken together, our findings revealed that agmatine has antioxidant activity against LPS-induced ROS accumulation in RAW 264.7 cells involving HO-1 expression induced by Nrf2 via PI3K/Akt pathway activation. [ABSTRACT FROM AUTHOR]