Abstract In this paper, the microstructure, mechanical properties, and corrosion behavior of friction stir welded (FSW) joints of the two aluminum alloys 6005A‐5083 were investigated and their correlation was discussed. In contrast to FSW joints of the same aluminum material, this results in a “V” shape curve of hardness distributed nonsymmetrically along the weld. The lowest hardness area occurs at the interface between the heat‐affected zone and the thermo‐mechanically affected zone of 6005A (6‐HAZ and 6‐TMAZ) due to the transformation of the β" phase under the influence of heat input during the stir friction process. This also leads to all tensile specimens fracturing in this area. The corrosion behavior of the FSW joint in acidic solution containing Cl − was determined by an exfoliation corrosion (EXCO) test, an intergranular corrosion (IGC) test, and potentiodynamic polarization measurements, based on the potential application in acid rain environment. The results showed that the corrosion resistance order in the acidic solution is: 6‐HAZ > NZ > 6‐BM > 5‐HAZ > 5‐BM. The 5‐BM has the worst corrosion resistance due to the high corrosion sensitivity of Al 3 Mg 2 in acidic solution. However, good corrosion resistances are shown in NZ and 6‐HAZ, which is related to a relatively homogeneous microstructure in NZ and a dissolution or coarsening of β" phases in 6‐HAZ because of frictional heat input.
The identification of medicinal materials is the premise and guarantee of drug safety. The majority of scientific researchers are bound to favor the simple, fast, effective, and inexpensive identification process of herbals. Rhodiola crenulata is a traditional Tibetan medicine grown at high altitudes, mainly distributed in Tibet, Yunnan, and Sichuan regions of China. Rhodiola crenulate possesses multiple bioactivities, such as anti-inflammatory, anti-hypoxia, and antioxidant properties, and has great potential for development. With the increasing market demand and a rapid decrease in resource content, a large number of confused products of Rhodiola crenulata have been troubling people. Therefore, this protocol introduces a standard process for the identification of Rhodiola crenulata in the field combined with routine laboratory testing. The combination of habitat, microscopic features, and thin-layer chromatography will undoubtedly identify Rhodiola crenulata quickly, efficiently, and economically, contributing to the continuous development of Tibetan medicine and the quality control of medicinal materials.
The effect of adding a small amount of Ag on the microstructure evolution and superplastic properties of Mg-Y-Er-Zn (WEZ612) alloys was systematically studied. The basal texture of the refined WEZ612 alloy produced by equal channel angular pressing was altered to a non-basal structure upon the addition of Ag. Ag addition also refined the grain size and promoted the formation of a large number of nano-14H-long period stacking ordered phases. Using high-resolution transmission electron microscopy, many nano-precipitated phases were detected on the basal plane of the Mg-Y-Er-Zn-1Ag (WEZ612–1Ag) alloy, The nano-precipitated phases on the basal plane improved the thermal stability of the alloy, lowered the deformation activation energy (Q), and improved the stress sensitivity index (m). At 523 K with a strain rate of 10−2 s−1, the Q value of WEZ612 was higher than that of WEZ612–1Ag (299.14 and 128.5 kJ mol−1, respectively). In contrast, the m value of the WEZ612 alloy (0.16) was lower than that of the WEZ612–1Ag alloy (0.46). At 623 K with a tensile rate of 10−2 s−1, the WEZ612 and WEZ612–1Ag alloys were elongated by 182% and 495%, respectively, with the latter exhibiting high-strain-rate and low-temperature superplasticity. The improved superplasticity of the WEZ612-1Ag alloy is attributed to the nano-precipitated phases, which effectively limit the cavity extension during superplastic deformation.
In this study, the influence of repair welding on microstructure evolution, mechanical properties, and corrosion resistance of SUS304-Q345B dissimilar metal active gas arc (MAG) welding plates was investigated via optical microscopy (OM), scanning electron microscopy (SEM), electron backscatter diffraction (EBSD), hardness, tensile, fatigue, intergranular corrosion, and electrochemical tests, in which the zero (R0), primary (R1), and secondary repair welding (R2) were performed by MAG welding. The results showed that, after repair welding, the δ-ferrite morphology in the weld evolved from a continuous dendritic shape to a dispersed worm-like structure and the bar ferrite in the heat-affected zone of SUS304 (HAZSUS304) evolved into short bar ferrite. The grain size of the weld was reduced due to the remelting caused by repair welding. The hardness of the weld increased first and then decreased which was related to the decrease of δ-ferrite morphology and grain size of weld. In the tensile test, all specimens were fractured at Q345B base material (BMQ345B), which revealed that repair welding had little effect on the tensile properties. The fatigue limit strength of R1 didn't reduce significantly, while the fracture position of R2 transferred from the SUS304 base material (BMSUS304) to the fusion line of SUS304 (FLSUS304). The corrosion resistance of R1 weld possessed the best corrosion resistance owing to the finer grain size and better δ-ferrite morphology. The results indicated that repair welding was feasible for the repair and reuse of welded joints, and it was of great importance in engineering applications of welded plates.
Cerebral ischemia/reperfusion injury (CIRI) is a major complication of acute ischemic stroke (AIS), characterized by calcium overload, oxidative stress, and cell apoptosis. In this study, we investigated the therapeutic potential of Genistein (Gen) in alleviating CIRI by focusing on its effects on the Wnt/Ca2+ signaling pathway. Using a rat model of cerebral ischemia/reperfusion and in vitro experiments on PC12 cells, we observed that Gen treatment reduced infarct size, improved neurological function, and mitigated calcium overload, oxidative stress, and apoptosis. Further analysis revealed that Gen regulates key proteins in the Wnt/Ca2+ signaling pathway, including Wnt5a and Frizzled-2, effectively preventing intracellular calcium accumulation and subsequent damage. The knockdown of Frizzled-2 confirmed the pathway's role in mediating calcium overload and subsequent damage. Our findings suggest that Gen alleviates CIRI by inhibiting the Wnt/Ca2+ signaling pathway, positioning it as a promising candidate for therapeutic intervention in stroke treatment.
During the immune response, B cells can enter the memory pathway, which is characterized by class switch recombination (CSR), or they may undergo plasma cell differentiation (PCD) to secrete immunoglobulin. Both of these processes occur in activated B cells, which are reported to relate to membrane-association proteins and adaptors. Protein 4.1R acts as an adaptor, linking membrane proteins to the cytoskeleton, and is involved in many cell events such as cell activation and differentiation, and cytokine secretion. However, the effect of 4.1R on regulating B-cell fate is unclear. Here, we show an important association between B-cell fate and 4.1R. In vitro, primary B cells were stimulated with lipopolysaccharide combined with interleukin-4; results showed that 4.1R-deficient (4.1R-/- ) cells compared with wild-type (4.1R+/+ ) B cells augmented expression of activation-induced cytidine deaminase and germline, resulting in increased IgG1+ B cells, whereas the secretion of IgG1 and IgM was reduced, and CD138+ B cells were also decreased. Throughout the process, 4.1R regulated canonical nuclear factor (NF-κB) rather than non-canonical NF-κB to promote the expression of CSR complex components, leading to up-regulation of B-cell CSR. In contrast, 4.1R-deficient B cells showed reduced expression of Blimp-1, which caused B cells to down-regulate PCD. Furthermore, over-activation of canonical NF-κB may induce apoptosis signaling to cause PCD apoptosis to reduce PCD number. In summary, our results suggest that 4.1R acts as a B-cell fate regulator by inhibiting the canonical NF-κB signaling pathway.
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