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The changes that occur in the microstructure of crystalline and amorphous Cu-P-Sn-Ni filler metals during the heating process were studied by high-temperature microscopy, and the composition of solders at certain temperatures were analyzed by scanning electron microscopy and X-ray diffraction. The amorphous solder was observed to transform from amorphic to crystalline during the process of heating and distinct surface morphology changes were apparent, while the internal structure of the crystalline brazing filler metal was found to be relatively stable. During the heating process, the amorphous brazing filler metal formed a ϒ-Cu solid solution with a small amount of Cu3P compounds, Cu88Sn22 and (Cu, Ni)3P phase compounds, ultimately forming the Cu88Sn22 + Ni12P5 + (Cu, Ni)3P3 three-element eutectic structure.

W-Cu alloy and 1Cr18Ni9 steel were brazed with NiCrSiBFeTi and NiMnSiCuZr filler metals in a vacuum furnace. The main microstructure of the NiCrSiBFeTi brazing seam region was a Ni-based solid solution of W, Cu, Cr, and Fe dissolved in the Ni phase and intermetallic compounds CrB and TiCr2. The main microstructure of the NiMnSiCuZr brazing seam region was a Ni-based solid solution of Cu, Cr, and Fe dissolved in the Ni phase Fe-based solid solution of Ni, Cu, and Cr dissolved in the Fe phase and intermetallic compounds Mn5Si3, Ni3Si, and Ni7Zr2. The elements Ni, Si, and Ti contained in the NiCrSiBFeTi filler metal and the elements Ni, Mn, and Si contained in the NiMnSiCuZr filler metal were more easily diffused into the interface of W-Cu alloy compared with that of 1Cr18Ni9 steel. The shear strength values of NiCrSiBFeTi joint and NiMnSiCuZr joint were approximately 285 and 249 MPa, respectively, and fracture of the two joints occurred at the interface near the W-Cu alloy side. The fracture morphology of the former was identified as cleavage brittle fracture, and the latter was identified as intergranular brittle fracture.

W75-Cu and W55-Cu alloys were brazed with a Cu-based filler metal under the process parameters of a brazing temperature of 1060°C and a holding time of 30 min in a vacuum furnace with a vacuum level >6×10-3 Pa. The microstructure, element distribution, phase constituents, four-point bending strength, and fracture morphology of the brazed joint were studied with a series of standard methods. The results indicated that the main microstructure of the brazing seam region was a Cu-based solid solution of Mn and Co dissolved in the Cu phase. The element Cu and a little element W from two sides of the base metals transited into the brazing seam region, and the elements Cu, Mn, and Co contained in the brazing filler metal diffused into the interface or even substrates. The main phases that existed in the brazed joint were Cu-rich phase Cu(Mn,Co), simple substance of W, simple substance of Cu, and trace amounts of Cu0.4W0.6. The four-point bending strength was about 950 MPa, and fracture occurred at the interface near the W75-Cu alloy side. The fracture morphology of the W75-Cu/W55-Cu brazed joint was identified as mixed ductile-brittle.

This thesis is a discussion on obtaining a vacuum brazing joint of W-Cu alloy and 18-8 stainless steel with Cu-Mn-Co filler metal under the process parameter of a brazing temperature of 1060°C and holding time of 1 h. Four-point bending strength was tested at room temperature. Microstructure, microhardness, and element distribution near the interface of the brazed seam were observed via micro sclerometer, scanning electron microscope (SEM), and energy disperse spectroscopy (EDS) methods. Finally, analysis of the existence for phase composition near the interface was conducted using X-ray diffraction. Corresponding to a four-point bend strength of 780 MPa, there was a plain-interface, dense microstructure without obvious microdefects that formed. Microhardness values increased near the interface of the brazed joint and decreased gradually to the center of the brazed seam. Element distribution indicated that elements (Cu, Mn, Co) from the filler metal diffused into the interface or even substrates, and Fe and Cu element, together with a little of W element, from the substrates dissolved into the brazed seam region. Fracture morphology of the W-Cu/18-8 steel joint was identified as a mixed feature of fracture type. Moreover, the brazing seam contained mainly a Cu-rich phase, W0.4Cu0.6, α-Fe, and simple substance of W, together with a little of Co0.7Fe0.3.

Objective: This study aims to investigate the effect of Bacillus subtilis WB800N on diabetic wounds. Methods: Haematoxylin & eosin (H&E) staining was used to observe the healing of skin wounds. Collagen deposition was assessed by Masson staining. Western blotting and qRT‐PCR were used to detect vascular endothelial‐related factors (VWF), CD31, TLR2, NLRP3, ASC and Caspase‐1 expression. 16S rDNA sequencing detected microbiota distribution. The concentrations of IL‐1β and IL‐37 were measured by ELISA. Apoptosis was measured by the TUNEL assay. Results: Compared with the control group, wound healing was delayed in diabetic mice. The wound area in the Bacillus subtilis group decreased more significantly than the diabetic wound group. H&E staining showed that Bacillus subtilis WB800N promoted wound healing and increased re‐epithelialization. Masson staining showed that Bacillus subtilis WB800N increased collagen deposition in mice with diabetic wounds. Bacillus subtilis WB800N upregulated VWF and CD31 protein expression in diabetic wounds mice. The 16S rDNA results showed that Bacillus subtilis WB800N reduced the diversity of the gut microbiota of diabetic wounds mice and regulated the microbial composition. At the genus level, Bacillus subtilis WB800N reduced the relative abundance of Muribaculaceae and CG − 005 in diabetic wounds mice, whilst increasing the relative abundance of Lactobacillus. Bacillus subtilis WB800N increased the expression of TLR2, NLRP3, ASC and Caspase‐1. Bacillus subtilis WB800N increased the concentrations of IL‐1β and IL‐37 in serum. Bacillus subtilis WB800N upregulated cell apoptosis. The TLR2 antagonist Sparstolonin B (SsnB) reduced the expression of TLR2, NLRP3, ASC, Caspase‐1, IL‐1β and IL‐37 and the apoptosis in diabetic wounds mice, whilst the combined intervention of Bacillus subtilis and SsnB reversed the effect of SsnB treatment alone. Conclusion: Bacillus subtilis WB800N alleviated diabetic wound healing by regulating gut microbiota homeostasis and TLR2. Significance and impact of research: Our findings might provide potential therapeutic targets for diabetic wounds. [ABSTRACT FROM AUTHOR]