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In order to investigate the effect of microalloying element composite adjustment on the corrosion resistance of Q345qE bridge steel, the influences of alloy element Cr, Ni, and Cu composite adjustment on the corrosion resistance of Q345qE bridge steel were studied by confocal laser scanning microscopy (CLSM), electrochemical workstation, field emission scanning electron microscopy (FE-SEM), and X-ray diffraction (XRD). Results showed that the compactness and protectiveness of the rust layer were improved after the composite adjustment of Cr, Ni and Cu microalloying elements. The Cr element in the rust layer on the Q345qE bridge steel surface could be enriched in the inner rust layer, which effectively blocked the penetration and transmission of corrosive ions such as Cl- and enhanced the protective ability of the rust layer on the substrate. After alloying element adjustment, the proportion of α-FeOOH that was more stable than γ-FeOOH in the rust layer of Q345qENH steel increased. Generally, Q345qE bridge steel with composite adjustment by microalloying elements possessed better corrosion resistance compared to ordinary Q345qE in 3.5% NaCl solution.

To study the source of inclusions in casting billets, 10% BaCO3, 10% SrCO3, and 10% La2O3 were used as tracers into the steel ladle, tundish covering flux, and tundish-coating refractories, respectively, during the production of non-oriented silicon steel. The steel and slag samples were taken from the related working procedure, and scanning electron microscopy (SEM) and a mi-croscope were used to analyze the morphology and composition of inclusions. Experimental results show that the large inclusions in non-oriented silicon steel are mainly SiO2, Al2O3, and aluminosilicate, resulting from the protecting slag and secondary oxidation.

The changes of total oxygen(T. O.) and N contents,the evolution of non-metallic inclusions,and the characteristic of macro-inclusions in casting billets of 50 CrVA spring steel produced by the BOF-LF-CC process were studied by continuous sampling at different stages. Results show that the average contents of T. O. and N are 106×10-6 and 13×10-6 at LF-start,respectively,and they become 15×10-6 and 39×10-6 in billets,indicating that the deoxidization effect in the LF refining process is obvious. However,reoxidation phenomenon is obvious in the transportation and casting processes,so it is necessary to strengthen the steel stream protection from ladle to tundish. The CaO-Al2O3-MgO and CaO-Al2O3-SiO2 composite oxide inclusions are the main inclusions in billets,the Al2O3 content in those inclusions is as high as 60%-70%,and no low-melting inclusion is obtained. The low-melting inclusion can be obtained by increasing the slag basicity or feeding a proper content of Ca wire. Large-size inclusions are primarily composed of CaO and CaOAl2O3-SiO2-(MgO) spherical oxides as well as a certain proportion of pure Al2O3 inclusions. It is necessary to extend the soft stirring time in the ladle to make inclusions float fully.

To improve the effect of LF refining on SPHC steel, thermodynamics software FactSage was used to analyze the physi-cochemical properties of the LF refining slag system, and then the corresponding optimization scheme was verified by industrial verifi-cation. Experimental results show that at the end of LF refining, the total oxygen T[O] in steel decreases from 24×10-6 to 20×10-6, the total removal rate of micro inclusions increases from 56.67% to 71.54%, and the amount of large inclusions decreases to 42.45 mg/10 kg from 85.42 mg/10 kg by the optimization of the LF refining slag system.

Objective: Wear‐induced aseptic loosening has been accepted as one of the main reasons for failure of total hip arthroplasty. Ceramic wear debris is generated following prosthesis implantation and plays an important part in the upregulation of inflammatory factors in total hip arthroplasty. The present study investigates the influence of ceramic debris on osteoblasts and inflammatory factors. Methods: Ceramic debris was prepared by mechanical grinding of an aluminum femoral head and added to cultures of MC3T3‐E subclone 14 cells at different concentrations (i.e. 0, 5, 10, and 15 μg/mL). Cell proliferation was evaluated using a Cell Counting Kit (CCK‐8), and cell differentiation was assessed by mRNA expression of alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). In addition, cell bio‐mineralization was evaluated through alizarin red S staining, and release of tumor necrosis factor alpha (TNF‐α), interleukin‐1 beta (IL‐1β), and interleukin‐6 (IL‐6) was measured through enzyme‐linked immunosorbent assays (ELISA). Furthermore, mRNA expression of Smad1, Smad4, and Smad5 and protein expression of phosphorylated Smad1, Smad4, and Smad5 were measured by reverse transcriptase polymerase chain reaction (RT‐PCR) and western blotting. Results: The ceramic debris had irregular shapes and sizes, and analysis of the size distribution using a particle size analyzer indicated that approximately 90% of the ceramic debris was smaller than 3.2 μm (2.0 ± 0.4 μm), which is considered clinically relevant. The results for mRNA expression of ALP, OCN, and OPN and alizarin red S staining indicated that cell differentiation and bio‐mineralization were significantly inhibited by the presence of ceramic debris at all tested concentrations (P < 0.05, and the values decreased gradually with the increase of ceramic debris concentration), but the results of the CCK‐8 assay showed that cell proliferation was not significantly affected (P > 0.05; there was no significant difference between the groups at 1, 3, and 5 days). In addition, the results of ELISA, RT‐PCR, and western blotting demonstrated that ceramic debris significantly promoted the release of inflammatory factors, including TNF‐α, IL‐β, and IL‐6 (P < 0.05, and the values increased gradually with the increase of ceramic debris concentration), and also greatly reduced the mRNA expression of Smad1, Smad4, and Smad5 (the values decreased gradually with the increase of ceramic debris concentration) as well as protein expression of phosphorylated Smad1, Smad4, and Smad5. Conclusion: Ceramic debris may affect differentiation and bio‐mineralization of MC3T3‐E subclone 14 cells through the bone morphogenetic protein/Smad signaling pathway. [ABSTRACT FROM AUTHOR]