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The relevant experiments and studies were conducted to address the metallurgical defects such as subcutaneous bubbles and slag inclusions occurring during the enamel steel continuous casting process. According to the high-temperature experimental results, calculations were made to determine the changes in viscosity and tension due to the steel reaction with the slag. Based on the experimental findings, there was a notable variation in the content of SiO2 and Al2O3 in the slag before and after the reaction. The concentration of the element Al in the steel melt significantly decreased, whereas the concentration of Ti showed a minimal change. These observations indicate that the reduction of SiO2 at the slag–steel interface is predominantly attributed to the role of Al. The calculation results showed that at 300 s of reaction time, the viscosity rapidly increased from 0.108 to 0.133 Pa·s and then slowly increased to 0.155 Pa·s; The interfacial tension rapidly decreased from its initial value of 1,380 mJ·m−2 to a minimum of 1,320 mJ·m−2, and it then slowly increased to an equilibrium state. Therefore, the main cause of the occurrence of porosity defects in the enamel steel continuous casting process is the reduction of interfacial tension between slag, steel, and gas caused by the reaction between the slag and steel, as well as the foaming of the slag.

Basic magnesium sulfate cement (BMSC) is a kind of magnesium oxide (MgO)–magnesium sulfate (MgSO4)–water (H2O) modified ternary cementitious material prepared from light burned magnesia, magnesium sulfate heptahydrate, water and additives. The effects of α-magnesium oxide/magnesium sulfate ratio (MO/MS), water/magnesium sulfate ratio (W/MS), sand-to-binder ratio (s/b) and superplasticiser dosage (SPD) on the performance of BMSC mortar were studied for the first time in this work. The results showed that for, optimal 28-day flexural strength, α-MO/MS = 10:1, W/MS = 16:1, s/b = 0.8 and SPD = 0.3%. For optimal 28-day compressive strength, α-MO/MS = 8:1, W/MS = 14:1, s/b = 0.6 and SPD = 0.4%. For best water resistance, α-MO/MS = 12.5:1, W/MS = 14:1, s/b = 0.2 and SPD = 0.1%. Based on these results, the basic mix proportion ranges of BMSC mortar should be α-MO/MS = 8:1–12.5:1, W/MS = 14:1–16:1, s/b = 0.2–0.6 and SPD = 0.1–0.4%. [ABSTRACT FROM AUTHOR]

Parathyroid hormone (PTH) and its related peptide (PTH-related peptide 1-34) are two of the Food and Drug Administration-approved bone-promoting drugs for age-related osteoporosis. Treatment with PTH stimulates bone formation. However, the molecular mechanisms of PTH-mediated osteoblast differentiation and cell proliferation are still not completely understood. In this study, we showed that PTH induced endoplasmic reticulum (ER) stress in osteoblasts through the PKR-like endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor 2α (EIF2α)-activating transcription factor 4 (ATF4)-signaling pathway. After separately blocking PERK-EIF2α-ATF4 signaling with two different inhibitors [AMG'44 and integrated stress response inhibitor (ISRIB)] or specific small interfering RNA for PERK and ATF4, the following targets were all downregulated: expression of osteoblast differentiation markers [runt-related transcription factor 2 (Runx2), alkaline phosphatase (Alp), type I collagen (Col1a1), and osteocalcin (Ocn)], cell proliferation markers (CyclinE, CyclinD, and CDC2), amino acid import (Glyt1), and metabolism-related genes (Asns). Additionally, Alp-positive staining cells, Alp activity, matrix mineralization, Ocn secretion, and cell proliferation indexes were inhibited. Interestingly, we found that salubrinal enhanced PTH-induced osteoblast differentiation and proliferation by maintenance of phosphorylation of EIF2α. Furthermore, we observed that PTH increased the association between heat shock protein 90 (HSP90) and PERK and maintained PERK protein stabilization in the early stages of PTH-induced ER stress. Treatment of MC3T3-E1 cells with geldanamycin, an HSP90 inhibitor, decreased PERK protein expression and inhibited osteoblast differentiation and cell proliferation upon PTH treatment. Taken together, our data demonstrate that PTH regulates osteoblast differentiation and cell proliferation, partly by activating the HSP90-dependent PERK-EIF2α-ATF4 signaling pathway.