ABSTRACT
When aluminium-rich phase minerals are added to Portland cement, Al atoms will enter the C-S-H and Al, then a substitution reaction will occur, forming a hydrated silica-calcium aluminate (C-A-S-H), which changes the molecular structure of the cement material. Due to limitations in experimental methods, the research on the bonding effect between corroded ions and Al-substituted structures is still unclear. Here, the mechanism of an Al substitution reaction affecting the adsorption of chloride and sulphate ions was studied using simulation. The C-A-S-H model of aluminium random substitution was built, evaluating the binding effects among the C-A-S-H, and sulphate and chloride ions. The results demonstrated that the C-A-S-H structure generated by the Al substitution reaction increased the physical adsorption capacity of the chloride and sulphate ions. The adsorption capacity of the sulphate ions was 13.26% higher than that before the Al substitution, and the adsorption capacity of chloride ions was 21.32% higher than that before the Al substitution. The addition of high aluminium phase minerals caused the interfacial flocculants C-A-S-H and C-S-H to connect and intertwine in the the interface transition zone (ITZ) structure. The addition of high-alumina phase minerals improves the microstructure of concrete hydration products, improving the physical and mechanical properties and durability of concrete. After the addition of 20% lithium slag, the sulphate ion erosion content and the chloride ion erosion content of the concrete decreased by 13.65% and 15.72%, respectively. This paper provides a deeper understanding of the effect of high-alumina phase admixtures on concrete at the micro-scale.
ABSTRACT
BACKGROUND: Interleukin- (IL-) 18 is a proinflammatory cytokine related to cardiovascular diseases, including hypertension and atherosclerosis. This study is aimed at determining whether IL-18 is related to aortic dissection (AD) and identifying the underlying mechanisms. METHODS: IL-18 expression in human aorta samples from AD (n = 8) and non-AD (NAD, n = 7) patients was measured. In addition, the IL-18, IL-6, interferon- (IFN-) γ, and IL-18-binding protein (IL-18BP) concentrations in plasma samples collected from the NAD and AD patients were detected. The effects of IL-18 on macrophage differentiation and smooth muscle cell (SMC) apoptosis were investigated in vitro. RESULTS: IL-18 expression was significantly increased in the aorta samples from the AD patients compared with those from the NAD patients, especially in the torn section. Aortic IL-18 was mainly derived from macrophages and also partly derived from CD4+ T lymphocytes and vascular SMCs. Plasma IL-18, IFN-γ, and IL-6 levels were significantly higher in the AD group than in the NAD group, and the IL-18 levels were positively correlated with the IFN-γ and IL-6 levels. In addition, plasma IL-18BP and free IL-18 levels were also elevated in the AD group. Linear regression analysis showed that the IL-18 level was independently associated with the presence of AD. In addition, anti-mouse IL-18-neutralizing monoclonal antibodies (anti-IL-18 nAb) inhibited angiotensin II-induced M1 macrophage differentiation and SMC apoptosis in vitro. CONCLUSION: IL-18 may participate in AD by regulating macrophage differentiation and macrophage-induced SMC apoptosis.
