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With the utilisation of recycled aggregate concrete (RAC) in building construction, the durability of this material requires particular attention, especially in terms of chloride penetration. This paper presents a numerical study on the chloride diffusion mechanism within RAC. Considering the random distribution of recycled coarse aggregates (RCA), a five-phase RAC model – including new mortar, adherent old mortar, new interfacial transition zone (ITZ), old ITZ and original natural coarse aggregates – is proposed to predict the effective diffusion coefficient of chlorides in RAC. The parametric studies, based on a series of critical factors (i.e. volume fraction of RCA, adhesive ratio of old mortar, chloride diffusivity of adherent old mortar, thicknesses of old and new ITZs and chloride diffusivity of old and new ITZs), reveal the properties of each phase and their individual impact on the effective diffusion coefficient of chlorides in RAC. The results obtained indicate that, interestingly, the effective diffusion coefficient tends to vary in terms of its relationships with high-quality adherent old mortar, lower adhesive ratio of old mortar, smaller thickness of ITZs and relatively superior chloride penetration resistance of ITZs, which cannot be found from existing models and experiments.

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The pathogenesis of atherosclerosis is accompanied by chronic inflammation with changes in the stiffness of the coronary artery wall. Being the main component of the vascular media, the smooth muscle cells (SMCs) are crucial to maintain blood vessel function. SMCs are mechano-sensitive, which can rapidly adapt to the fluctuations in the microenvironment of the blood vessel, including the subtle changes of the vascular stiffness. However, how substrate stiffness influences the phenotype and inflammatory response of SMCs is not well understood. In this study, we investigated the effects of substrate stiffness on SMCs phenotype, inflammatory gene expression and the nuclear factorkappa B (NFκB) signaling pathway of vascular SMCs. From 1 kPa to 100 kPa, the SMCs cytoskeleton became more and more organized with the increase of the substrate stiffness, representing by the uniformed distribution of the stress fibers. SMCs cultured on both soft (1 kPa) and hard (100 kPa) substrate increased the expression of macrophage marker CD68 molecule (CD68) and Galectin 3 (LGALS3) and the inflammatory gene Interleukin-6 (IL-6) and Interleukin-1β (IL-1β) than those on 40 kPa substrate. Moreover, the protein expression level of phosphorylated nuclear factor kappa B inhibitor (p-IκB) was higher on either soft (1 kPa) or hard (100 kPa) substrate. In consistent, the dephosphorylated IκB showed a higher expression level on the substrate stiffness of 40 kPa. These results suggested that substrate stiffness played an important role in SMCs cell morphology, phenotype and inflammatory response by affecting NFκB signaling pathway.

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