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Lime is a widely used construction and building material. As an alkali activator, lime can reduce costs, improve safety of on-site construction, and ensure environmental benefits. In this study, the effects of different lime contents on the physicomechanical characteristics and the hydration properties of circulating fluidized bed fly ash-blast furnace slag-based cementitious materials (CBCM) were evaluated. The results revealed that flowability and setting time of CBCM decreased with the increasing lime content. The mechanical properties first showed an increasing trend and then declined, achieving their optimal levels at 20 % lime content. Similar to the mechanical properties, the density of CBCM increased first and then decreased with the increase of lime content, enriching its maximum at the same lime amount. The main hydration products of CBCM are ettringite and C-(A)-S-H gel. Ettringite is mainly generated in large quantities within 3 days, which is the main reason for the early strength of CBCM. The highest reaction degree of calcium hydroxide was obtained at the lime content of 20 %, and a significant amount of dense foil-like C-(A)-S-H gel was formed. The calcium hydroxide precipitated once the lime content exceeded 20 %. The hydration reaction was blocked, and the hydration products were relatively reduced.

Alkali-activated materials prepared from industrial solid wastes have excellent performance, advancing the cement industry towards achieving the Net-zero emissions goal. However, the diverse synergistic effects of various solid waste types necessitate further investigation. In this study, the effect of different content (20 %, 30 %, 40 %, and 50 %) of ground granulated blast furnace slag (GGBFS) on the mechanical performance of circulating fluidized bed fly ash (CFBFA)-GGBFS-lime ternary cementitious materials (CGL) was investigated. The synergistic mechanism of GGBFS and CFBFA was elucidated through analyses of hydration heat, XRD, FT-IR, and SEM-EDS tests. The results indicated that GGBFS facilitated sulfate consumption during the early hydration stage, promoting the dissolution of CFBFA. This, in turn, enhanced the availability of sulfate, calcium, and active silicon-aluminum phases for CGL hydration, ultimately leading to an improvement in their overall hydration degree. Conclusively, the optimal synergistic effect between CFBFA and GGBFS was observed at a GGBFS content of 40 %, with a compressive strength of 32.84 MPa at 28 days. However, excessive GGBFS content (50 %) could lead to the premature formation of a “hydration barrier membrane”, negatively affecting the sustained hydration of CGL. This work presented an eco-friendly approach to the resource utilization of CFBFA, particularly in terms of mineral resource consumption, and held promising prospects for applications in projects.

Senescence of bone marrow mesenchymal stem cells (BMSCs) is one of the leading causes of osteoporosis. SIRT3, an essential NAD-dependent histone deacetylase, is highly correlated with BMSC senescence-mediated bone degradation and mitochondrial/heterochromatic disturbance. S-sulfhydration of cysteine residues favorably enhances SIRT3 activity by forming persulfides. Nevertheless, the underlying molecular mechanism of SIRT3 S-sulfhydration on mitochondrial/heterochromatic homeostasis involved in BMSC senescence remains unknown. Here, we demonstrated that CBS and CSE, endogenous hydrogen sulfide synthases, are downregulated with BMSC senescence. Exogenous H2S donor NaHS-mediated SIRT3 augmentation rescued the senescent phenotypes of BMSCs. Conversely, SIRT3 deletion accelerated oxidative stress-induced BMSC senescence through mitochondrial dysfunction and the detachment of the heterochromatic protein H3K9me3 from the nuclear envelope protein Lamin B1. H2S-mediated SIRT3 S-sulfhydration modification rescued the disorganized heterochromatin and fragmented mitochondria induced by the S-sulfhydration inhibitor dithiothreitol, thus leading to elevated osteogenic capacity and preventing BMSC senescence. The antisenescence effect of S-sulfhydration modification on BMSCs was abolished when the CXXC sites of the SIRT3 zinc finger motif were mutated. In vivo, aged mice-derived BMSCs pretreated with NaHS were orthotopically transplanted to the ovariectomy-induced osteoporotic mice, and we proved that SIRT3 ameliorates bone loss by inhibiting BMSC senescence. Overall, our study for the first time indicates a novel role of SIRT3 S-sulfhydration in stabilizing heterochromatin and mitochondrial homeostasis in counteracting BMSC senescence, providing a potential target for the treatment of degenerative bone diseases.