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In this paper, recycled carbon fiber reinforced polymer (CFRP) mixture (CFRP-M, including recycled carbon fiber and powder) and refined recycled CFRP fiber (CFRP-F, mostly recycled carbon fiber) were added to cement to study the influence of addition on the flexural strength, compressive strength, and fluidity of cement-based materials. The recycled CFRP were prepared by mechanically processing the prepreg scraps generated during the manufacture of CFRP products. For comparison, commercial carbon fiber powder was also added in cement and the performance was compared to that of addition of recycled CFRP. The hydration products and strengthening mechanism of cement-based materials were analyzed by Fourier Transform Infrared Spectroscopy (FTIR) and Scanning Electron Microscope (SEM). The results show that the recycled CFRP has limited impact on the compressive strength but has an obvious improvement in the flexural strength of cement-based composites. Notably, CFRP-F is superior to CFRP-M in the reinforcement of cement-based materials. When the mass content of CFRP-F is 5%, the fluidity is 100 mm, and the flexural strength of specimens can be increased by up to 43.55%. Through XRD, FTIR, and SEM analysis, it is found that the main mechanism of recycled CFRP reinforced cement-based materials is the “bridging effect” induced by fibers and can prevent or delay the development of cracks. The recycled CFRP has no influence on the hydration process and will not introduce any new hydration products. Current research not only provides a theoretical basis for the design and use of recycled CFRP to reinforce cement-based composites but also offers a solution to relieve environmental pressure and improve resource utilization. [ABSTRACT FROM AUTHOR]

: Porphyromonas gingivalis (P. gingivalis) is one of the major pathogens causing periodontitis and apical periodontitis (AP). Long noncoding RNA (lncRNA) can regulate cellular mineralization and inflammatory diseases. The aim of this study was to investigate the role and mechanism of lncRNA in P. gingivalis-stimulated cementoblast mineralization. In vivo, C57BL/6 mice were divided into the healthy, the AP, and AP + P. gingivalis groups (n = six mice per group). Micro computed tomography, immunohistochemistry staining, and fluorescence in situ hybridization were used to observe periapical tissue. In vitro, cementoblasts were treated with osteogenic medium or P. gingivalis. Pluripotency associated transcript 3 (Platr3), interleukin 1 beta (IL1B), and osteogenic markers were analyzed by quantitative real-time polymerase chain reaction and western blot. RNA pull-down and RNA immunoprecipitation assays were used to detect proteins that bind to Platr3. RNA sequencing was performed in Platr3-silenced cementoblasts. In vivo, P. gingivalis promoted periapical tissue destruction and IL1B expression, but inhibited Platr3 expression. In vitro, P. gingivalis facilitated IL1B expression (P < 0.001), whereas suppressed the expression of Platr3 (P < 0.001) and osteogenic markers (P < 0.01 or 0.001). In contrast, Platr3 overexpression alleviated the repressive effect of P. gingivalis on cementoblast mineralization (P < 0.01 or 0.001). Furthermore, Platr3 bound to nudix hydrolase 21 (NUDT21) and regulated the nuclear factor-κB (NF-κB) signaling pathway. Knocking down NUDT21 suppressed osteogenic marker expression and activated the above signaling pathway. Collectively, the results elucidated that Platr3 mediated P. gingivalis-suppressed cementoblast mineralization through the NF-κB signaling pathway by binding to NUDT21. [ABSTRACT FROM AUTHOR]