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Rebar is an extremely important building material. The cooling rate and the presence of niobium (Nb) element are key factors influencing the overall performance of rebars. In this work, the high-strength rebar’s microstructure, precipitated phase, and mechanical properties were characterized using scanning electron microscopy, transmission electron microscopy, HVS-1000 hardness tester, and MTS810 universal tensile testing machine. The results showed that a shift in cooling rate from 0.3 to 3°C·s−1 resulted in noticeable changes in the microstructures of rebars, particularly between Nb-free and Nb-containing variants. In the case of Nb-containing rebars, there was an increase of 8.26% in the proportion of pearlite, along with a decrease of 10.63 μm in the average grain size of ferrite. Furthermore, the lamellar spacing of pearlite experienced a decrease of 0.0495 μm, the proportion of low-angle grain boundaries saw an increment of 4.13%, and the size of the precipitated phase (Nb, Ti, V) C reduced by 18.9 nm. These changes collectively led to a significant increase in hardness (98.56 HV), yield strength (179.02 MPa), and ultimate strength (199.43 MPa). The resultant fracture morphology manifested as a dimple pattern.

HRB500E rebar is a low-alloy high-strength steel with excellent mechanical properties and good plasticity but suffers from deficient corrosion resistance. This can be solved by adding trace elements, including rare earth elements. Herein, the corrosion-resistant behavior of rebar was evaluated by weightlessness testing and electrochemical measurements, and the effects of Ce on the structural evolution of the corrosion product layer were investigated by scanning electron microscopy (SEM), Electron Probe X-ray Micro-Analyzer (EPMA), X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS). The results showed that adding Ce to the rebar improved the densification of the reinforcing surface corrosion products, as well as reduced the corrosion rate of the experimental rebar. Compared to C0 sample without Ce, the rebar sample containing 0.044 wt.% Ce displayed increased Ecorr by 0.051 V, decreased Icorr by 15.573 mA cm−2, enhanced Rc of the corrosion product layer by 112.71 Ω cm2, incremented α-FeOOH content in the corrosion product layer, and boosted ratio of α/γ* in the corrosion product layer by 10.11%. Furthermore, the oxide (CeO2) formed by Ce in the corrosion layer of the rebar bar surface existed in the rust layer, resulting in a stable corrosion product layer with improved blocking ability of the corrosive medium. Overall, the addition of Ce at certain ratios looks promising to produce HRB500E rebar with excellent corrosion resistance and extended service life under harsh conditions. [ABSTRACT FROM AUTHOR]

Sodium–glucose cotransporter 2 inhibitors, efficacious antidiabetic agents that have cardiovascular and renal benefits, can promote pancreatic β-cell regeneration in type 2 diabetic mice. However, the underlying mechanism remains unclear. In this study, we aimed to use multiomics to identify the mediators involved in β-cell regeneration induced by dapagliflozin. We showed that dapagliflozin lowered blood glucose level, upregulated plasma insulin level, and increased islet area in db/db mice. Dapagliflozin reshaped gut microbiota and modulated microbiotic and plasmatic metabolites related to tryptophan metabolism, especially l-tryptophan, in the diabetic mice. Notably, l-tryptophan upregulated the mRNA level of glucagon-like peptide 1 (GLP-1) production–related gene (Gcg and Pcsk1) expression and promoted GLP-1 secretion in cultured mouse intestinal L cells, and it increased the supernatant insulin level in primary human islets, which was eliminated by GPR142 antagonist. Transplant of fecal microbiota from dapagliflozin-treated mice, supplementation of l-tryptophan, or treatment with dapagliflozin upregulated l-tryptophan, GLP-1, and insulin or C-peptide levels and promoted β-cell regeneration in db/db mice. Addition of exendin 9-39, a GLP-1 receptor (GLP-1R) antagonist, or pancreatic Glp1r knockout diminished these beneficial effects. In summary, treatment with dapagliflozin in type 2 diabetic mice promotes β-cell regeneration by upregulating GLP-1 production, which is mediated via gut microbiota and tryptophan metabolism. Article Highlights: Sodium–glucose cotransporter 2 inhibitors, novel and efficacious antidiabetic agents, can preserve β-cell mass in type 2 diabetic animals, but the mechanism remains unclear. We find that dapagliflozin reshapes gut microbiota, improves microbiotic and plasmatic metabolites related to tryptophan metabolism, and increases glucagon-like peptide 1 (GLP-1) production mediated via tryptophan metabolism. GLP-1−GLP-1 receptor signaling participates in the dapagliflozin-induced β-cell regeneration. Our study reveals that the gut microbiota–tryptophan metabolism–GLP-1 axis is a novel mechanism of β-cell regeneration induced by dapagliflozin and provides experimental evidence for its β-cell protection in treating type 2 diabetes. [ABSTRACT FROM AUTHOR]