Rotating bending (52.5 Hz) and ultrasonic (20 kHz) fatigue tests were performed on the specimens of a bearing steel, which were quenched and tempered at 150°C, 300°C, 450°C and 600°C, respectively, to investigate the influence of strength level and loading frequency on the fatigue behavior in veryhigh-cycle regime. Influences on fatigue resistance of materials, characteristics of S-N curves and transition of crack initiation site were discussed. The specimens with higher strength showed interior fracture mode in very-high-cycle regime and with slight frequency effect, otherwise cracks all initiate from the surface and the fatigue strength was much higher under ultrasonic cycling.
This paper studies the formation mechanism of fine granular area (FGA) in high-strength steels and predicts the threshold value of its formation. Fatigue experiments are carried out by using rotating bending and ultrasonic fatigue testing machines on a high carbon chromium steel (GCr15) with three different heat treatments. The results show that the range of stress intensity factor at the periphery of FGA (K FGA) keeps constant with an average value of 5.2 MPa m 1/2 , which is close to the traditional crack growth threshold (K th,0), 5.0 MPa m 1/2. A theoretical model based on the plastic zone at crack tip is proposed to predict the value of K FGA and the predictions are in good agreement with experimental data.
Intestinal microbiota dysbiosis is an established characteristic of ulcerative colitis (UC). Regulating the gut microbiota is an attractive alternative UC treatment strategy, considering the potential adverse effects of synthetic drugs used to treat UC. Kaempferol (Kae) is an anti-inflammatory and antioxidant flavonoid derived from a variety of medicinal plants. In this study, we determined the efficacy and mechanism of action of Kae as an anti-UC agent in dextran sulfate sodium (DSS)-induced colitis mice. DSS challenge in a mouse model of UC led to weight loss, diarrhea accompanied by mucous and blood, histological abnormalities, and shortening of the colon, all of which were significantly alleviated by pretreatment with Kae. In addition, intestinal permeability was shown to improve using fluorescein isothiocyanate (FITC)–dextran administration. DSS-induced destruction of the intestinal barrier was also significantly prevented by Kae administration via increases in the levels of ZO-1, occludin, and claudin-1. Furthermore, Kae pretreatment decreased the levels of IL-1β, IL-6, and TNF-α and downregulated transcription of an array of inflammatory signaling molecules, while it increased IL-10 mRNA expression. Notably, Kae reshaped the intestinal microbiome by elevating the Firmicutes to Bacteroidetes ratio; increasing the linear discriminant analysis scores of beneficial bacteria, such as Prevotellaceae and Ruminococcaceae; and reducing the richness of Proteobacteria in DSS-challenged mice. There was also an evident shift in the profile of fecal metabolites in the Kae treatment group. Serum LPS levels and downstream TLR4-NF-κB signaling were downregulated by Kae supplementation. Moreover, fecal microbiota transplantation from Kae-treated mice to the DSS-induced mice confirmed the effects of Kae on modulating the gut microbiota to alleviate UC. Therefore, Kae may exert protective effects against colitis mice through regulating the gut microbiota and TLR4-related signaling pathways. This study demonstrates the anti-UC effects of Kae and its potential therapeutic mechanisms, and offers novel insights into the prevention of inflammatory diseases using natural products.
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