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In order to evaluate the increase in the flexural strength of a 3D braided C/SiC composite comprised with a thin pyrolytic carbon (PyC) interlayer (TI C/SiC) under a load of 60 MPa with an amplitude of ±20 MPa at an oxygen partial pressure of 8000 Pa, the effect of temperature, oxidation and stress value on the length change in the sample, fracture behavior, residual flexural strength and fracture morphology were studied up to 1500 °C. It was found that the gauge length change behaviors of the material are related to (i) the positive damage of the thin interlayer and (ii) to the negative damage of the C phase. The most serious damage of TI C/SiC under 60 ± 20 MPa occurs in an oxygen partial pressure of 17,000 Pa at 1300 °C. When the oxygen partial pressure and/or the temperature are reduced, the positive C phase damage is relieved. In the case that the oxygen partial pressure, temperature and stress increase, the negative C phase damage is facilitated. The oxidation mechanism of the C phase is controlled by the inward diffusion of oxygen from the sample surface to the center; however, a higher stress is considered to change the oxygen diffusion mechanism by increasing the reaction of the C phase, with oxygen causing a widening of microcracks. [ABSTRACT FROM AUTHOR]

Yttria-stabilized zirconia (YSZ, Y2O3-ZrO2) ceramic with titanium dioxide nanoparticle (nanoTiO2) is prepared using conventional pressureless and two-step sintering (TSS) methods. The microstructure, phase composition, and mechanical properties of TSS-TiO2-ZrO2-Y2O3 nanocomposite ceramics are compared to those of the ceramics sintered using conventional sintering. The effect of TSS and nanoparticles on the sintering densification of the YSZ ceramics is investigated. X-ray diffractometry revealed that nanoTiO2 destabilizes c-ZrO2 and stabilizes t-ZrO2 in the YSZ. In addition, TSS is more conducive for grain refinement and sintering densification of the TiO2-ZrO2-Y2O3 nanocomposite ceramics; the average grain size of the samples decreased from 1.446 (conventional sintering) to 0.492 μm (TSS). Meanwhile, the relative density and sintering shrinkage of the TSS-1450 sample reached the maximum (98.23% and 22.92%, respectively) at a nanoTiO2 fraction of 7 wt%. The maximum microhardness and bending strength of the TSS-1450 ceramic matrix with 7-wt% nanoTiO2 were 1823 HV and 505 MPa, respectively. The nanoparticles distributed in the grain boundary induce the crack to the matrix, which induces the transgranular fracture, and nanoTiO2 improves the densification and mechanical properties of YSZ ceramics more than titanium dioxide microparticles. [ABSTRACT FROM AUTHOR]

Background: Smad7 is protective in a mouse model of rheumatoid arthritis. Here we investigated whether Smad7-expressing CD4 + T cells and the methylation of Smad7 gene in CD4 + T cells contribute to the disease activity of RA in patients., Methods: Peripheral CD4 + T cells were collected from 35 healthy controls and 57 RA patients. Smad7 expression by CD4 + T cells were determined and correlated with the clinical parameters of RA including RA score and serum levels of IL-6, CRP, ESR, DAS28-CRP, DAS28-ESR, Swollen joints and Tender joints. Bisulfite sequencing (BSP-seq) was used to determine the DNA methylation in Smad7 promoter (-1000 to +2000) region in CD4 + T cells. In addition, a DNA methylation inhibitor, 5-Azacytidine (5-AzaC), was added to CD4 + T cells to examine the possible role of Smad7 methylation in CD4 + T cell differentiation and functional activity., Results: Compared to the heath controls, Smad7 expression was significantly decreased in CD4 + T cells from RA patients and inversely correlated with the RA activity score and serum levels of IL-6 and CRP. Importantly, loss of Smad7 in CD4 + T cell was associated with the alteration of Th17/Treg balance by increasing Th17 over the Treg population. BSP-seq detected that DNA hypermethylation occurred in the Smad7 promoter region of CD4 + T cells obtained from RA patients. Mechanistically, we found that the DNA hypermethylation in the Smad7 promoter of CD4 + T cells was associated with decreased Smad7 expression in RA patients. This was associated with overreactive DNA methyltransferase (DMNT1) and downregulation of the methyl-CpG binding domain proteins (MBD4). Inhibition of DNA methylation by treating CD4 + T cells from RA patients with 5-AzaC significantly increased Smad7 mRNA expression along with the increased MBD4 but reduced DNMT1 expression, which was associated with the rebalance in the Th17/Treg response., Conclusion: DNA hypermethylation at the Smad7 promoter regions may cause a loss of Smad7 in CD4 + T cells of RA patients, which may contribute to the RA activity by disrupting the Th17/Treg balance., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Hu, Xu, He, Shan, Zhou, Wang, Bai, Shang, Nie, Pan, Lan and Wang.)