Dense B 4 C–SiC–CrB 2 ternary composites were fabricated via reactive hot pressing with B 4 C and chromic silicides (84 wt% CrSi 2 +16 wt% CrSi) as raw materials. The effects of chromic silicides on the densification, phase components, microstructure and performance of the prepared composites were investigated. The reaction mechanism and toughening mechanism were also studied. The results indicated that the chromic silicides were the reactive sintering aids which reacted with B 4 C and C to introduce CrB 2 and SiC in the matrix in situ. Partial B 4 C, CrB 2 and SiC formed the eutectic liquid phase, which enhanced the densification of B 4 C. The addition of chromic silicides enhanced the densification and fracture toughness while reduced the hardness. The good comprehensive performances of 435 MPa flexural strength , 4.09 MPa m 1/2 fracture toughness and 33.11 GPa hardness were obtained in the composites fabricated with 10 wt% chromic silicides. The higher addition amounts of chromic silicides resulted in the larger-size SiC, which reduced the flexural strength. The transgranular fracture of SiC and partial CrB 2 , the existing phenomena such as microcracks , crack branching and crack deflection could cumulatively improve the fracture toughness of the materials.
Rong Tu,Jiaojiao Li,Mingpu Jia,Qizhong Li,Meijun Yang,Song Zhang,Takashi Goto
B 4 C–CrB 2 composites were prepared by arc-melting using B 4 C and CrB 2 powders as raw materials. The eutectic composition of B 4 C–CrB 2 system was 30B 4 C–70CrB 2 (mol%) with a labyrinth-like irregularly layered eutectic microstructure, composed of B 4 C phase about 1–2 μm in thickness dispersing in CrB 2 matrix, much smaller than raw powders. The interface of the eutectic composite was well bonded, and there were edge dislocations at the interface to alleviate the interface mismatch. The eutectic temperature of B 4 C–CrB 2 composites was approximately 2200 K. At the eutectic composition, the B 4 C–CrB 2 composites showed the maximum Vickers hardness (24.6 GPa) and fracture toughness (4.3 MPa m 1/2 ) at room temperature.
Purpose Nephrotic syndrome (NS) is the main cause of the increasing end-stage renal disease (ESRD) patients worldwide. Podocytes are considered the crucial cells involved in the progression of NS, and their damage can directly lead to proteinuria. The objective of this study was to explore the protective effects of xanthohumol (XN) on podocyte injury. Methods Adriamycin (ADR)-induced podocyte injury in vivo and in vitro models were established to explore the effects of XN on adriamycin nephropathy (AN) by urine and serum biochemical assay, periodic acid-schiff (PAS) staining, immunohistochemistry, immunofluorescence, western blot, and real-time quantitative PCR (RT-qPCR). Results The results showed that XN could upregulate the expressions of podocyte specific marker Wilms’ tumor protein 1 (Wt1), and glomerular filtration related functional proteins such as Nephrin, Synaptopodin, Zonula occludens 1 (ZO-1), and Crumbs2 (Crb2) as well as downregulate the expression of podocyte injury marker Desmin in ADR-treated podocytes to restrain the podocyte actin cytoskeleton disruption. Conclusion Our study showed that XN treatment significantly attenuated ADR-induced podocyte injury, suggesting that XN may be a potential therapy option for patients with NS.
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