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  • Author: Ye Han x
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Abstract

This study is to investigate the role of the coating of TiO2 nanoparticles deposited on wool fibers against high-intensity ultraviolet B (UVB), ultraviolet A (UVA), and visible light irradiation. The properties of tensile and yellowness and whiteness indices of irradiated TiO2-coated wool fibers are measured. The changes of TiO2-coated wool fibers in optical property, thermal stability, surface morphology, composition, molecular structure, crystallinity, and orientation degree are characterized using diffuse reflectance spectroscopy, thermogravimetric analysis, scanning electronic microscopy, energy-dispersive X-ray spectroscopy, Fourier-transform infrared spectroscopy, and X-ray diffraction techniques. Experimental results show that the tensile properties of anatase TiO2-coated wool fibers can be degraded under the high-intensity UVB, UVA, and visible light irradiation for a certain time, resulting in the loss of the postyield region of stress–strain curve for wool fibers. The coating of TiO2 nanoparticles makes a certain contribution to the tensile property, yellowness and whiteness indices, thermal stability, and surface morphology of wool fibers against high-intensity UVB, UVA, and visible light irradiation. The high-intensity UVB, UVA, and visible light can result in the photo-oxidation deterioration of the secondary structure of TiO2-coated wool fibers to a more or less degree. Meanwhile, the crystallinity and orientation degree of TiO2 coated wool fibers decrease too.

Abstract

Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker CD248/endosialin are known to play an important regulatory role in the development of liver fibrosis. Additionally, hypoxia microenvironment and hypoxia-inducible factor (HIF) are involved in the regulation of CD248/endosialin. Therefore, we hypothesize that hypoxia microenvironment which develops due to BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then affects the function of HSC and development of liver fibrosis. To confirm the hypothesis, two major investigations are necessary: (1) in the BCS animal model and clinical studies, the relationship between the severity of liver fibrosis and the expression of HIF and CD248/endosialin in HSC will be explored; and (2) in the in vitro cell system, the effect of hypoxic microenvironment, HIF-1α or HIF-2α, on the expression of CD248/endosialin in HSC will be explored. It will be important to elucidate whether HIF signaling pathway regulates the expression of CD248/endosialin, thereby inducing the development of BCS-related liver fibrosis.