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In this work, K2Ti4O9 whiskers are prepared by adding a certain amount of NaCl as the whisker reaction slow-release agent. Rutile TiO2 whiskers are obtained by ion exchange and microwave sintering method with K2Ti4O9 whiskers as templates. The surface morphology and crystal structure of K2Ti4O9 whiskers are analyzed and characterized by scanning electron microscope (SEM), X-ray diffractometer (XRD), X-ray photoelectron spectroscopy (XPS), and energy-dispersive X-ray spectroscopy (EDS). One-dimensional conductive whiskers of fluorine-doped tin dioxide-coated rutile titanium dioxide (FTO@TiO2) were prepared by the hydrothermal chemical combined precipitation method. Under the optimized conditions, the resistivity of the conductive whiskers was 0.625 kΩ, and the Hunter whiteness is 80.3. Additionally, FTO@TiO2 conductive nanomaterials were dispersed into acrylic polymer emulsion (APE) to make antistatic slurry and coat it on the surface of the polyester fabric. After the antistatic coating has dried, FTO@TiO2 whiskers are located in the coating mold; FTO@TiO2 whiskers bridge each other to form a current path, so that the fabric has antistatic properties. Under the best experimental parameters, the FTO@TiO2 whiskers possessed excellent electrical conductivity, and the surface resistance of the coated fabric can reach 106 Ω, and it presented certain antistatic properties as well. [ABSTRACT FROM AUTHOR]

Abstract: The influence of Li loading on the activity and selectivity of Rh–Fe/γ-Al2O3 catalysts for the synthesis of ethanol from syngas was explored. The catalysts were characterized by means of XRD, N2 adsorption, TPR, XPS, CO-TPD, and DRIFTS. Introduction of Li into Rh–Fe catalyst inhibited the Rh reducibility, which could stabilize oxidized Rh species. This led to the significant increase of Rh+/Rh0 ratio over reduced catalysts, and then Rh+ became the major Rh species on the surface of reduced Li promoted catalyst. The enhanced Rh+ content improved the generation and stabilization of gem-dicarbonyls Rh+(CO)2 species on Rh+ sites, which was indicated by CO adsorption behavior. It can be concluded that the addition of Li facilitated CO insertion ability and simultaneously suppressed CO dissociation ability. Lower hydrocarbons selectivity and higher ethanol selectivity were observed on Li modified Rh–Fe catalysts. The catalyst with 0.5 wt% Li exhibited the highest selectivity being 30.2% to ethanol.Graphical Abstract: [ABSTRACT FROM AUTHOR]

Alongshan virus (ALSV) is a newly discovered pathogen in the Flaviviridae family, characterized by a unique multi-segmented genome that is distantly related to the canonical flaviviruses. Understanding the pathogenic mechanism of this emerging segmented flavivirus is crucial for the development of effective intervention strategies. In this study, we demonstrate that ALSV can infect various mammalian cells and induce the expression of antiviral genes. Furthermore, ALSV is sensitive to IFN-β, but it has developed strategies to counteract the host's type I IFN response. Mechanistically, ALSV's nonstructural protein NSP1 interacts with and degrades human STAT2 through an autophagy pathway, with species-dependent effects. This degradation directly inhibits the expression of interferon-stimulated genes (ISGs). Additionally, NSP1-mediated degradation of STAT2 disrupts mitochondrial dynamics, leading to mitophagy and inhibition of mitochondrial biogenesis. This, in turn, suppresses the host's innate immune response. Interestingly, we found that inhibiting mitophagy using 3-methyladenine and enhancing mitochondrial biogenesis with the PPARγ agonist pioglitazone can reverse NSP1-mediated inhibition of ISGs, suggesting that promoting mitochondrial mass could serve as an effective antiviral strategy. Specifically, the NSP1 methyltransferase domain binds to the key sites of F175/R176 located in the coiled-coil domain of STAT2. Our findings provide valuable insights into the intricate regulatory cross talk between ALSV and the host's innate immune response, shedding light on the pathogenesis of this emerging segmented flavivirus and offering potential intervention strategies.IMPORTANCEAlongshan virus (ALSV), a segmented flavivirus belonging to the Flaviviridae family, was first identified in individuals who had been bitten by ticks in Northeastern China. ALSV infection is responsible for causing Alongshan fever, a condition characterized by various clinical symptoms, including fever, headache, skin rash, myalgia, arthralgia, depression, and coma. There is an urgent need for effective antiviral therapies. Here, we demonstrate that ALSV is susceptible to IFN-β but has developed mechanisms to counteract the host's innate immune response. Specifically, the ALSV nonstructural protein NSP1 interacts with STAT2, leading to its degradation via an autophagy pathway that exhibits species-dependent effects. Additionally, NSP1 disrupts mitochondrial dynamics and suppresses mitochondrial biogenesis, resulting in a reduction in mitochondrial mass, which ultimately contributes to the inhibition of the host's innate immune response. Interestingly, we found that inhibiting mitophagy and promoting mitochondrial biogenesis can reverse NSP1-mediated suppression of innate immune response by increasing mitochondrial mass. These findings provide valuable insights into the molecular mechanisms of ALSV pathogenesis and suggest potential therapeutic targets against ALSV infection.