Mo-doped TiO2 nanotube arrays are prepared successfully by a combined method of direct current (DC) magnetron sputtering and anodic oxidation. The doping amount of Mo can be modified by changing the number of molybdenum blocks on the Ti target while a Ti–Mo alloy film is prepared by magnetron sputtering on a metal Ti substrate, following a Mo-doped TiO2 nanotube array grown by anodization. Morphology test shows that the doping of Mo could inhibit the phase transition and growth of crystal of TiO2. X-ray photoelectron spectroscopy (XPS) results show that Mo has successfully been embedded in the TiO2 crystal lattice and mainly exists in the valence states of Mo6+. Mo-doping samples show slightly increased visible light absorption as the red shift of TiO2 absorption edge with the band gap dropping from 3.24 to 3.16 eV with 0.5 at.% Mo doping. The enhanced photocurrent is demonstrated for a 0.5 at.% Mo-doped TiO2 electrode. Through photoelectric performance testing under UV-visible light irradiation, the nanotube array film with a Mo-doped content of 0.5% produced the maximum photocurrent density, which is about four times the undoped TiO2 nanotube array film, exhibiting a considerable photoelectric effect gain. The controllable Mo doping TiO2 nanotube array film prepared by this combining technique is expected as a promising material for efficient applications in photoelectric conversion.
Background: The industrial vinegar residue (VR) from solid-state fermentation, mainly cereals and their bran, will be a potential feedstock for future biofuels because of their low cost and easy availability. However, utilization of VR for butanol production has not been as much optimized as other sources of lignocellulose, which mainly stem from two key elements: (i) high biomass recalcitrance to enzymatic sugar release; (ii) lacking of suitable industrial biobutanol production strain. Though steam explosion has been proved effective for bio-refinery, few studies report SE for VR pretreatment. Much of the relevant knowledge remains unknown. Meanwhile, recent efforts on rational metabolic engineering approaches to increase butanol production in Clostridium strain are quite limited. In this study, we assessed the impact of SE pretreatment, enzymatic hydrolysis kinetics, overall sugar recovery and applied atmospheric and room temperature plasma (ARTP) mutant method for the Clostridium strain development to solve the long-standing problem. Results: SE pretreatment was first performed. At the optimal condition, 29.47% of glucan, 71.62% of xylan and 22.21% of arabinan were depolymerized and obtained in the water extraction. In the sequential enzymatic hydrolysis process, enzymatic hydrolysis rate was increased by 13-fold compared to the VR without pretreatment and 19.60 g glucose, 15.21 g xylose and 5.63 g arabinose can be obtained after the two-step treatment from 100 g VR. Porous properties analysis indicated that steam explosion can effectively generate holes with diameter within 10-20 nm. Statistical analysis proved that enzymatic hydrolysis rate of VR followed the Pseudop-second-order kinetics equation and the relationship between SE severity and enzymatic hydrolysis rate can be well revealed by Boltzmann model. Finally, a superior inhibitortolerant strain, Clostridium acetobutylicum Tust-001, was generated with ARTP treatment. The water extraction and enzymolysis liquid gathered were successfully fermented, resulting in butanol titer of 7.98 g/L and 12.59 g/L of ABE. Conclusions: SE proved to be quite effective for VR due to high fermentable sugar recovery and enzymatic hydrolysate fermentability. Inverse strategy employing ARTP and repetitive domestication for strain breeding is quite feasible, providing us with a new tool for solving the problem in the biofuel fields.
Objective To screen for immune genes that play a major role in Kawasaki disease and to investigate the pathogenesis of Kawasaki disease through bioinformatics analysis. Methods Kawasaki disease‐related datasets GSE18606, GSE68004, and GSE73461 were downloaded from the Gene Expression Omnibus database. Three microarrays were integrated and standardized to include 173 Kawasaki disease samples and 101 normal samples. The samples were analyzed using CIBERSORT to obtain the infiltration of 22 immune cells and analyze the differential immune cells in the samples and correlations. The distribution of the samples was analyzed using principal component analysis (PCA). Immune‐related genes were downloaded, extracted from the screened samples and analyzed for differential analysis (different expression genes [DEG]) and weighted gene co‐expression network analysis (WGCNA). We constructed coexpression networks, and used the cytohobbe tool in Cytoscape to analyze the coexpression networks and select the immune genes that played a key role in them. Results Immune cell infiltration analysis showed that B cells naive, T cells CD8, natural killer (NK) cells activated, and so forth were highly expressed in normal samples. T cells CD4 memory activated, monocytes, neutrophils, and so forth were highly expressed in Kawasaki disease samples. PCA results showed a significant difference in the distribution of normal and Kawasaki disease samples. From the screened samples, 97 upregulated and 103 downregulated immune‐related genes were extracted. WGCNA analysis of DEG yielded 10 gene modules, of which the three most relevant to Kawasaki disease were red, yellow, and gray modules. They were associated with cytokine regulation, T‐cell activation, presentation of T‐cell receptor signaling pathways, and NK cell‐mediated cytotoxicity. CXCL8, CCL5, CCR7, CXCR3, and CCR1 were identified as key genes by constructing a coexpression network. Conclusion Our study shows that we can distinguish normal samples from Kawasaki disease samples based on the infiltration of immune cells, and that CXCL8, CCL5, CCR7, CXCR3, and CCR1 may play important roles in the development of Kawasaki disease.
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