In this study, a radio frequency magnetron sputtering process was used to deposit F-doped ZnO (FZO) films on polyimide (PI) substrates. The thermal expansion effect of PI substrates induces distortion and bending, causing FZO films to peel and their electrical properties and crystallinity to deteriorate. To address these shortcomings, oxygen (O2) plasma was used to pretreat the surface of PI substrates using a plasma-enhanced chemical vapor deposition system before the FZO films were deposited. The effects of O2 plasma pretreatment time on the surface water contact angle, surface morphologies, and optical properties of the PI substrates were investigated. As the pretreatment time increased, so did the roughness of the PI substrates. After the FZO films had been deposited on the PI substrates, variations in the surface morphologies, crystalline structure, composition, electrical properties, and optical properties were investigated as a function of the O2 plasma pretreatment time. When this was 30 s, the FZO films had optimal optical and electrical properties. The resistivity was 3.153 × 10−3 Ω-cm, and the transmittance ratios of all films were greater than 90%. The X-ray photoelectron spectroscopy spectra of the FZO films, particularly the peaks for O1s, Zn 2p1/2, and Zn 2p3/2, were determined for films with O2 plasma pretreatment times of 0 and 30 s. Finally, a HCl solution was used to etch the surfaces of the deposited FZO films, and silicon-based thin-film solar cells were fabricated on the FZO/PI substrates. The effect of O2-plasma pretreatment time on the properties of the fabricated solar cells is thoroughly discussed.
PDL is an effective and safe therapeutic modality for managing vascular anomalies in Chinese patients. We determined that differentiating and identifying IH subtypes prior to treatment could be a useful parameter for predicting therapeutic results. Lesion colour, sites, and hypertrophic changes in PWS are relevant therapeutic factors. PDL parameters and techniques differ according to the various vascular anomalies to achieve optimal results.
The objective of this study was to form auto shredder residue-derived fuel (ASRDF) by using an extrusion apparatus, to solve the disposal problems of auto shredder residue (ASR)
Background and Aims Chronic kidney disease (CKD) is an urgent public health issue in the world. However, effective treatments for intervention of CKD remain undefined. Phosphate (Pi) is an essential element for synthesis of DNA, RNA, ATP, phospholipid membranes, and for regulation of phosphorylation/dephosphorylation, cellular signaling and metabolic pathways. Solute carrier family 34 (SLC34) is responsible for Pi absorption in the small intestine. However, the role of SLC34 in progression of CKD is still unknown. Method A membrane protein, solute carrier family 34 member 2 (SLC34A2), was discovered by using big data mining from the National Center for Biotechnology Information (NCBI). SLC34A2 was overexpressed in human proximal tubular cells, HK-2, by Lipofectamine 3000. RNA sequencing was carried out to uncover SLC34A2-mediated signaling pathways by using Illumina platform. Apoptosis was evaluated by Annexin V-PI staining and TEUNEL assay in cells and mouse kidneys, respectively. Cell cycle was measured by flow cytometry. Unilateral ureteral obstruction (UUO) and bilateral renal ischemia-reperfusion injury (bIRI) were employed to generate CKD mouse models. Results By using big data mining from the NCBI, we identified a membrane protein, SLC34A2, was upregulated in various types of nephropathies including diabetic nephropathy, focal segmental glomerulosclerosis, minimal change disease, ANCA-associated vasculitis. Overexpression of SLC34A2 suppressed viability of HK-2 cells. RNA sequencing revealed that apoptosis and cell cycle are high scored pathways modulated by SLC34A2. The results were further verified in HK-2 cells. Ectopic SLC34A2 promoted apoptosis via downregulation of BCL-2. Moreover, SLC34A2 induced cell cycle arrest in S phase via downregulation of CDK2. CKD mouse models of UUO and bIRI were carried out to confirm in vitro findings. In mice kidneys, the expression of Slc34a2 in UUO and bIRI groups was superior to that in sham groups. Enriched Bax and TUNEL-positive cells were observed in the fibrotic kidneys of mice. Moreover, increased expression of p21 and downregulated Cyclin A2 in the fibrotic kidneys further confirmed that Slc34a2 induced cell cycle arrest in S phase. Conclusion Slc34a2 induced apoptosis and halted cell cycle in S phase, resulting in subsequent tubulointerstitial fibrosis in mice. Our results suggest that targeting SLC34A2 might be a promising strategy for intervention of CKD.
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