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        Constructing Microstructures of Chlorinated Polyvinyl Chloride Microporous Membranes by Non-solvent Induced Phase Separation for High Permeate Flux and Rejection Performance

        Xiaomei Zhan,Jifeng Cheng,Li Xiang,Huiju Shao,Shuhao Qin 한국섬유공학회 2021 Fibers and polymers Vol.22 No.5

        To obtain the excellent permeate flux, rejection performance and mechanical properties, the chlorinated polyvinylchloride (CPVC) porous membrane was fabricated on the polyethylene terephthalate (PET) non-woven fabric by non-solventinduced phase separation (NIPS), using Tween80 (polyoxyethylene sorbitan monooleate) as a hydrophilic surfactant to regulate themicrostructure of the membrane. Porous skin layer and sub-layer were achieved when 3 wt.% Tween80 was added with asmall amount of deionized water as additive, and internal layer consisted of various finger-like holes. The forming mechanism ofmicrostructures was investigated according to the effects of Tween80 molecular chain structure on the viscosity and surface tensionof casting solution. Significantly, the modified membranes obviously exhibited higher pure water flux, which was increasedby 257 % compared with the pristine membrane. The rejection to ink suspension was over 99 %. Furthermore, the antifoulingperformance of modified membrane was also greatly improved on account of the above microstructure and more hydrophilicsurface. This study provides a new idea for the construction of membrane microstructure and the hydrophilic modification.

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        Sputum Transcriptomics Reveals FCN1+ Macrophage Activation in Mild Eosinophilic Asthma Compared to Non-Asthmatic Eosinophilic Bronchitis

        Zhan Wenzhi,Luo Wei,Zhang Yulong,Xiang Keheng,Chen Xiaomei,Shen Shuirong,Huang Chuqing,Xu Tingting,Ding Wenbin,Chen Yuehan,Lin Mingtong,Pan Xinghua,Lai Kefang 대한천식알레르기학회 2024 Allergy, Asthma & Immunology Research Vol.16 No.1

        Purpose: Eosinophilic asthma (EA) and non-asthmatic eosinophilic bronchitis (EB) share similar eosinophilic airway inflammation. Unlike EA, EB did not present airway hyperresponsiveness or airflow obstruction. We aimed to compare the mechanism underlying the different manifestations between EA and EB via sputum transcriptomics analysis. Methods: Induced-sputum cells from newly physician-diagnosed EA, EB patients, and healthy controls (HCs) were collected for RNA sequencing. Results: Bulk RNA sequencing was performed using sputum cells from patients with EA (n = 18), EB (n = 15) and HCs (n = 28). Principal component analysis revealed similar gene expression patterns in EA and EB. The most differentially expressed genes in EB compared with HC were also shared by EA, including IL4, IL5 IL13, CLC, CPA3, and DNASE1L3. However, gene set enrichment analysis showed that the signatures regulating macrophage activation were enriched in EA compared to EB. Sputum cells were profiled using single-cell RNA sequencing. FABP4+ macrophages, SPP1+ macrophages, FCN1+ macrophages, dendritic cells, T cells, B cells, mast cells, and epithelial cells were identified based on gene expression profiling. Analysis of cell-cell communication revealed that interactions between FCN1+ macrophages and other cells were higher in EA than in EB. A wealth of transforming growth factor beta (TGF-β) and vascular endothelial growth factor (VEGF) interactions between FCN1+ macrophages and other cells have been shown in EA. The gene expression levels of EREG, TGFBI, and VEGFA in FCN1+ macrophages of EA were significantly higher than those of EB. Furthermore, signatures associated with the response to TGF-β, cellular response to VEGF stimulus and developmental cell growth were enriched in FCN1+ macrophages of EA compared to those of EB. Conclusions: FCN1+ macrophage activation associated with airway remodeling processes was upregulated in EA compared to that in EB, which may contribute to airway hyperresponsiveness and airflow obstruction.

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