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RISS 인기검색어
- 검색키워드
- 저자 : Cheng‑Qiong Luo (검색결과 3 건)
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Depth-enhanced integral imaging system based on spatial filtering
Yan Xing,Qiong-Hua Wang,Cheng-Gao Luo,Huan Deng,Da-Hai Li 한국정보디스플레이학회 2015 Journal of information display Vol.16 No.2
An integral imaging system enabling an enhanced depth of field is proposed based on spatial filtering. In the proposed system, spatial filtering is used on each elemental image to obtain a depth-enhanced elemental image in the pickup stage, and the obtained elemental images are composed to form an elemental image array for the computational reconstruction in the display stage. A preliminary experiment was carried out, and the experiment results verified the feasibility of the system.
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Branched polymeric prodrug/programmed cell death 4 complexes for combinational cancer therapy
Yu‑Jing He,Lei Xing,Peng‑Fei Cui,Jia‑Liang Zhang,Jian‑Bin Qiao,Cheng‑Qiong Luo,Ge Jiang,Hu‑Lin Jiang 한국약제학회 2017 Journal of Pharmaceutical Investigation Vol.47 No.2
Here, we demonstrate a co-delivery system constructed by integrating chemotherapeutic molecules into branched polymeric prodrug which can condense nucleic acids. Demethylcantharidate (DCA) was chosen as a model drug and premodified through nucleophilic substitution reaction by its two carboxylic groups with allyl chloride. The synthesized intermediate (DCA-dially) was then used to polymerize with tris (2-aminoethyl) amine (TAEA) through progressively ammonolysis reaction. The obtained poly (DCA-alt-TAEA) (DCAT) was used to pack PDCD4 into spherical-like nanoparticles through electrostatic interaction. Gel retardation assays implied that DCAT could integrate DNA at the weight ratio of 1 and protect it from digestion by nuclease. Acid-base titration experiments showed that DCAT obtained preferable buffering capability which was beneficial for the endosomal escape of DCAT/PDCD4 complexes. Cellular tests involving gene transfection efficiency and cytotoxicity indicated that DCA and PDCD4 co-delivered by the complexes significantly and synergistically suppressed the viability of SMMC-7721 cells. These results suggest that integrating chemotherapeutic molecules into nucleic acid-packing polymeric prodrug as cationic polymer/PDCD4 complexes is a highly efficient way to co-deliver chemotherapeutic drugs and nucleic acids for cancer therapy.
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IL-33 promotes IL-10 production in macrophages: a role for IL-33 in macrophage foam cell formation
Hai-Feng Zhang,Mao-Xiong Wu,Yong-Qing Lin,Shuang-Lun Xie,Tu-Cheng Huang,Pin-Ming Liu,Ru-Qiong Nie,Qin-Qi Meng,Nian-Sang Luo,Yang-Xin Chen,Jing-Feng Wang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
We evaluated the role of IL-10- in IL-33-mediated cholesterol reduction in macrophage-derived foam cells (MFCs) and the mechanism by which IL-33 upregulates IL-10. Serum IL-33 and IL-10 levels in coronary artery disease patients were measured. The effects of IL-33 on intra-MFC cholesterol level, IL-10, ABCA1 and CD36 expression, ERK 1/2, Sp1, STAT3 and STAT4 activation, and IL-10 promoter activity were determined. Core sequences were identified using bioinformatic analysis and sitespecific mutagenesis. The serum IL-33 levels positively correlated with those of IL-10. IL-33 decreased cellular cholesterol level and upregulated IL-10 and ABCA1 but had no effect on CD36 expression. siRNA-IL-10 partially abolished cellular cholesterol reduction and ABCA1 elevation by IL-33 but did not reverse the decreased CD36 levels. IL-33 increased IL-10 mRNA production but had little effect on its stability. IL-33 induced ERK 1/2 phosphorylation and increased the luciferase expression driven by the IL-10 promoter, with the highest extent within the − 2000 to − 1752 bp segment of the 5′-flank of the transcription start site; these effects were counteracted by U0126. IL-33 activated Sp1, STAT3 and STAT4, but only the STAT3 binding site was predicted in the above segment. Site-directed mutagenesis of the predicted STAT3-binding sites (CTGCTTCCTGGCAGCAGAA→CTGCCTGGCAGCAGAA) reduced luciferase activity, and a STAT3 inhibitor blocked the regulatory effects of IL-33 on IL-10 expression. Chromatin immunoprecipitation (CHIP) confirmed the STAT3-binding sequences within the − 1997 to − 1700 and − 1091 to − 811 bp locus regions. IL-33 increased IL-10 expression in MFCs via activating ERK 1/2 and STAT3, which subsequently promoted IL-10 transcription and thus contributed to the beneficial effects of IL-33 on MFCs.
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