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71.
72.
制备了金-海藻酸钙-几丁聚糖微胶囊,提出了修饰用于蛋白质药物靶向传输的多糖载体-几丁聚糖的新方法,该方法通过在几丁聚糖微胶囊表面结合金的纳米微粒使微胶囊表面结构发生变化,从而改变微胶囊的性质,这种修饰方法目前未见报道.文中对制备条件进行了优化,并对金-海藻酸钙-几丁聚糖微胶囊的粒径分布进行了表征.文中选择在pH值为5时反应2 h,制得的柠檬酸体系和丙烯酸体系的金-海藻酸钙.几丁聚糖微胶囊的平均直径分别为216.686um和196.850um. 相似文献
73.
厦门广电集团6信道高清转播车改造方案 总被引:1,自引:0,他引:1
介绍了厦门广电集团6信道高清转播车改造背景,从实用性、经济性的角度出发,介绍了详细的车体改造方案、系统方案和视音频方案等. 相似文献
74.
相变微胶囊将相变材料包封在壳材中,有效解决了相变材料的泄漏等问题,是一种性能良好的相变储能材料,在热能储存领域具有广泛的应用。但因其壳材的存在削弱了内部相变材料与外部环境间的热传导,降低了相变微胶囊的热导率,制约了其实际应用范围。因此,对相变微胶囊进行改性是增强导热的有效途径。本文介绍相变微胶囊的组成与结构,并从声子-声子与电子-声子相互作用的角度,概述微观尺度下的导热机理。在此基础上,分别从芯材和壳材2个方面对相变微胶囊导热增强改性进行阐述,通过定量数据和导热机理对改性相变微胶囊的导热增强效果进行分析论述,同时,概括了改性相变微胶囊在纺织调温、浆料和建筑领域的应用。最后,对相变微胶囊导热性能增强的研究前景和挑战以及实际应用方向进行了展望。 相似文献
75.
Cong Ge Xuebin Xu Fei Ma Jianmin Zhou Changwen Du 《International journal of molecular sciences》2022,23(13)
Benefitting from the special structure of the leaf cuticle layer, plants have natural hydrophobicity and anti-fouling abilities. Inspired by the leaf surface structure, a biomimetic modification strategy was raised to improve the surface hydrophobicity of polyacrylate coating for controlled release fertilizer. Double-layer (polyacrylate and carnauba wax) coated fertilizer was obtained after biomimetic modification. The quality of controlled release fertilizer modified with the carnauba wax was greatly enhanced, and the coating material was effectively saved. The surface appearance of polyacrylate-coated fertilizer was improved for the surface blemish was repaired by the loaded carnauba wax. The characterizations by Fourier transform infrared spectroscopy indicated that the hydrogen bonds were formed between the water-based polyacrylate membrane and the carnauba wax layers. By optimizing the content of polyacrylate and carnauba wax, the release duration of the fertilizer was effectively prolonged, which was improved from 1 month to more than 2 months after the biomimetic modification. Therefore, biological wax as an environmentally-friendly natural material that has showed a broad potential in the application of coated controlled release fertilizer. 相似文献
76.
灰色负荷预测的参数修正法 总被引:16,自引:2,他引:16
本文提出灰色预测模型GM(1,1)的α参数作正方法,实验表明本方法应用于电力系统负荷预测有较高的精度。 相似文献
77.
78.
Hui-Min Zhang Fei-Fei Qi Jun Wang Yuan-Yuan Duan Li-Li Zhao Yun-Dan Wang Tong-Cun Zhang Xing-Hua Liao 《International journal of molecular sciences》2022,23(12)
Gastric cancer (GC) is the fifth most common cancer and the third deadliest cancer in the world, and the occurrence and development of GC are influenced by epigenetics. Methyltransferase-like 3 (METTL3) is a prominent RNA n6-adenosine methyltransferase (m6A) that plays an important role in tumor growth by controlling the work of RNA. This study aimed to reveal the biological function and molecular mechanism of METTL3 in GC. The expression level of METTL3 in GC tissues and cells was detected by qPCR, Western blot and immunohistochemistry, and the expression level and prognosis of METTL3 were predicted in public databases. CCK-8, colony formation, transwell and wound healing assays were used to study the effect of METTL3 on GC cell proliferation and migration. In addition, the enrichment effect of METTL3 on DEK mRNA was detected by the RIP experiment, the m6A modification effect of METTL3 on DEK was verified by the MeRIP experiment and the mRNA half-life of DEK when METTL3 was overexpressed was detected. The dot blot assay detects m6A modification at the mRNA level. The effect of METTL3 on cell migration ability in vivo was examined by tail vein injection of luciferase-labeled cells. The experimental results showed that METTL3 was highly expressed in GC tissues and cells, and the high expression of METTL3 was associated with a poor prognosis. In addition, the m6A modification level of mRNA was higher in GC tissues and GC cell lines. Overexpression of METTL3 in MGC80-3 cells and AGS promoted cell proliferation and migration, while the knockdown of METTL3 inhibited cell proliferation and migration. The results of in vitro rescue experiments showed that the knockdown of DEK reversed the promoting effects of METTL3 on cell proliferation and migration. In vivo experiments showed that the knockdown of DEK reversed the increase in lung metastases caused by the overexpression of METTL3 in mice. Mechanistically, the results of the RIP experiment showed that METTL3 could enrich DEK mRNA, and the results of the MePIP and RNA half-life experiments indicated that METTL3 binds to the 3’UTR of DEK, participates in the m6A modification of DEK and promotes the stability of DEK mRNA. Ultimately, we concluded that METTL3 promotes GC cell proliferation and migration by stabilizing DEK mRNA expression. Therefore, METTL3 is a potential biomarker for GC prognosis and a therapeutic target. 相似文献
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