The m6A Methyltransferase METTL3-Mediated N6-Methyladenosine Modification of DEK mRNA to Promote Gastric Cancer Cell Growth and Metastasis

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.     

MILP formulations for highway petrol station replenishment in initiative distribution mode

To investigate highway petrol station replenishment in initiative distribution mode,this paper develops a mixed-integer linear programming(MILP)model with minim...     

Integrated Analysis of Microarray,Small RNA,and Degradome Datasets Uncovers the Role of MicroRNAs in Temperature-Sensitive Genic Male Sterility in Wheat

Temperature-sensitive genic male sterile (TGMS) line Beijing Sterility 366 (BS366) has been utilized in hybrid breeding for a long time, but the molecular mechanism underlying male sterility remains unclear. Expression arrays, small RNA, and degradome sequencing were used in this study to explore the potential role of miRNA in the cold-induced male sterility of BS366. Microspore observation showed defective cell plates in dyads and tetrads and shrunken microspores at the vacuolated stage. Differential regulation of Golgi vesicle transport, phragmoplast formation, sporopollenin biosynthesis, pollen exine formation, and lipid metabolism were observed between cold and control conditions. Pollen development was significantly represented in the 352 antagonistic miRNA-target pairs in the integrated analysis of miRNA and mRNA profiles. The specific cleavage of ARF17 and TIR1 by miR160 and miR393 were found in the cold-treated BS366 degradome, respectively. Thus, the cold-mediated miRNAs impaired cell plate formation through repression of Golgi vesicle transport and phragmoplast formation. The repressed expression of ARF17 and TIR1 impaired pollen exine formation. The results of this study will contribute to our understanding of the roles of miRNAs in male sterility in wheat.     

基于低温直接键合的血细胞计数芯片结构制备

研究了一种新颖的微流管道血细胞计数器的结构及其工作原理,采用流体动力学对其液体分层流动特性进行了仿真分析,结合图形制备和低温直接键合工艺制作了硅基微流体管道血细胞计数器结构,并采用红外透射方法对微流体管道结构进行了检测.对封闭管道的流通性及结构的键合强度也进行了测量.研究分析表明,采用上述工艺制备的微流体芯片结构与电子器件兼容性好,具有良好的化学惰性和热稳定性,而且管道结构规则,精度高,键合界面层薄,具有较好的应用前景.     

一个微分差分方程组数学模型周期正解的存在唯一性

本文考虑再生资源开发问题 ,建立了非线性微分差分方程组的数学模型 ,获得了该模型周期连续正解存在唯一的充分必要条件。     

抗腐蚀低密度水泥浆体系的研究

分析了地层水腐蚀油井水泥的机理,并通过大量试验研究,开发出了密度为1.30—1.50 g/cm~3的低密度水泥浆体系。同时在模拟腐蚀性地层水中,对该体系水泥浆凝结硬化形成的水泥石试件的耐久性和浆体的综合工程性能进行了评价。结果表明,该低密度水泥浆体系耐地层水腐蚀能力强,综合工程性能良好,可满足易漏浅井防止腐蚀性地层水腐蚀套管外壁的固井要求。     

高黏度牛顿流体中砂粒运动实验研究

为了解决疏松砂岩稠油油藏开采过程中的砂粒运移问题,基于固液两相流理论及实验流体力学理论,利用研制的高黏度流体颗粒自由沉降实验装置,分别开展了高黏度牛顿流体中球形颗粒的自由沉降实验、砂粒的自由沉降实验和不同含砂体积分数下混合黏度变化规律实验,根据实验结果,建立了不同粒径范围的阻力系数模型以及混合黏度模型。研究表明,高黏油混合黏度存在相应的临界值,在实验条件下,含砂体积分数为0.1%时,混合黏度达到最低,不利于携砂。结合上述模型和实验结果,建立了高黏度牛顿流体中的砂粒运动模型,揭示了高黏介质中颗粒的特定运移规律,为今后稠油携砂流动规律理论研究奠定了基础。      

仪器安装板振动环境虚拟试验和验证技术研究

基于商用有限元软件MSC.Patran和Nastran,研究了导弹仪器安装板结构的振动环境预示技术。建立了仪器安装板的三维实体模型,单机仪器使用质点模拟,并通过MPC法与安装板连接;设置了多种阻尼特性,通过模态叠加法预示了该仪器安装板在振动条件下的结构动力学环境,通过振动试验验证了预示结果。研究发现,使用大阻尼能较好地预示该仪器安装板结构的动力学环境。