3G移动可视电话系统测试方案设计

本文主要设计了开发3G移动可视电话系统过程中,在VT系统设计完成后脱离其它软件模块进行有效测试的几套方案。首先介绍了具有独创性的针对CommDevice的Loopback方案的基本编程思路与部分程序代码,对COITI-H0耐ce以外的模块进行陕速检测;第二套利用简单便捷的VIVA手机＋MD8470A的Loopback方案对手机整体效果进行初步检测;第三套通过VIVA手机到DNA的测试方案复杂但精确性高。本文中设计的各套方案各有优劣,具有可调性高,测试效果好的特点,合理使用各种测试方案,对于提高可视电话开发速度和产品质量都有很大帮助。     

二次雷达目标数据处理软件设计

航管设备二次雷达捕获的目标数据A模式与C模式混杂,且每次扫描、询问某一确定目标的过程中需要对目标进行多次询问,导致数据量大大增加,后端数据处理压力增大.为解决上述问题,论文提出一种目标数据处理方案,首先对接收到的A、C模式数据进行点迹合并,再对批号数据与无批号数据分流处理,通过点迹关联、滤波跟踪、航迹管理等综合处理输出目标数据.试验结果表明该设计方案可实现目标航迹快速起始,并且在目标高机动、断续、交叉等复杂情况下能连续、稳定输出数据,具有较好实用价值.     

一种基于89C52的新型风压测量仪的研制

该仪器是基于89C52的单片机系统,采用12位AD574A转换器,针对现有风压测量仪器功能上的不足,实现了实时送显和平均送显功能,满足了测量风压时不同情况下的使用要求,尤其适用于风机系统管道内各种压力参数的测量.系统设计了RS232通讯接口,为进一步开发风机性能测试系统奠定了基础.     

一种基于FPGA的调制指数可调的数字化调频方案

该方案实际上是一个输出频率受控的直接数字频率合成(DDS)系统。通过A/D转换器件将调制信号转换成数字信号,用该数字信号控制DDS的频率控制字,形成输出频率受模拟信号控制的正弦波,从而实现了调频。通过在A/D转换值后补零的方法,可控制调频波的调制指数。系统由FPGA实现。EDA软件Max PlusⅡ的仿真和系统的实际输出波形都表明该数字化调频系统的调制指数可在很大范围内变化。     

多路高压放大器输出直流电压监测与显示系统设计

在自适应光学系统中,自适应控制器AD输出控制信号需要通过高压放大器放大成高压电驱动压电陶瓷变形镜,从而实现波前实时校正.在实际系统中,往往需要对高压放大器输出电压进行实时监测.本系统采用小体积单片机C8051F310作为控制器,采用专用电表芯片CS5460A作为核心测量芯片,实现了单板对20路0～500 V直流电压的实时监测与显示,线性度优于0.2％.     

线型双酚A酚醛树脂的合成

对线型双酚A酚醛树脂的合成工艺及催化剂浓度、种类、反应时间、醛酚比等影响因素进行了研究。结果表明,随着反应物醛酚比的增大,产物中残留的BPA量呈下降趋势,软化点先上升后下降,在1.2左右出现峰值;随反应时间延长,产物的软化点升高,分子质量增大,残留BPA量减少,分子质量分散性增加;催化剂用量增大,分子质量增大,软化点增高,残留BPA含量降低。合理的催化剂用量为m(BPA)∶m(催化剂)=100∶20。以合成的BPAN代替双氰胺(D ICY)作环氧树脂EB454A80的固化剂,在相同的固化工艺条件下,固化物的Tg提高近12℃。     

Endometrial Epithelial ARID1A Is Required for Uterine Immune Homeostasis during Early Pregnancy

A growing body of work suggests epigenetic dysregulation contributes to endometriosis pathophysiology and female infertility. The chromatin remodeling complex subunit AT-rich interaction domain 1A (ARID1A) must be properly expressed to maintain normal uterine function. Endometrial epithelial ARID1A is indispensable for pregnancy establishment in mice through regulation of endometrial gland function; however, ARID1A expression is decreased in infertile women with endometriosis. We hypothesized that ARID1A performs critical operations in the endometrial epithelium necessary for fertility besides maintaining gland function. To identify alterations in uterine gene expression resulting from loss of epithelial ARID1A, we performed RNA-sequencing analysis on pre-implantation uteri from Ltf^iCre/+Arid1a^f/f and control mice. Differential expression analysis identified 4181 differentially expressed genes enriched for immune-related ingenuity canonical pathways including agranulocyte adhesion and diapedesis and natural killer cell signaling. RT-qPCR confirmed an increase in pro-inflammatory cytokine and macrophage-related gene expression but a decrease in natural killer cell signaling. Immunostaining confirmed a uterus-specific increase in macrophage infiltration. Flow cytometry delineated an increase in inflammatory macrophages and a decrease in uterine dendritic cells in Ltf^iCre/+Arid1a^f/f uteri. These findings demonstrate a role for endometrial epithelial ARID1A in suppressing inflammation and maintaining uterine immune homeostasis, which are required for successful pregnancy and gynecological health.     

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.