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℃。     

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19.     

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.     

Effective Natural Killer Cell Degranulation Is an Essential Key in COVID-19 Evolution

NK degranulation plays an important role in the cytotoxic activity of innate immunity in the clearance of intracellular infections and is an important factor in the outcome of the disease. This work has studied NK degranulation and innate immunological profiles and functionalities in COVID-19 patients and its association with the severity of the disease. A prospective observational study with 99 COVID-19 patients was conducted. Patients were grouped according to hospital requirements and severity. Innate immune cell subpopulations and functionalities were analyzed. The profile and functionality of innate immune cells differ between healthy controls and severe patients; CD56dim NK cells increased and MAIT cells and NK degranulation rates decreased in the COVID-19 subjects. Higher degranulation rates were observed in the non-severe patients and in the healthy controls compared to the severe patients. Benign forms of the disease had a higher granzymeA/granzymeB ratio than complex forms. In a multivariate analysis, the degranulation capacity resulted in a protective factor against severe forms of the disease (OR: 0.86), whereas the permanent expression of NKG2D in NKT cells was an independent risk factor (OR: 3.81; AUC: 0.84). In conclusion, a prompt and efficient degranulation functionality in the early stages of infection could be used as a tool to identify patients who will have a better evolution.