基于Dynamics AX的航天制造资源管理

在分析了航天制造企业信息化需求的基础上,提出了基于Dynamics AX的航天制造企业制造资源管理的解决方案;以典型航天制造企业为例,设计基于Dynamics AX系统的制造资源管理模块,其中包括设备管理、仪器仪表管理、工具管理、工装管理和计量管理.最后以设备管理模块为例,结合典型航天制造企业的特点,实现了设备上账、分账、调拨、停启用、闲置报废等功能,完成了对设备全生命周期的跟踪管理.     

基于EPA的新型结晶器液位控制系统

针对结晶器液位控制中硬件和软件算法方面存在的问题,设计一种基于微控制器MAX7651和以太网控制器AX88796的网络液位控制系统,该系统采用带校正补偿环节的专家模糊控制策略进行控制。仿真和测试结果证明系统具有良好的控制性能。     

黄芪甲苷对肝细胞放射损伤预防作用的机制研究

本文研究了黄芪甲苷(Astragaloside IV,ASIV)对肝细胞放射损伤防护的机制。以γ射线照射L-02细胞建立辐射损伤模型,分为对照组、黄芪甲苷组(80μg/mL)、照射组(4 Gy)、黄芪甲苷+照射组(80μg/mL+4Gy),于照射前12 h更换含有黄芪甲苷浓度为80μg/mL的培养基。采用流式细胞术检测黄芪甲苷对照后L-02细胞早期凋亡率及细胞周期的影响;以罗丹明123荧光探针检测黄芪甲苷对照后L-02细胞线粒体膜电位改变的影响;免疫荧光法观察γH2AX焦点数;通过Western Blot检测细胞中Nrf2、HO-1、NQO1的蛋白表达变化。结果显示:照后细胞凋亡率随着药物浓度的增加而降低,黄芪甲苷能有效的缓解电离辐射引起的细胞G2期阻滞;黄芪甲苷+照射组细胞线粒体膜电位均高于照射组;黄芪甲苷+照射组γH2AX焦点数明显少于照射组;照射组细胞内Nrf2、HO-1及NQO1表达升高,黄芪甲苷+照射组Nrf2、HO-1及NQO1表达则是随着药物浓度增加而降低。综上可知,黄芪甲苷对L-02细胞具有辐射损伤预防作用,其机制可能是通过Nrf2途径来减轻电离辐射所致的损伤。     

三元层状材料 M2AX的研究进展

三元层状陶瓷材料（M（n＋1）AXn）因其具有独特的力学、热学和电学性能而备受关注.本文综述其中的一个分支-M2AX相在计算材料学方面的最新结果,并归纳块材的力学性能和抗氧化性能的研究结果,文中还简述了该材料的热学和电学性能,并展望了M2AX系列材料的应用前景.     

γH2AX,a DNA Double-Strand Break Marker,Correlates with PD-L1 Expression in Smoking-Related Lung Adenocarcinoma

In recent years, the choice of immune checkpoint inhibitors (ICIs) as a treatment based on high expression of programmed death-ligand 1 (PD-L1) in lung cancers has been increasing in prevalence. The high expression of PD-L1 could be a predictor of ICI efficacy as well as high tumor mutation burden (TMB), which is determined using next-generation sequencing (NGS). However, a great deal of effort is required to perform NGS to determine TMB. The present study focused on γH2AX, a double-strand DNA break marker, and the suspected positive relation between TMB and γH2AX was investigated. We assessed the possibility of γH2AX being an alternative marker of TMB or PD-L1. One hundred formalin-fixed, paraffin-embedded specimens of lung cancer were examined. All of the patients in the study received thoracic surgery, having been diagnosed with lung adenocarcinoma or squamous cell carcinoma. The expressions of γH2AX and PD-L1 (clone: SP142) were evaluated immunohistochemically. Other immunohistochemical indicators, p53 and Ki-67, were also used to estimate the relationships of γH2AX. Positive relationships between γH2AX and PD-L1 were proven, especially in lung adenocarcinoma. Tobacco consumption was associated with higher expression of γH2AX, PD-L1, Ki-67, and p53. In conclusion, the immunoexpression of γH2AX could be a predictor for the adaptation of ICIs as well of as PD-L1 and TMB.     

The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?

It is widely stated that wild-type p53 either mediates the activation of cell cycle checkpoints to facilitate DNA repair and promote cell survival, or orchestrates apoptotic cell death following exposure to cancer therapeutic agents. This reigning paradigm has been challenged by numerous discoveries with different human cell types, including solid tumor-derived cell lines. Thus, activation of the p53 signaling pathway by ionizing radiation and other DNA-damaging agents hinders apoptosis and triggers growth arrest (e.g., through premature senescence) in some genetic backgrounds; such growth arrested cells remain viable, secrete growth-promoting factors, and give rise to progeny with stem cell-like properties. In addition, caspase 3, which is best known for its role in the execution phase of apoptosis, has been recently reported to facilitate (rather than suppress) DNA damage-induced genomic instability and carcinogenesis. This observation is consistent with an earlier report demonstrating that caspase 3 mediates secretion of the pro-survival factor prostaglandin E₂, which in turn promotes enrichment of tumor repopulating cells. In this article, we review these and related discoveries and point out novel cancer therapeutic strategies. One of our objectives is to demonstrate the growing complexity of the DNA damage response beyond the conventional “repair and survive, or die” hypothesis.     

某雷达双以太网接口的设计实现

阐述了一种嵌入式系统双以太网通讯接口的软硬件工业设计案例,该设计使用了AT89S52微处理器和AX88796L以太网控制芯片,运用TCP／IP协议,最终实现了某型雷达的以太网通讯需求。     

USB接口单片机的VoIP终端设计

介绍了一种以单片机SONIX2202、D类功放AX2012和语音芯片NY3P010AS8为核心设计的网络电话机,该装置通过USB接口连接到计算机上,可拨打国际国内长途电话及手机,系统还带有语音拨号等功能。本文对该装置的工作原理、硬件配置、软件设计及功能进行了详细论述,经样机实验证明,其各项功能均可很好地实现。     

Changes in the Number of Double-Strand DNA Breaks in Chinese Hamster V79 Cells Exposed to γ-Radiation with Different Dose Rates

A comparative investigation of the induction of double-strand DNA breaks (DSBs) in the Chinese hamster V79 cells by γ-radiation at dose rates of 1, 10 and 400 mGy/min (doses ranged from 0.36 to 4.32 Gy) was performed. The acute radiation exposure at a dose rate of 400 mGy/min resulted in the linear dose-dependent increase of the γ-H2AX foci formation. The dose-response curve for the acute exposure was well described by a linear function y = 1.22 + 19.7x, where “y” is an average number of γ-H2AX foci per a cell and “x” is the absorbed dose (Gy). The dose rate reduction down to 10 mGy/min lead to a decreased number of γ-H2AX foci, as well as to a change of the dose-response relationship. Thus, the foci number up to 1.44 Gy increased and reached the “plateau” area between 1.44 and 4.32 Gy. There was only a slight increase of the γ-H2AX foci number (up to 7) in cells after the protracted exposure (up to 72 h) to ionizing radiation at a dose rate of 1 mGy/min. Similar effects of the varying dose rates were obtained when DNA damage was assessed using the comet assay. In general, our results show that the reduction of the radiation dose rate resulted in a significant decrease of DSBs per cell per an absorbed dose.     

架构数字化示波器

传统的示波器不能保存图形,更不能对信号进行实时的分析处理。希望利用计算机和电子技术架构数字化多功能双踪甚至多踪示波器的做法来解决这个问题。同时比较以此架构的数字化示波器和传统的示波器的性能差别,指出两者的优劣。在系统的实现上,根据精度和成本提出了几种做法,主要分为直接使用计算机声卡架构和使用自行设计的数字电路实现两种。