基于误差估值累加开环校正的诱导式欺骗检测方法

诱导式卫星欺骗干扰可诱导航空器逐渐偏离预定航迹，难以被发现，因此及时有效地检测干扰是飞行安全的保障。在现有紧组合导航体制基础上，设计了一种基于误差估值累加开环校正的紧组合导航结构，并证明了其性能与传统闭环校正紧组合导航性能等效。在此结构中，将紧组合导航系统与自适应序贯概率比检测方法结合，提出了一种基于误差估值累加开环校正的诱导式欺骗检测方法，融合紧组合导航信息与其他不受欺骗影响的导航信息，构建欺骗检测统计量进行诱导式欺骗检测。仿真结果表明，开环校正结构可避免随时间累加的惯性导航系统误差所导致的组合导航滤波器发散问题，同时欺骗检测方法可进一步提高算法对“最坏”情形下微小诱导式欺骗的检测效果。     

A blockchain-based audit approach for encrypted data in federated learning

The development of data-driven artificial intelligence technology has given birth to a variety of big data applications. Data has become an essential factor to improve these applications. Federated learning, a privacy-preserving machine learning method, is proposed to leverage data from different data owners. It is typically used in conjunction with cryptographic methods, in which data owners train the global model by sharing encrypted model updates. However, data encryption makes it difficult to identify the quality of these model updates. Malicious data owners may launch attacks such as data poisoning and free-riding. To defend against such attacks, it is necessary to find an approach to audit encrypted model updates. In this paper, we propose a blockchain-based audit approach for encrypted gradients. It uses a behavior chain to record the encrypted gradients from data owners, and an audit chain to evaluate the gradients’ quality. Specifically, we propose a privacy-preserving homomorphic noise mechanism in which the noise of each gradient sums to zero after aggregation, ensuring the availability of aggregated gradient. In addition, we design a joint audit algorithm that can locate malicious data owners without decrypting individual gradients. Through security analysis and experimental evaluation, we demonstrate that our approach can defend against malicious gradient attacks in federated learning.     

具有保护肠上皮细胞HT-29免受大肠杆菌和H2O2损伤潜力的植物乳杆菌的筛选

益生菌可在肠道定植从而发挥抗炎或抗氧化活性，有利于宿主肠道健康。本实验研究了从新疆传统发酵乳制品中分离得到的8?株植物乳杆菌对大肠杆菌侵袭和过氧化氢刺激肠上皮细胞HT-29的保护作用。结果表明：在8?株植物乳杆菌中，植物乳杆菌35具有最高的黏附能力。植物乳杆菌35可通过取代、竞争、排阻的方式抑制大肠杆菌对HT-29细胞的黏附，抑制率分别为42.60%、59.17%、60.19%。植物乳杆菌35及其多糖可抑制大肠杆菌刺激HT-29细胞产生白细胞介素-8；同时保护HT-29细胞免受过氧化氢的损伤，增加超氧化物歧化酶、谷胱甘肽过氧化物酶活力水平并降低丙二醛含量。结论：植物乳杆菌35及其粗胞外多糖具有抑制大肠杆菌O157诱导的炎症性肠病的潜力。     

计算机通信及网络远程控制技术的应用与可靠性探究

随着社会的进步和发展,计算机网络通信技术已被应用到实际生活、生产的各个方面,对人们的生活、生产等产生了深刻的影响。为此,文章就计算机通信及网络远程控制技术在实际生活中的应用问题进行了探究,旨在借助先进科技促进社会实现更优质发展。     

基于改进残差特征蒸馏的轻量级超分辨率网络

基于深度学习的图像超分辨率算法通常采用递归的方式或参数共享的策略来减少网络参数，这将增加网络的深度，使得运行网络花费大量的时间，从而很难将模型部署到现实生活中。为了解决上述问题，本文设计一种轻量级超分辨率网络，对中间特征的关联性及重要性进行学习，且在重建部分结合高分辨率图像的特征信息。首先，引入层间注意力模块，通过考虑层与层之间的相关性，自适应地分配重要层次特征的权重。其次，使用增强重建模块提取高分辨率图像中更精细的特征信息，以此得到更加清晰的重建图片。通过大量的对比实验表明，本文设计的网络与其他轻量级模型相比，有更小的网络参数量，并且在重建精度和视觉效果上都有一定的提升。     

四氢姜黄素经PI3K/Akt信号通路对人血小板活化和聚集的调控作用

目的：探讨姜黄素的主要肠道代谢物四氢姜黄素（tetrahydrocurcumin，THC）对血小板活化和聚集的影响及其可能的分子机制。方法：在体外实验中，用不同浓度的THC（0、0.5、1、10 μmol/L）提前与健康人纯化血小板共同孵育40 min，然后加入凝血酶激活血小板2 min，用流式细胞术测定血小板表面CD62P和CD63的表达量，用酶联免疫吸附法测定血小板释放血小板因子-4（platelet factor-4，PF4）和趋化因子配体-5（chemokine ligand 5，CCL5）水平，用血小板聚集仪检测血小板释放ATP水平和血小板最大聚集率，用Western blot蛋白免疫印迹法检测血小板磷酸肌醇-3-激酶（phosphoinositide 3-kinase，PI3K）和Akt蛋白的磷酸化水平。结果：与模型组（血小板悬液中加入0.05%二甲基亚砜）相比，THC能抑制凝血酶诱导的血小板表面CD62P和CD63的表达，抑制PF4、CCL5和ATP的释放，降低血小板最大聚集率，下调PI3K和Akt蛋白的磷酸化水平，且呈浓度依赖效应，其中10 μmol/L的浓度下作用效果显著（P＜0.01、P＜0.001）。PI3K的特异性激动剂740 Y-P可部分逆转THC对PF4和CCL5释放和血小板聚集的抑制作用（P＜0.05、P＜0.01）。结论：THC具有显著抑制血小板活化和聚集的作用，其机制可能是THC可下调PI3K/Akt介导的信号通路。     

Techno-economic assessment of hydrogen refueling station: A case study in Croatia

Hydrogen refueling station (HRS) capacity and location depend on the users, which makes it difficult to select the most favorable option before potential users are actually identified. As in Croatia, at least for now, there are no hydrogen users, this study considers a wide range of HRS capacities and their different configurations. These include hydrogen production and charging station within one existing wind farm in Croatia or both nearby the users, the hydrogen production within the wind farm and the charging station nearby the users, while hydrogen is delivered to the station with a tube trailer, and configuration of hydrogen production within the wind farm with a mobile charging station in case of several users in different locations. Each HRS configuration is evaluated by the obtained levelized cost of hydrogen depending on the capital, and operation and maintenance costs within the HRS techno-economic analysis provided.     

火花放电原子发射光谱类型标准化校正方式的探讨

在国内,火花放电原子发射光谱分析广泛使用类型标准化进行方法校正。在国外,标准和文献中鲜见使用此方法的相关论述。类型标准化主要采用平移校正和转动校正两种方式,哪种方式更加合理也鲜见报道。国外设备类型标准化的默认设置优先采用转动校正方式,相关国内标准对最优校正方式的规定尚不明确,此默认设置的合理性有待探讨。实验选用低合金钢20CrNi2Mo、R407标准样品和不锈钢317L、0Cr18Ni9标准样品,引用国内相关标准,以正确度临界差为评判依据,模拟类型标准化样品和待测样品“十分接近”和“接近”两种情况下平移校正和转动校正的数据正确度。经数据统计分析,平移校正分析结果均满足要求,转动校正结果在“接近”情况下部分元素不满足要求。结合相关国家标准中元素含量范围和精密度数据进行分析,通过计算允许最大偏倚量并制作曲线图方式展开分析,得出如下结论:在满足文中类型标准化控制要点前提下,分析设置更适合于采用平移校正方式。     

Adaptation to Endoplasmic Reticulum Stress Enhances Resistance of Oral Cancer Cells to Cisplatin by Up-Regulating Polymerase η and Increasing DNA Repair Efficiency

Endoplasmic reticulum (ER) stress response is an adaptive program to cope with cellular stress that disturbs the function and homeostasis of ER, which commonly occurs during cancer progression to late stage. Late-stage cancers, mostly requiring chemotherapy, often develop treatment resistance. Chemoresistance has been linked to ER stress response; however, most of the evidence has come from studies that correlate the expression of stress markers with poor prognosis or demonstrate proapoptosis by the knockdown of stress-responsive genes. Since ER stress in cancers usually persists and is essentially not induced by genetic manipulations, we used low doses of ER stress inducers at levels that allowed cell adaptation to occur in order to investigate the effect of stress response on chemoresistance. We found that prolonged tolerable ER stress promotes mesenchymal–epithelial transition, slows cell-cycle progression, and delays the S-phase exit. Consequently, cisplatin-induced apoptosis was significantly decreased in stress-adapted cells, implying their acquisition of cisplatin resistance. Molecularly, we found that proliferating cell nuclear antigen (PCNA) ubiquitination and the expression of polymerase η, the main polymerase responsible for translesion synthesis across cisplatin-DNA damage, were up-regulated in ER stress-adaptive cells, and their enhanced cisplatin resistance was abrogated by the knockout of polymerase η. We also found that a fraction of p53 in stress-adapted cells was translocated to the nucleus, and that these cells exhibited a significant decline in the level of cisplatin-DNA damage. Consistently, we showed that the nuclear p53 coincided with strong positivity of glucose-related protein 78 (GRP78) on immunostaining of clinical biopsies, and the cisplatin-based chemotherapy was less effective for patients with high levels of ER stress. Taken together, this study uncovers that adaptation to ER stress enhances DNA repair and damage tolerance, with which stressed cells gain resistance to chemotherapeutics.