疫情下电磁场理论课程的网络教学

本文主要总结了新冠疫情期间作者的电磁场理论课程在线教学经验。对比分析了录播和直播的优缺点后,选择录播教学方式。基于超星网络教学平台,展示了录播网络教学的具体措施,包括网上答疑和学习效果检查以及在线批改作业等。给出了网络教学可以为线下教学继续使用的方法和手段,为疫情结束后的正常教学提供了新的网络教学补充措施。     

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。     

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。     

广义正交码索引调制系统的性能分析

摘 要：为了提高码索引调制（code index modulation，CIM）系统的传输效率，提出了一种具有更低复杂度的单输入单输出（single input single output，SISO）的广义正交码索引调制（generalized orthogonal code index modulation，GQCIM）系统。CIM 系统使用扩频码和星座符号传输信息，但只能激活两个扩频码索引和一个调制符号。而 GQCIM 系统以一种新颖的方式克服了只激活一个调制符号的限制，同时充分利用了调制符号的正交性，增加扩频码索引以传输更多的额外信息位，提高了系统的传输效率。此外，分析了GQCIM系统的理论性能，推导了误码率性能的上界。通过蒙特卡罗仿真验证了GQCIM系统的性能，对比发现GQCIM系统的理论和仿真性能一致。而且在相同的传输效率下，结果显示GQCIM系统的性能优于同样具有正交性的调制系统，如广义码索引调制（generalized code index modulation，GCIM）系统、CIM系统、码索引调制-正交空间调制（code index modulation aided quadrature spatial modulation，CIM-QSM）系统、码索引调制-正交空间调制（code index modulation aided spatial modulation，CIM-SM）系统、脉冲索引调制（pulse index modulation，PIM）系统。     

Convolutional Neural Network Auto Encoder Channel Estimation Algorithm in MIMO-OFDM System

Higher transmission rate is one of the technological features of prominently used wireless communication namely Multiple Input Multiple Output-Orthogonal Frequency Division Multiplexing (MIMO–OFDM). One among an effective solution for channel estimation in wireless communication system, specifically in different environments is Deep Learning (DL) method. This research greatly utilizes channel estimator on the basis of Convolutional Neural Network Auto Encoder (CNNAE) classifier for MIMO-OFDM systems. A CNNAE classifier is one among Deep Learning (DL) algorithm, in which video signal is fed as input by allotting significant learnable weights and biases in various aspects/objects for video signal and capable of differentiating from one another. Improved performances are achieved by using CNNAE based channel estimation, in which extension is done for channel selection as well as achieve enhanced performances numerically, when compared with conventional estimators in quite a lot of scenarios. Considering reduction in number of parameters involved and re-usability of weights, CNNAE based channel estimation is quite suitable and properly fits to the video signal. CNNAE classifier weights updation are done with minimized Signal to Noise Ratio (SNR), Bit Error Rate (BER) and Mean Square Error (MSE).     

一种新的密码本原:棘轮密钥交换的定义、模型及构造

在传统密码学应用中,人们总假定终端是安全的,并且敌手只存在于通信信道上。然而,主流的恶意软件和系统漏洞给终端安全带来了严重和直接的威胁和挑战,例如容易遭受存储内容被病毒破坏、随机数发生器被腐化等各种攻击。更糟糕的是,协议会话通常有较长的生存期,因此需要在较长的时间内存储与会话相关的秘密信息。在这种情况下,有必要设计高强度的安全协议,以对抗可以暴露存储内容和中间计算结果(包括随机数)的敌手。棘轮密钥交换是解决这一问题的一个基本工具。文中综述了密码本原——棘轮密钥交换,包括单向、半双向和双向等棘轮密钥交换的定义、模型及构造,并展望了棘轮密钥交换的未来发展趋势。     

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.     

Radiation- and Photo-Induced Oxidation Pathways of Methionine in Model Peptide Backbone under Anoxic Conditions

Within the reactive oxygen species (ROS) generated by cellular metabolisms, hydroxyl radicals (HO^•) play an important role, being the most aggressive towards biomolecules. The reactions of HO^• with methionine residues (Met) in peptides and proteins have been intensively studied, but some fundamental aspects remain unsolved. In the present study we examined the biomimetic model made of Ac-Met-OMe, as the simplest model peptide backbone, and of HO^• generated by ionizing radiation in aqueous solutions under anoxic conditions. We performed the identification and quantification of transient species by pulse radiolysis and of final products by LC-MS and high-resolution MS/MS after γ-radiolysis. By parallel photochemical experiments, using 3-carboxybenzophenone (CB) triplet with the model peptide, we compared the outcomes in terms of short-lived intermediates and stable product identification. The result is a detailed mechanistic scheme of Met oxidation by HO^•, and by CB triplets allowed for assigning transient species to the pathways of products formation.