个性化学习路径推荐综述

近年来，伴随着现代信息技术的迅猛发展，以人工智能为代表的新兴技术在教育领域得到了广泛应用，引发了学习理念和方式的深刻变革.在这种大背景下，在线学习超越了时空的限制，为学习者“随时随地”学习提供了更多的可能性，从而得到了蓬勃发展.然而，在线学习中师生时间、空间分离的特征，导致教师无法及时掌握学生的学习状态，一定程度上制约了在线学习中教学质量的提升.面对多元化的学习需求及海量学习资源，如何迅速完成学习目标、降低学习成本、合理分配学习资源等问题成为限制个人和时代发展的重大问题.然而，传统的“一刀切”的教育模式已经不能满足人们获取知识的需求了，需要一个更高效、更科学的个性化教育模式，以帮助学习者以最小的学习成本最大限度地完成学习目标.基于以上背景，如何自动高效识别学习者特征，高效地组织和分配学习资源，为每一位学习者规划个性化路径，成为面向个体的精准化教育资源匹配机制研究中亟待解决的问题.系统地综述并分析了当前个性化学习路径推荐的研究现状，并从多学科领域的角度分析了对于同一问题的不同研究思路，同时也归纳总结了当前研究中最为主流的核心推荐算法.最后，强调当前研究存在的主要不足之处.     

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。     

基于重要度排序的配电自动化终端优化布局方法

针对配电自动化终端优化布局问题，提出了一种基于重要度排序的终端优化布局方法。首先以等年值综合费用为目标函数，供电可靠性和投入产出比为双重约束建立了配电自动化终端优化布局模型。然后通过分析配电自动化终端对供电可靠性提升的影响，给出各个节点的“二遥”及“三遥”终端安装重要度定义及计算公式。最后采用枚举法确定最优终端安装数量，基于节点终端安装重要度排序确定终端的最优安装位置。该方法考虑了已布局节点对剩余节点终端安装重要度的影响，能够在降低计算量的同时兼顾布局合理性。运用所提方法RBTS-BUS2系统及扩充模型进行终端优化布局并与智能优化算法的布局结果进行对比，验证了本文方法的有效性及优越性。     

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。     

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.