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。     

基于可供性的文化意象交互式智能音箱设计研究

目的 探索将文化民俗有效融入现代产品中的技术思路，保留并延续中华传统文化的生命力，有助于提升用户体验。方法 分析可供性与文化意象之间的主客观互通性;挖掘交互式智能音箱中的可供性触点;构建形态、感官、认知及情境四类可供性的设计框架;以楚文化意象为例进行设计实践，对智能音箱的产品造型与交互操作方式进行设计，并进行设计评价。结果 在可供性理论指导下的楚文化意象交互式智能音箱产品外观及交互体验设计较好地满足了设计目标和用户需求。结论 可供性有助于文化意象的正确提取与转化，可将意象抽象为具有实际意义的设计要素，帮助用户在生理与认知两个层面理解产品的使用方法，同时进一步回味、体验文化内涵和文化精髓。     

Green Measurements for Software Product Based on Sustainability Dimensions

Software is a central component in the modern world and vastly affects the environment’s sustainability. The demand for energy and resource requirements is rising when producing hardware and software units. Literature study reveals that many studies focused on green hardware; however, limited efforts were made in the greenness of software products. Green software products are necessary to solve the issues and problems related to the long-term use of software, especially from a sustainability perspective. Without a proper mechanism for measuring the greenness of a particular software product executed in a specific environment, the mentioned benefits will not be attained. Currently, there are not enough works to address this problem, and the green status of software products is uncertain and unsure. This paper aims to identify the green measurements based on sustainable dimensions in a software product. The second objective is to reveal the relationships between the elements and measurements through empirical study. The study is conducted in two phases. The first phase is the theoretical phase, where the main components, measurements and practices that influence the sustainability of a software product are identified. The second phase is the empirical study that involved 103 respondents in Malaysia investigating current practices of green software in the industrial environment and further identifying the main sustainability dimensions and measurements and their impact on achieving green software products. This study has revealed seven green measurements of software product: Productivity, Usability, Cost Reduction, Employee Support, Energy Efficiency, Resource Efficiency and Tool Support. The relationships are statistically significant, with a significance level of less than 0.01 (p = 0.000). Thus, the hypothesised relationships were all accepted. The contributions of this study revolve around the research perspectives of the measurements to attain a green software product.     

样品前处理QuEChERS法及新型吸附材料在水产品中抗生素残留分析中的应用进展

抗生素的不合理使用，给水产品带来了一系列的潜在食用安全风险。品种繁多且残留痕量的抗生素也为食品安全检测带来了新的挑战，发展准确、快速、简便、高效且安全的前处理方法尤为重要。QuEChERS法作为一种新型样品前处理技术，现已逐渐应用到水产品抗生素残留检测中，并可实现较好的回收率。由于水产品中蛋白质和脂类含量高，样品基质复杂，使用经典QuEChERS法无法满足抗生素分析需求，改良其提取方法和净化方法是保证分析结果的关键。本文综述QuEChERS法原理特点，总结归纳其在针对水产品抗生素分析上的主要方法改良手段，并就近十年来改良QuEChERS法在水产品抗生素残留分析中的应用进行文献归纳，同时介绍新型吸附材料在该领域的使用，为探索新的净化方式提供参考，以期帮助检测人员持续优化改进QuEChERS法，推动和扩大QuEChERS法在水产品抗生素残留分析中的应用范围。     

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.