激光打孔技术在光伏背板玻璃上的应用

双玻光伏组件以其抗PID性强、防隐裂、防水汽透过、抗蜗牛纹、可靠性优异、轻量化等诸多优点,在晶硅太阳能组件市占比逐步提高。双玻光伏组件用背板玻璃一般需要预留出线孔,光伏背板玻璃的出线孔主要有两种打孔方式:金钢钻上下同步钻孔的模式和激光打孔。激光打孔以其易维护、可异形孔加工、效率高、生产成本低等优势得到各大玻璃厂的认可。通过分析在实际生产中激光打孔出现的打孔缺陷问题,提出了改善措施,有助于工厂的降本增效。     

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。     

钢混结构大型厂房整体式爆破拆除

采用整体式控制爆破拆除方案对华电扬州电厂钢筋混凝土框-排架结构厂房进行了爆破拆除。爆破前,对汽机房、厂房外墙和楼梯进行了预处理。将厂房划分为3个爆区,采用非电多回路网格式爆破网路,依靠东侧锅炉房倒塌施加在西侧锅炉房上的倾覆力矩,有效地克服了西侧锅炉房向西倒的难题,可为同类工程提供一定的参考。     

地应力条件下的凿岩爆破数值模拟

为了研究地应力对凿岩爆破的影响,采用DDA方法模拟爆炸应力波作用下考虑地应力条件时的单孔和多孔凿岩爆破破岩过程。模拟发现,随着初始地应力水平的增加,裂纹扩展半径和破岩区域面积减小,裂纹发育主方向趋于地应力的最大主应力方向,初始地应力对裂纹的抑制和引导作用明显;初始地应力水平的增加,对拉伸裂纹的抑制作用更为显著,从而降低了拉伸破坏对爆破破岩的贡献。模拟也表明,在初始地应力存在的条件下,通过对爆破载荷和炮孔布置进行针对性的优化,可以克服地应力带来的影响,并取得预期的爆破效果。本研究对地应力条件下的凿岩爆破工程具有理论和参考意义。     

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。     

受老空水威胁工作面巷道防治水实践

针对高庄煤矿3_上1104回风巷为沿空掘巷,巷道掘进期间受3_上1102老空水威胁,掘进开采存在严重的水患安全问题,采用超前打设疏水孔的方案来治理老空水威胁,对巷道采用调向增大护巷煤柱厚度等措施实现巷道安全快速掘进,探放水期间无淹巷情况发生,探放水后巷道顶板和上帮无淋水现象发生。     

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.