A review of thin film electrolytes fabricated by physical vapor deposition for solid oxide fuel cells

The ohmic resistance in solid oxide fuel cells (SOFCs) mainly comes from the electrolyte, which can be reduced by developing novel electrolyte materials with higher ionic conductivity and/or fabricating thin-film electrolytes. Among various kinds of thin-film fabrication technology, the physical vapor deposition (PVD) method can reduce the electrolyte thickness to a few micrometers and mitigate the issues associated with high-temperature sintering, which is necessary for wet ceramic methods. This review summarizes recent development progress in thin-film electrolytes fabricated by the PVD method, especially pulsed laser deposition (PLD) and magnetron sputtering. At first, the importance of the substrate surface morphology for the quality of the film is emphasized. After that, the fabrication of thin-film doped-zirconia and doped-ceria electrolytes is presented, then we provide a brief summary of the works on other types of electrolytes prepared by PVD. Finally, we have come to the summary and made perspectives.     

Experimental study and model predictions on helium release in an enclosure with single or multiple vents

This paper presents experiments performed at Canadian Nuclear Laboratories (CNL) to examine the dispersion behaviour of helium in a polycarbonate enclosure that was representative of a residential parking garage. The purpose was to gain a better understanding of the effect of buoyancy- or wind-driven natural ventilation on hydrogen dispersion behaviour. Although hydrogen dispersion studies have been reported extensively in the literature, gaps still exist in predictive methods for hazard analysis. Helium, a simulant for hydrogen, was injected near the centre of the floor with a flow rate ranging from 5 to 75 standard litres per minute through an upward-facing nozzle, resulting in an injection Richardson number ranging between 10^?1 and 10². The location of the nozzle varied from the bottom of the enclosure to near the ceiling to examine the impact of the nozzle elevation on the development of a stratified layer in the upper region of the enclosure. When the injection nozzle was placed at a sufficiently low elevation, the vertical helium profile always consisted of a homogenous layer at the top overlaying a stratified layer at the bottom. To simulate outdoor environmental conditions, a fan was placed in front of each vent to examine the effect of opposing or assisting wind on the dispersion. The helium transients in the uniform layer predicted with analytical models were in good agreement with the measured transients for most tests. Model improvements are required for adequately predicting transients with primarily stratified profiles or strong opposing wind.     

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。     

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.