Influence of high energy ball milling on structural,microstructural and optical properties of TiO2 nanoparticles

The influence of high-energy ball milling on structural, microstructural, and optical properties of TiO₂ by modifying the nanoparticle size was studied. Five samples were extracted at different milling times (0, 2, 4, 8, and 13 h). The average particle sizes estimated by dynamic light scattering (DLS) were 205, 155.8, 116.8, 82.9, and 82.7 nm at 0, 2, 4, 8, and 13 h, respectively. X-ray diffraction analysis confirmed progressive broadening of the peaks as the milling time elapsed. Besides, a correlation was found between d spacing and the average crystal size. The UV–Vis diffuse reflectance spectra of TiO₂ revealed a decrease in reflectance due to particle size reduction. Similarly, an alteration of the bandgap transition energy was presented, whose values gradually decreased from 2.966 eV to 2.861 eV for the sample without and with the maximum duration milling performed (13 h), respectively. Likewise, the SEM analysis showed a distribution in nanoparticle size that became more homogeneous and smaller average grain size as the milling duration was longer.     

水力空化改质对重质原油沥青质及性质的影响

利用水力空化过程产生局部的高温、高压、高射流以及强大的剪切力等极端化学物理条件改质处理沙特重质原油，试验结果表明：沙特重质原油经过水力空化改质后粘度由13.61降低至7.22mm2/s，残碳由7.16%降低至6.48%，实沸点蒸馏后减压渣油降低1个百分点。进一步采用APPI FT-IR MS、XRD、FT-IR、SEM和粒度分布等技术研究了水力空化改质对沙重原油分子组成，沥青质团聚体微晶结构、沥青质胶束粒径分布、沥青质官能团、沥青质形貌等方面的影响，从分子角度阐述空化改质重油的机理。研究结果表明：水力空化改质后沙重原油分子量分布、芳烃类化合物缔合作用变小；沥青质对低DBE化合物吸附性能降低；沥青质团聚体微晶结构更加松散；沥青质胶束粒度分布降低；沥青质分子相互团聚作用力减弱。进一步考察了水力空化改质前后减压渣油延迟焦化性能，改质处理后焦炭产率降低1.85个百分点，液体收率和气体产率分别增加1.52和0.33个百分点，水力空化改质对沥青质性质、结构特点的改善能够有效的提高其加工性能。     

基于双时间点检测的毫米波雷达人流量监测方法

针对现有基于视频监控的人流量统计方案成本高、算法复杂且不利于个人隐私保护的局限性，利用毫米波雷达体积小、成本低、分辨率高的特点，提出了一种基于双时间点检测的人流量监测方法。该方法先获取人体目标散射点位置和多普勒频移信息来构成点云数据，然后根据多普勒频移正负来判断人体的运动方向，并筛选具有高多普勒频移值的点云数据以降低干扰点对聚类结果的影响；在双时间点对特定区域内人员数量进行统计，并根据双时间点之间所获取的点云数据聚类结果对所统计人员数据进行修正。实验结果表明，该方法能够用匿名的方式以较高的正确率统计人员进出。     

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。     

Effect of the particle size ratio on macro- and mesoscopic shear characteristics of the geogrid-reinforced rubber and sand mixture interface

As a new type of material for civil engineering projects, the rubber and sand mixture is widely used in roadbed fillers, offering environmental benefits over traditional tyre disposal methods. This study uses a large-scale direct shear apparatus to examine the interface shear properties of the geogrid-reinforced rubber and sand mixture, considering different particle size ratios (r), rubber contents, and normal stresses. Based on indoor tests, direct shear models of the mixture with different values of r are established in PFC^3D, revealing the meso-mechanical mechanism of the mixture in the direct shear process. The results show that when r is greater than 1, incorporating a certain amount of rubber particles can increase the shear strength of the mixture. The r values of 15.78, 7.63, and 3.98 correspond to an optimal rubber content of 30%, 10%, and 20%, respectively. When r is less than 1, mixing rubber particles can only reduce the shear strength of the mixture. When the rubber content is low, the smaller the value of r, the greater is the thickness of the shear band. Furthermore, the normal and tangential contact forces are greater. The fabric anisotropy evolution law of the mixture is consistent with the change in the contact force distribution.     

Structural,optical, cytotoxicity,and antimicrobial properties of MgO,ZnO and MgO/ZnO nanocomposite for biomedical applications

In this study, MgO nanoparticles were successfully fabricated and incubated inside ZnO NPs to form MgO/ZnO nanocomposite for biomedical applications. The x-ray diffraction analysis of MgO, ZnO, and MgO/ZnO has shown the single-phase x-ray diffraction patterns through X'pert High score. The crystallite sizes were calculated as 18 nm, 42 nm, and 53 nm, respectively. The average particle size of MgO, ZnO, and MgO/ZnO nanopowders depicted from secondary electron images of field emission electron microscopy were 56 nm, 400 nm, and 450 nm, respectively. The presence of MgO NPs inside ZnO NPs was confirmed by transmission electron microscopy. The elemental dispersive spectroscopy of MgO, given the peaks of oxygen and magnesium, also showed only zinc and oxygen peaks in ZnO, which confirms no other impurities in MgO and ZnO powders. The elemental analysis of MgO/ZnO nanocomposite showed the peaks of Zinc and Oxygen, along with a tiny peak of Mg. The photoluminescence and UV–vis spectroscopy revealed the absorbance fluorescence limit of the nanomaterials. Fourier transform infrared spectroscopy confirmed the several groups present in the nanocomposite. The biocompatibility of MgO, ZnO, and MgO/ZnO was observed with human peripheral blood mononuclear cells. The cytotoxicity studies were also performed against human cancer (liver and breast) cell lines. The MgO, ZnO, and MgO/ZnO exhibited the antimicrobial properties against Escherichia coli and Staphylococcus aureus.     

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.