Insight into the Impact of Oxidative Stress on the Barrier Properties of Lipid Bilayer Models

As a new field of oxidative stress-based therapy, cold physical plasma is a promising tool for several biomedical applications due to its potential to create a broad diversity of reactive oxygen and nitrogen species (RONS). Although proposed, the impact of plasma-derived RONS on the cell membrane lipids and properties is not fully understood. For this purpose, the changes in the lipid bilayer functionality under oxidative stress generated by an argon plasma jet (kINPen) were investigated by electrochemical techniques. In addition, liquid chromatography-tandem mass spectrometry was employed to analyze the plasma-induced modifications on the model lipids. Various asymmetric bilayers mimicking the structure and properties of the erythrocyte cell membrane were transferred onto a gold electrode surface by Langmuir-Blodgett/Langmuir-Schaefer deposition techniques. A strong impact of cholesterol on membrane permeabilization by plasma-derived species was revealed. Moreover, the maintenance of the barrier properties is influenced by the chemical composition of the head group. Mainly the head group size and its hydrogen bonding capacities are relevant, and phosphatidylcholines are significantly more susceptible than phosphatidylserines and other lipid classes, underlining the high relevance of this lipid class in membrane dynamics and cell physiology.     

Collaborative Action of Microglia and Astrocytes Mediates Neutrophil Recruitment to the CNS to Defend against Escherichia coli K1 Infection

Escherichia coli K1 is a leading cause of neonatal bacterial meningitis. Recruitment of neutrophils to the central nervous system (CNS) via local immune response plays a critical role in defense against E. coli K1 infection; however, the mechanism underlying this recruitment remains unclear. In this study, we report that microglia and astrocytes are activated in response to stimulation by E. coli K1 and/or E. coli K1-derived outer membrane vesicles (OMVs) and work collaboratively to drive neutrophil recruitment to the CNS. Microglial activation results in the release of the pro-inflammatory cytokine TNF-α, which activates astrocytes, resulting in the production of CXCL1, a chemokine critical for recruiting neutrophils. Mice lacking either microglia or TNF-α exhibit impaired production of CXCL1, impaired neutrophil recruitment, and an increased CNS bacterial burden. C-X-C chemokine receptor 2 (CXCR2)-expressing neutrophils primarily respond to CXCL1 released by astrocytes. This study provides further insights into how immune responses drive neutrophil recruitment to the brain to combat E. coli K1 infection. In addition, we show that direct recognition of E. coli K1 by microglia is prevented by the K1 capsule. This study also reveals that OMVs are sufficient to induce microglial activation.     

Nurr1 Is Not an Essential Regulator of BDNF in Mouse Cortical Neurons

Nurr1 and brain-derived neurotrophic factor (BDNF) play major roles in cognition. Nurr1 regulates BDNF in midbrain dopaminergic neurons and cerebellar granule cells. Nurr1 and BDNF are also highly expressed in the cerebral cortex, a brain area important in cognition. Due to Nurr1 and BDNF tissue specificity, the regulatory effect of Nurr1 on BDNF in different brain areas cannot be generalized. The relationship between Nurr1 and BDNF in the cortex has not been investigated previously. Therefore, we examined Nurr1-mediated BDNF regulation in cortical neurons in activity-dependent and activity-independent states. Mouse primary cortical neurons were treated with the Nurr1 agonist, amodiaquine (AQ). Membrane depolarization was induced by KCl or veratridine and reversed by nimodipine. AQ and membrane depolarization significantly increased Nurr1 (p < 0.001) and BDNF (p_AQ < 0.001, p_KCl < 0.01) as assessed by real-time qRT-PCR. However, Nurr1 knockdown did not affect BDNF gene expression in resting or depolarized neurons. Accordingly, the positive correlation between Nurr1 and BDNF expression in AQ and membrane depolarization experiments does not imply co-regulation because Nurr1 knockdown did not affect BDNF gene expression in resting or depolarized cortical neurons. Therefore, in contrast to midbrain dopaminergic neurons and cerebellar granule cells, Nurr1 does not regulate BDNF in cortical neurons.     

同轴式双空心抽油杆下入深度设计方法

同轴式双空心抽油杆加热系统可有效解决高凝油井井筒易结蜡、稠油井产液黏度较高的问题,但考虑油井生产效率、开采成本及综合的经济效益,需要计算出最佳的抽油杆下入深度。以井口出油温度最优为目标,同轴式双空心抽油杆下入深度、循环水进口温度为约束条件,建立了井口出油温度C计算模型。利用该模型进行求解时,先用迭代法进行同轴式双空心抽油杆下入深度优化,然后在优化结果基础上进行抽油机载荷校核。建立的井口出油温度计算模型及同轴式双空心抽油杆下入深度确定方法,在现场13口油井进行了应用。结果表明,该方法避免了以前设计人员凭经验确定抽油杆下深的弊端,可靠性更高,且有效时率平均提高14.1百分点,既满足了生产需要又节省了油井开发成本。      

脉冲光源原子吸收光谱仪信号数字处理软件的设计

通过实验室设计的脉冲光源钨丝原子吸收光谱仪,采集到一个分析信号和光源载波叠加的复合信号。为了从中提取原子吸收分析信号,首先对该复合信号进行数值微分,确定光源脉冲载波每个峰的坐标和相应的峰高,算出每个载波峰位相应的吸光度值,绘制吸收峰轮廓图;然后根据辛普森(Simpson)数值积分原理,求出吸收峰的面积,从而得到积分吸光度值。在微软公司的Visual Basic 6．0开发平台上,编写了实现上述功能的软件,以图形和数值的方式,同时输出每次测定结果。该软件系统和钨丝原子吸收光谱仪硬件系统相配合,对铜标准溶液的测试结果为:检出限为0．0133μg/ml,线性范围为0．10- 4．0μg／ml,对1．0μg／ml Cu(n=10)测定的精密度为RSD=4．05％。     

现浇混凝土蜂巢空腹楼盖技术的应用

蜂巢空腹楼盖技术是采用蜂巢芯在现浇混凝土板中铸塑成内部空间承力单元,形成传力明确的现浇混凝土双向网格肋空心楼盖水平结构体系。它的传力骨架是通过柱与柱(墙)之间实心暗梁或明梁,结合蜂巢空腹板工肋上下翼缘形成一个大的工字形截面梁,使其抗侧移刚度、位移、强度和变形等各方面均能满足设计要求。     

Acute T-Cell-Driven Inflammation Requires the Endoglycosidase Heparanase-1 from Multiple Cell Types

It has been accepted for decades that T lymphocytes and metastasising tumour cells traverse basement membranes (BM) by deploying a battery of degradative enzymes, particularly proteases. However, since many redundant proteases can solubilise BM it has been difficult to prove that proteases aid cell migration, particularly in vivo. Recent studies also suggest that other mechanisms allow BM passage of cells. To resolve this issue we exploited heparanase-1 (HPSE-1), the only endoglycosidase in mammals that digests heparan sulfate (HS), a major constituent of BM. Initially we examined the effect of HPSE-1 deficiency on a well-characterised adoptive transfer model of T-cell-mediated inflammation. We found that total elimination of HPSE-1 from this system resulted in a drastic reduction in tissue injury and loss of target HS. Subsequent studies showed that the source of HPSE-1 in the transferred T cells was predominantly activated CD4⁺ T cells. Based on bone marrow chimeras, two cellular sources of HPSE-1 were identified in T cell recipients, one being haematopoiesis dependent and the other radiation resistant. Collectively our findings unequivocally demonstrate that an acute T-cell-initiated inflammatory response is HPSE-1 dependent and is reliant on HPSE-1 from at least three different cell types.     

分离用无机膜及其在食品中的应用

概述了无机膜的种类、特点,同时介绍了无机膜在食品分离中的研究应用情况及今后的发展前景。     

阵列波导光栅薄膜的制备及性能

以一种特定成分的有机硅为原料,采用溶胶-凝胶法,在硅基片上制备出用于光波导器件的薄膜.通过折射率和厚度测试及XPS成分测试验证了此薄膜具有较好的均匀性、厚度和光学特性,满足光波导器件的要求.分析了溶胶-凝胶法中常见的龟裂现象的原因以及采预防方法.利用这种薄膜结合微电子加工工艺制备出光波导器件阵列波导光栅.     

近海大气环境下锈蚀平面钢框架抗震性能试验研究及有限元分析

焊接空心球节点(WHSJs)自1966年被提出以来,已经广泛地应用于空间网格结构中,至今已有55年的应用历史。由于环境的侵蚀、后期维护不到位等,焊接球节点锈蚀的现象屡见不鲜。该文针对随机锈蚀后焊接空心球节点的抗压承载力的变化规律进行了研究,基于随机有限元分析方法进行了大量的随机数值分析,研究了锈蚀深度概率分布模型对抗压承载力折减系数的影响;利用曲线拟合技术提出了折减系数下限和上限曲线的理论计算公式;通过随机有限元的大量分析结果揭示了抗压折减系数随锈蚀深度概率分布模型的变化规律;提出了用于预测抗压折减系数概率分布模型的拟合公式;通过对具有不同几何参数的焊接空心球节点的分析,得到了该文结论对不同几何尺寸下焊接球节点的适用性。研究结果表明,所提出的方法可以准确确定随机锈蚀焊接空心球节点抗压承载力折减系数的随机概率分布模型,可为随机锈蚀焊接球节点承载力的评估提供理论分析基础。