并联旁侧支路风流逆转次序的实验研究

为研究上行通风网络火灾中并联旁侧支路风流逆转次序的问题,设计并制作了一个包含3条并联支路的小型模拟实验台.在其中1条支路中设置了燃烧器,用来模拟火灾支路;另两条模拟旁侧支路.取旁侧支路长度及初始风速(点火前的风速)的不同组合,分别进行模拟实验.利用热线风速仪和烟迹观测了两条旁侧支路中风流逆转的过程.结果表明:上行风流火灾中两条并联的旁侧支路可以在不同时刻发生风流逆转;风流逆转次序取决于两条支路长度与初始风速的乘积之比;长度与初始风速乘积较小的支路将较早发生风流逆转.     

基于CFD的新型风幕控尘装置的模拟研究及其应用

针对传统风幕控尘装置设备多、空间小、掘进机移动不便等诸多不足之处,⌒进行了优化设计。为确保新型风幕控尘装置的实际应用效果,指导现场防尘系统设计,确定抽出式风机风筒安设位置,依(山西某矿掘进巷道工作面1:1建立了物理几何模型,并利用计算流体动力学(CFD)进行模拟。根(湍流模型特性及流体运动特点,选取拉格朗日法离散相模型对掘进巷道粉尘浓度分布进行了模拟分析并进行现场实践。结果显示,所选物理几何模型参数设置合理,拟合精度达到预测要求;加装新型风幕控尘装置前后,粉尘浓度下降对比明显;距底板2.1 m处安设抽出式风机风筒时,系统降尘效果显著。     

Numerical simulation of particle deposition in obstructive human airways

To investigate airflow pattern and its impact on particle deposition, finite-volume based computational fluid dynamics (CFD) simulations were conducted in the diseased triple-bifurcation airways. Computations were carried out for twenty Reynolds numbers ranging from 100 to 2 000 in the step of 100. Particles in the size range of 1–10 μm were conducted. Two particle deposition mechanisms (gravitational sedimentation and inertial impaction) were considered. The results indicate that there are strong relationship between airflow structures and particle deposition patterns. Deposition efficiency is different for different particles in the whole range of the respiratory rates. Particles in different sizes can deposit at different sites. Smaller particles can be uniformly deposited at the inside wall of the considered model. Larger particles can be mainly deposited in the proximal bifurcations. Deposition fraction varies a lot for different inlet Reynolds numbers. For lower Reynolds numbers, deposition fraction is relatively small and varies a little with varying the diameters. For higher Reynolds numbers, there is a most efficient diameter for each Reynolds number to target the aerosols at the specific site.     

Genetic Deletion of Mmp9 Does Not Reduce Airway Inflammation and Structural Lung Damage in Mice with Cystic Fibrosis-like Lung Disease

Elevated levels of matrix metalloprotease 9 (MMP-9) and neutrophil elastase (NE) are associated with bronchiectasis and lung function decline in patients with cystic fibrosis (CF). MMP-9 is a potent extracellular matrix-degrading enzyme which is activated by NE and has been implicated in structural lung damage in CF. However, the role of MMP-9 in the in vivo pathogenesis of CF lung disease is not well understood. Therefore, we used β-epithelial Na⁺ channel-overexpressing transgenic (βENaC-Tg) mice as a model of CF-like lung disease and determined the effect of genetic deletion of Mmp9 (Mmp9^-/-) on key aspects of the pulmonary phenotype. We found that MMP-9 levels were elevated in the lungs of βENaC-Tg mice compared with wild-type littermates. Deletion of Mmp9 had no effect on spontaneous mortality, inflammatory markers in bronchoalveolar lavage, goblet cell metaplasia, mucus hypersecretion and emphysema-like structural lung damage, while it partially reduced mucus obstruction in βENaC-Tg mice. Further, lack of Mmp9 had no effect on increased inspiratory capacity and increased lung compliance in βENaC-Tg mice, whereas both lung function parameters were improved with genetic deletion of NE. We conclude that MMP-9 does not play a major role in the in vivo pathogenesis of CF-like lung disease in mice.     

Lactoferrin Ameliorates Ovalbumin-Induced Asthma in Mice through Reducing Dendritic-Cell-Derived Th2 Cell Responses

Asthma is a chronic respiratory disease with symptoms such as expiratory airflow narrowing and airway hyperresponsiveness (AHR). Millions of people suffer from asthma and are at risk of life-threatening conditions. Lactoferrin (LF) is a glycoprotein with multiple physiological functions, including antioxidant, anti-inflammatory, antimicrobial, and antitumoral activities. LF has been shown to function in immunoregulatory activities in ovalbumin (OVA)-induced delayed type hypersensitivity (DTH) in mice. Hence, the purpose of this study was to investigate the roles of LF in AHR and the functions of dendritic cells (DCs) and Th2-related responses in asthma. Twenty 8-week-old male BALB/c mice were divided into normal control (NC), ovalbumin (OVA)-sensitized, and OVA-sensitized with low dose of LF (100 mg/kg) or high dose of LF (300 mg/kg) treatment groups. The mice were challenged by intranasal instillation with 5% OVA on the 21st to 27th day after the start of the sensitization period. The AHR, cytokines in bronchoalveolar lavage fluid, and pulmonary histology of each mouse were measured. Serum OVA-specific IgE and IgG1 and OVA-specific splenocyte responses were further detected. The results showed that LF exhibited protective effects in ameliorating AHR, as well as lung inflammation and damage, in reducing the expression of Th2 cytokines and the secretion of allergen-specific antibodies, in influencing the functions of DCs, and in decreasing the level of Th2 immune responses in a BALB/c mouse model of OVA-induced allergic asthma. Importantly, we demonstrated that LF has practical application in reducing DC-induced Th2 cell responses in asthma. In conclusion, LF exhibits anti-inflammation and immunoregulation activities in OVA-induced allergic asthma. These results suggest that LF may act as a supplement to prevent asthma-induced lung injury and provide an additional agent for reducing asthma severity.     

Extracellular Vesicles and Asthma—More Than Just a Co-Existence

Extracellular vesicles (EVs) are membranous structures, which are secreted by almost every cell type analyzed so far. In addition to their importance for cell-cell communication under physiological conditions, EVs are also released during pathogenesis and mechanistically contribute to this process. Here we summarize their functional relevance in asthma, one of the most common chronic non-communicable diseases. Asthma is a complex persistent inflammatory disorder of the airways characterized by reversible airflow obstruction and, from a long-term perspective, airway remodeling. Overall, mechanistic studies summarized here indicate the importance of different subtypes of EVs and their variable cargoes in the functioning of the pathways underlying asthma, and show some interesting potential for the development of future therapeutic interventions. Association studies in turn demonstrate a good diagnostic potential of EVs in asthma.     

Lysophosphatidylserine Induces MUC5AC Production via the Feedforward Regulation of the TACE-EGFR-ERK Pathway in Airway Epithelial Cells in a Receptor-Independent Manner

Lysophosphatidylserine (LysoPS) is an amphipathic lysophospholipid that mediates a broad spectrum of inflammatory responses through a poorly characterized mechanism. Because LysoPS levels can rise in a variety of pathological conditions, we sought to investigate LysoPS’s potential role in airway epithelial cells that actively participate in lung homeostasis. Here, we report a previously unappreciated function of LysoPS in production of a mucin component, MUC5AC, in the airway epithelial cells. LysoPS stimulated lung epithelial cells to produce MUC5AC via signaling pathways involving TACE, EGFR, and ERK. Specifically, LysoPS- dependent biphasic activation of ERK resulted in TGF-α secretion and strong EGFR phosphorylation leading to MUC5AC production. Collectively, LysoPS induces the expression of MUC5AC via a feedback loop composed of proligand synthesis and its proteolysis by TACE and following autocrine EGFR activation. To our surprise, we were not able to find a role of GPCRs and TLR2, known LyoPS receptors in LysoPS-induced MUC5AC production in airway epithelial cells, suggesting a potential receptor-independent action of LysoPS during inflammation. This study provides new insight into the potential function and mechanism of LysoPS as an emerging lipid mediator in airway inflammation.     

提高四气门气缸盖进气道一致性工艺措施浅析

进气道性能及其性能一致性偏差是四气门气缸盖的关键指标之一,其性能参数为进气涡流比和流量系数,涡流比大小代表进缸气流旋转程度,流量系数代表进气量多少,对柴油机燃油燃烧效果和排放有很大影响。因一般四气门气缸盖至少有一个是切向进气道,其气道性能参数对制造偏差非常敏感,本文通过总结试制中的各种方案,总结了三种对进气道一致性影响比较大的因素以及保证性能一致性的工艺措施。     

深部软岩巷道围岩变形特征及全锚索支护机理

针对新元煤矿9102原回风巷的围岩大变形及支护构件变形失效等问题,分析了复杂高水平应力和垂直应力场作用下原回风巷顶板围岩的裂隙发育状况及围岩变形破坏特征,结合现场实际决定在原回风巷20 m处重新开掘一条回风巷。采用数值模拟分析了新掘回风巷的围岩应力环境,结合原有支护及现场实践提出了全锚索支护技术,并阐明其支护机理。现场监测表明,新掘回风巷采用全锚索支护技术后,巷道围岩变形明显减少,且支护构件无变形失效,实现了对深部软岩巷道的围岩控制。