高瓦斯矿井孤岛综放采空区遗煤自燃综合防治技术

针对国阳二矿高瓦斯自燃煤层综放开采的实际情况,分析了"U+Ⅱ"型孤岛综放面采空区遗煤自燃特点及危险性。利用单元法对孤岛面的漏风状况进行了实测,并通过数值模拟分析了综放采空区内的漏风流场,根据采空区自燃"三带"的渗流风速确定了可能自燃带的范围,表明采空区漏风是"U+Ⅱ"型孤岛综放面采空区遗煤自燃的主要危险因素。在此基础上,结合实际情况系统地制定了以有效控制采空区漏风和重点发火区域注胶为主的综合防灭火技术措施,为有效控制综放采空区遗煤自燃,实现矿井高产高效、安全生产提供技术保障。实践表明,运用控制工作面风量与高抽巷负压、均压堵漏、压注胶体防灭火材料及加快工作面推进速度等综合防灭火技术防治高瓦斯矿井"U+Ⅱ"型孤岛综放面采空区遗煤自燃是可行的。     

水网藻对铜绿微囊藻的化感作用及对氮磷去除能力研究

通过测定藻液D680和叶绿素a浓度,研究了水网藻种植水对铜绿微囊藻生长的影响,探讨了在分离培养和共生培养2种条件下水网藻对铜绿微囊藻的抑制作用,并考察了水网藻对氮磷的去除能力.结果表明,水网藻对铜绿微囊藻有较强的抑制作用,在水网藻种植水作用8 d后,铜绿微囊藻死亡率达92%;不同浓度的水网藻对铜绿微囊藻的抑制作用不同,...     

六氯苯对离体鱼肝线粒体抗氧化酶的作用

采用差速离心法从鲫鱼肝脏中提取线粒体,用不同浓度(0,2,4,8,16,32mg/L)六氯苯对其体外染毒30min.测定线粒体超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,用聚丙烯酰胺凝胶电泳法分析其同工酶谱,并检测线粒体中丙二醛(MDA)含量.结果显示,SOD和GSH-Px活性及其同工酶的活性表达均呈现出低浓度六氯苯作用下被激活,高浓度六氯苯作用下被抑制的变化趋势.在高浓度六氯苯(32mg/L)作用下线粒体中MDA含量显著增加.说明六氯苯的毒性作用可能为一种自由基机制,即低浓度的六氯苯导致线粒体内活性氧自由基(ROS)生成量少量增加,SOD和GSH-Px及其同工酶活性由于氧化应激的诱导被激活;随着六氯苯浓度增加,线粒体内ROS生成量大量增加,并破坏了SOD和GSH-Px的抗氧化活性,导致其活力下降或丧失,自由基含量增加,线粒体脂质过氧化加剧.     

隔油调节罐设计浅论

就隔油调节罐设置的目的、容积的确定、设置的位置、收油设施的设计、污油的加热排泥、排油的操作控制、消防措施及污油的输送等问题阐述了自己的看法。     

钙稳态失调与镉肝细胞毒性关系的研究

分别从细胞外钙对镉肝细胞毒性的影响.细胞内总钙和游离钙含量变化以及钙移位酶活力的变化等方面探讨了镉对肝细胞的毒性与细胞内钙稳态失调的关系.结果表明:镉对大鼠游离肝细胞的毒作用并非由于引起细胞外钙内流所致,也不是由于干扰了细胞内钙隔离系统功能所致.     

Connectivity of Streams and Wetlands to Downstream Waters: An Integrated Systems Framework

Interest in connectivity has increased in the aquatic sciences, partly because of its relevance to the Clean Water Act. This paper has two objectives: (1) provide a framework to understand hydrological, chemical, and biological connectivity, focusing on how headwater streams and wetlands connect to and contribute to rivers; and (2) briefly review methods to quantify hydrological and chemical connectivity. Streams and wetlands affect river structure and function by altering material and biological fluxes to the river; this depends on two factors: (1) functions within streams and wetlands that affect material fluxes; and (2) connectivity (or isolation) from streams and wetlands to rivers that allows (or prevents) material transport between systems. Connectivity can be described in terms of frequency, magnitude, duration, timing, and rate of change. It results from physical characteristics of a system, e.g., climate, soils, geology, topography, and the spatial distribution of aquatic components. Biological connectivity is also affected by traits and behavior of the biota. Connectivity can be altered by human impacts, often in complex ways. Because of variability in these factors, connectivity is not constant but varies over time and space. Connectivity can be quantified with field‐based methods, modeling, and remote sensing. Further studies using these methods are needed to classify and quantify connectivity of aquatic ecosystems and to understand how impacts affect connectivity.     

Thallium(I) and thallium(III) induce apoptosis in isolated rat hepatocytes by alterations in mitochondrial function and generation of ROS

Environmental metal toxins, generated through diverse anthropogenic activities, constitute one of the major contaminants that have led to global dispersion of these toxic metals in the ecosystem. Thallium is one of these widely dispersed metals that produce severe adverse effects on human and biological systems. The influence of thallium(I) and thallium(III) on the early events that trigger apoptosis signaling were examined in freshly isolated rat hepatocytes. In addition, the role of oxidative stress, and mitochondria in the induction of apoptosis were also investigated. Incubation of thallium(I) and thallium(III) with isolated rat hepatocytes generated reactive oxygen species (ROS), collapse of mitochondrial membrane potential, activation of caspases cascade, and appearance of apoptosis phenotype. Mitochondrial permeability transition (MPT) pore sealing agents (cyclosporine A and carnitine) and ATP generators (L-glutamine, fructose, and xylitol) inhibited the activation of caspase-3 and apoptosis, indicating that both the cations activated apoptosis signaling via mitochondrial pathway. Pretreatment of hepatocytes with antioxidants (α-tocopherol or deferoxamine) also blocked caspase-3 activation induced by these cations, suggesting that oxidative stress may be directly involved in a mitochondrial MPT pore opening and activation of caspases cascade. These findings contribute to a better understanding of the mechanisms that mediate thallium-induced apoptosis in isolated rat hepatocytes.