石油资源流动空间结构的要素解析

石油资源横向流动是以源地、汇地、中转交流地及其间的运输通道为构架的资源空间运移系统,具有显著的空间特征。为解决现有的资源流动空间结构研究中,研究对象及其内涵各异,且相互不成体系的问题,论文以石油资源横向流动为例,借鉴哈格特的空间结构认知模式,将石油资源流动的空间结构系统地解析为流动节点、流动关系、通道网络和流场四大要素,并分别对其空间内涵、特征、意义以及研究重点与相应方法进行分析,进而探讨了其对于资源流动机制与流动优化研究的促进作用,从而使得石油资源流动空间结构的研究体系更加系统、严密,并可为其他资源的流动研究提供借鉴。     

资源产权与道德的起源:演化博弈论的诠释

论文在一个演化经济学视角下考察资源产权和道德(以下简称为产权和道德)自生自发问题。首先,简略地梳理了产权生发研究的历史;介绍了应用博弈论,特别是演化博弈论研究产权生发问题的近况,并指出其不足之处在于博弈支付的社会经济学含义模糊和无法揭示行为博弈与博弈环境相互作用、共同演化的过程。其次,扩展了生物遗传学中适应度的概念,使其适于社会演化分析;分析了社会经济学适应度的构成及其与竞争类型的关系。第三,为了说明行为博弈与博弈环境之间的相互作用关系,在传统复制者动态方程组中,引入状态方程(或组)。第四,采用改进后的复制者动态方程组分析产权和道德自生自发的机理和过程,指出产权和道德都是人类无节制争斗和无约束生育的产物。最后,分析了洛克社会的三大不足,及其继续演化的动力。     

Sodium cyanide-induced modulations in the activities of some oxidative enzymes and metabolites in the fingerlings of Cyprinus carpio (Linnaeus)

Carp fingerlings exposed to a sublethal concentration (0.5?mg?L^?1) of sodium cyanide showed a steady decrement over a 7-day period in respiratory rate, rise in lactate dehydrogenase (LDH), and fall in succinate dehydrogenase (SDH) activities followed by variations in lactic and pyruvate levels. Changes in these enzyme activities might be due to impaired oxidative metabolism and severe cellular damage leading to the release of these enzymes. Decline in the activities of SDH and LDH clearly represents a shift from aerobic to anaerobic metabolism as evidenced by elevated lactate and decline in pyruvate levels. The shift to anaerobic metabolism is also reflected by severe drop in the respiratory rate of the fish. This may be a consequence of the blockage of electron transfer from cytochrome c oxidase to molecular oxygen, thus ceasing cellular respiration and it can lead to cellular hypoxia even in the presence of normal hemoglobin oxygenation. Hence, we indirectly reconfirm the inhibition of oxidative metabolism by sodium cyanide. Alterations in behavioral pattern induced by sublethal sodium cyanide exposure may be due to the combination of cytotoxic hypoxia with lactate acidosis, which depresses the central nervous system (CNS); as the brain is the most sensitive site to anoxia, it results in impaired CNS function.     

Assessing environmental exposure and health impacts of gold mining in Ghana

Understanding the extent to which people are being exposed to environmental contaminants helps to identify those populations which may be disproportionately exposed to the contaminants of potential public health concern. This study represents the first report of a comparison of heavy metal arsenic (As), mercury (Hg), cadmium (Cd), cobalt (Co), copper (Cu), lead (Pb), platinum (Pt), zinc (Zn), and manganese (Mn) concentrations in the blood of residents of mining and non-mining communities in Ghana. Blood sampling, health records, and interviews were used in this study to establish the links between the levels of contaminants and health effects in humans within a mining and non-mining community in Ghana. Results of this study show that mean concentration of As in blood in Tarkwa Nsuaem Municipality/Prestea-Huni Valley District (TNMA/PHVD) (mining communities) and Cape Coast Metropolis (CCMA) (non-mining community) was 18- and 2-fold higher, respectively, than the WHO guideline value of 0.002?mg?L^?1. The mean concentrations of As, Cd, Pb, Hg, and Mn were elevated up to 20-fold higher in the blood of resident adults and children in TNMA/PHVD than in CCMA. The risk of acute respiratory infections in the exposed populations of TNMA and PHVD were approximately 41- and 12-fold greater than the unexposed group. The risk of diabetes mellitus in the exposed populations of TNMA and PHVD were also approximately 20- and 4-fold higher than the unexposed group. In TNMA and PHVD, 40 blood donors were suffering from hyperkeratosis or pigmentation unlike their CCMA counterparts. Data suggest a potential association between mining activities and the levels of these heavy metals. However, the proportion of anthropogenic contribution to the levels of these metals in the blood remains uncertain. This uncertainty seems to be the umbrella under which both government and mining companies continue to hide, leading to inaction.     

Cytotoxicity of single-walled carbon nanotubes,multi-walled carbon nanotubes,and chrysotile to human lung epithelial cells

Carbon nanotubes (CNTs) have found numerous applications in various industries. Recently, adverse effects of these materials on human and animal cells in vitro have been reported. In the present study, the cytotoxicity of single-walled carbon nanotubes (SWCNTs), multi-walled carbon nanotubes (MWCNTs), and chrysotile asbestos in human lung epithelial cells has been studied using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cells were exposed for 6 h and 24 h to between 0.97 and 1500 μg mL^?1 of CNTs and chrysotile fibers prepared in two culture media containing 5% serum and 0.5% dimethylsulfoxide. Dose–response curves were obtained to determine the nonobservable adverse effect concentration and the half-maximum inhibitory concentration (IC₅₀). The way of dispersion affects the cytotoxicity of CNTs. For MWCNT, the toxicological indexes were lower than for SWCNT. Chrysotile fibers were even less cytotoxic than CNTs. Therefore, workplace control measures are recommended as priority for occupational and environmental conditions.     

Manufactured silver and gold nanoparticles-induced apoptosis by caspase-pathway in human cell lines

Abstract

Metallic nanoparticles have emerged as an important class of nanomaterials for a wide range of industrial and medical applications. Because of the intensive commercial applications, risk assessment of these nanoparticles is of great importance. In the present study, the human hepatoma and leukemia cells were used to characterize the apoptotic effects of silver nanoparticles (4.7 and 42?nm) and gold nanoparticles (30?nm). Apoptotic cells were identified by chromatin condensation and flow cytometry analysis, using Annexin V/PI, TUNEL and caspase activation assays. Flow cytometry analysis showed that the three metallic nanoparticles induced apoptotic cell death in a concentration and time dependent-manner. Moreover, the three nanoparticles induced activation of caspase-3 and -7 in hepatoma and leukemia cells. Apoptotic effects were stronger after exposure of both cell lines with 4.7?nm silver nanoparticles than those obtained with 42?nm silver and 30?nm gold nanoparticles. In conclusion, silver (4.7 and 42?nm) and gold (30?nm) nanoparticles induced apoptosis in hepatoma and leukemia cells via the caspase dependent pathway. The smaller silver nanoparticles (4.7?nm) had a greater ability to induce apoptosis in both cell lines.     

Chromosome damage in individuals exposed to heavy metals†

Testing the mutagenic activity of environmental pollutants has become an important area of modern environmental science and prophylactic medicine. The most suitable method for short‐term mutagenicity testing on man, at present, are chromosome studies on somatic cells of exposed individuals. Mutation types analyzed by such studies are of high practical relevance as indicator system of genetic damage induced in man under in vivo conditions. A rather large series of such studies has been dedicated to the action of heavy metals on individuals contacted with these metals under therapeutic, ecological or occupational conditions or by intoxication. Lead, cadmium, chromium, nickel, mercury, zinc and other metals as well as their compounds have been under study. Analyses of that kind, of course, are hampered by difficulties with the distinct estimation of the actual load as well as unclear conditions of exposition, e.g. simultaneous exposition to different metals.

Results obtained till now arouse some suspicion of a direct or indirect mutagenic activity in man by certain chromium and platinum compounds, arsenic, mercury, and combinations of lead with other heavy metals (cadmium, zinc, arsenic, antimony, etc.). Life style, above all smoking habits, well may act comutagenic. In most cases, however, mutagenic activity of metals and metal compounds apparently is clearly superposed by their toxic activity. In specific cases, chromosome studies also may contribute to discover sources of ecological exposition and to monitor occupational load by heavy metals.     

DNA damage in mouse organs and in human sperm cells by bisphenol A

Abstract

The in vivo genotoxic potential of bisphenol A using the comet assay in mice and in human sperm cells in vitro without metabolizing enzymes was studied. Male mice were exposed by oral gavage to the following doses of bisphenol A (0 125, 250 and 500?mg/kg body weight). DNA damage was investigated in liver, kidney, testes, urinary bladder, colon and lungs cells. In testicular cells, a significant increase in DNA strand breaks was observed in the lowest, but not in the medium or highest dose groups. Histopathological investigation of the testicular samples did not show any treatment dose-related effects. No DNA strand breaks were observed in any of the other investigated tissues. In human sperm cells in vitro, bisphenol A did not induce DNA strand breaks.     

Oxidative stress and changes in locomotor behavior and gill morphology of Gambusia affinis exposed to chromium

Sublethal effects of chromium trioxide on mosquito fish, Gambusia affinis, were carried out for 28 days on day 4, 8, 12, 16, 20, 24, and 28. The sublethal effects of chromium (LC₁₀, 77.62?mg?L^?1) on antioxidant enzymes, thiobarbituric acid reactive substance (TBARS), locomotor behavior, and gill morphology were studied. The antioxidant enzymes like superoxide dismutase (SOD) and catalase were induced throughout the exposure span of 28 days. Percent induction was also increase with the days of exposure. Lipid peroxidation product, malondialdehyde was enhanced in the viscera tissue of chromium-exposed fish. Perturbation of locomotor behavior like decrease in distance travelled (m?min^?1) and in swimming speed (cm?s^?1) was observed in exposed fish. Chromium toxicity caused alterations in gill morphology like hypertrophy and hyperplasia in secondary lamellae followed by detached epithelium with severe necrosis. It can be concluded from the results that Cr intoxication in Gambusia fish, caused induction in antioxidant enzymes and lipid peroxidation, plus changes in gill morphology and locomotor behavior.     

Determination of oxidative stress markers and serum cholinesterase among pesticide sprayers in southern Brazil

Small farmers generally spray pesticides manually and often do not use complete protective equipment. The standard test to detect pesticide exposure, which may be associated with toxicity, is the determination of serum cholinesterase, but in chronic exposure to low doses, this test is less sensitive. In this study, in a group sampled among pesticide sprayers without signs of intoxication, cholinesterase, thiobarbituric acid reactive substances (TBARS), catalase (Cat), and superoxide dismutase (Sod) activities were analyzed. Cholinesterase activity was only slightly lower in the farmer group in relation to the control group. However, TBARS and Cat activities were 3-fold increased in the farmers in comparison to the controls. Sod activity was similar in both groups. The group of pesticide sprayers that did not use the complete protective equipment presented a significantly higher level of TBARS than the group that used the complete protective equipment. Therefore, the determination of TBARS and catalase can be useful to identify individuals that are chronically exposed to low doses of pesticides.