基于模糊聚类的PM_(2.5)拟合组分选择模型的研究

提出了一种新的PM2.5源成分谱拟合组分选择模型,在充分考虑拟合过程的物理意义的基础上,采用聚类正确率作为组分选择的依据.实验验证,该模型能够准确获取较好的拟合主组分,相比与经验选或者手动盲选所得拟合结果,我们提出的模型将成功拟合(误差范围在0~0.05之间)的比例由40%提升到83%.     

大气中挥发性有机化合物(VOCs)的人为来源研究

在2002年春、夏、秋、冬四季对环境大气中挥发性有机化合物的组成和变化规律进行了研究,在此基础上运用CMB8.0受体模型对各类污染源进行了源解析,得到受体点各人为污染源的年平均贡献率分别为:汽车尾气62%,汽油挥发9%,石油液化气10%,涂料6%,石油化工6%,未知源6%.对不同物种贡献的分析显示,环境大气中的乙烯、苯和甲苯等化合物主要来自于汽车尾气的排放,异戊烷来自于汽油的挥发,石油液化气、涂料、石油化工分别对大气中的异丁烷、正己烷和2,4-二甲基戊烷贡献量最大.     

京津冀水源涵养生态服务供体区与受体区范围的划分

京津冀水资源问题已经严重制约区域经济发展,定量分析研究区水源涵养生态服务供受关系,有助于深刻理解区域上下游之间的生态联系,促进区域生态公平,实现区域社会持续健康发展.利用降水储量法、水量平衡法及水源涵养生态服务供体区与受体区划分方法,分析2000-2010年京津冀净水源涵养量空间格局,划分研究区水源涵养生态服务供体区和受体区范围.结果表明:①冀北燕山山区净水源涵养量最高,年均值为65.24~81.35 mm,其次是冀西太行山山区,年均值为46.47~61.28 mm;净水源涵养量负值区主要分布在东部沿海和大中小城市,年均值为-130.46~-152.39 mm.②水源涵养生态服务供体区占研究区面积的41.42%,单位面积（m2,下同）平均净供水量为0.03~0.07 m3;水源涵养生态服务平衡区面积占25.01%;水源涵养生态服务受体区面积占33.57%,单位面积平均净需水量为0.18~0.41 m3,是供体区供水能力的6倍左右.③从流域来看,滦河流域的承德市为天津市、秦皇岛市及唐山市供应水资源,年均供水总量为23.7×108 m3;永定河流域的张家口市为北京市供应水资源,年均供水总量为5.3×108 m3;大清河流域的保定市为北京市及天津市西南部供应水资源,年均供水总量为8.2×108 m3;但子牙河流域和漳卫河流域供水能力严重不足.研究显示,燕山山区和太行山山区为水源涵养生态服务供体区,东部沿海和大中小城市为主要水源涵养生态服务受体区,水源涵养生态服务供体区净水源涵养能力不能满足水源涵养生态服务受体区需水量,整个研究区供受关系严重失衡.      

源解析中环境受体数据处理与扩展方法的建立

本文对包含污染源或气象条件等发生剧烈变化且数据量小的实测受体数据进行了正态扩展,得到扩展数据.同时,利用PMF和PCA模型验证了扩展方法得到的数据量是否能满足模型的要求.结果表明,扩展范围和扩展受体成分谱个数是两个影响扩展数据合理性的主要因素,最佳扩展条件为:扩展范围取标准差的0.5倍,扩展受体成分谱个数为6个.通过53 h算法标记出每个化学成分时间序列中能够代表污染源或气象条件等发生剧烈变化的值并给出对应的估计值.将与估计值的相对误差(RE)超过80%的被标记的值剔除,其余的替换成估计值,发现扩展后PCA解析结果与原始数据处理后数据解析结果基本一致,能够得到主要贡献的污染源及贡献率;若将被标记的值全部剔除后,则不适合做PCA解析;仅通过PMF验证,且扩展数据与原始数据的解析结果中污染源类的判断一致.将受体数据各化学成分的时间序列中代表污染源或气象条件等发生剧烈变化的值替换成53 h算法给出的估计值,对于受体数据量小且用无源成分谱的多元统计方法解析无法给出结果的情况下的源解析有更大价值.     

工频磁场诱导人FL细胞膜EGF的受体聚簇及噪声磁场的干预

为了研究50Hz工频磁场对人源细胞膜表皮生长因子(epidermal growth factor,EGF)的受体聚簇现象的可能诱导作用及噪声磁场的干预,将人羊膜细胞FL(human amniotic cells)分别用EGF、不同强度(0.05、0.1、0.2、0.4mT)工频磁场、噪声磁场、工频磁场和噪声磁场叠加的复合场处理15 min后,用间接免疫荧光染色法标记,并用激光共聚焦显微镜观察细胞膜表皮生长因子(EGF)的受体的聚簇现象.结果表明,0.1、0.2、0.4mT工频磁场辐照FL细胞15 min可诱导细胞膜EGF的受体发生聚簇,但0.05mT工频磁场辐照时,细胞膜不出现EGF受体的明显聚簇.0.2mT噪声磁场则不能诱导细胞膜EGF受体的聚簇;当0.2mT噪声磁场与0.1、0.2mT工频磁场叠加后,可抑制工频磁场诱导的细胞膜EGF受体聚簇,但不能完全抑制0.4mT工频磁场诱导的细胞膜EGF受体聚簇.研究结果表明,一定强度的工频磁场能诱导细胞膜EGF受体的聚簇;其作用阈值在0.05～0.1mT之间;噪声磁场对工频磁场诱导膜受体聚簇的干预作用存在剂量-效应关系.     

Effects of estrone on the early life stages and expression of vitellogenin and estrogen receptor genes of Japanese medaka (Oryzias latipes)

The fertilized eggs of Japanese medaka (Oryzias latipes) were exposed to estrone (E1) at 5–5000 ng L⁻¹ for 15 d, and the hatched fry were exposed continuously to the same concentrations for the additional 15 d. Adverse effects on hatchability, time to hatching, and gross abnormalities occurred at 50 ng L⁻¹ or above. Then the fry were divided into a continual exposure group, and a water recovery group. When the fry were exposed to E1 for another 60 d, there was a decrease in the hepatosomatic index (HSI) of males and the influence disappeared in the water recovery group. The gonadosonatic index (GSI) of females at 500 ng L⁻¹ decreased significantly in another 60 d exposure. While the fry were maintained in dechlorinated tap water for 60 d, a significant decrease in female GSI was observed at 50 ng L⁻¹ or above. An increased GSI was found in males in both continual exposure and water recovery groups at all E1 treatments. Quantitative RT-PCR showed that vitellogenin-I (Vtg-I) gene expressions in the female liver were significantly down-regulated at 50 ng L⁻¹ in the continual exposure group, and at 500 ng L⁻¹ in the water recovery group, while male Vtg-I genes were significantly up-regulated for all E1 treatments. In addition, all E1 treatments caused sex reversal of males. These results suggest that E1 at 5 ng L⁻¹ or above have unrecoverable impacts on the gonadal growth and development of medaka, even if only early life stages were exposed to E1.     

PCDD/Fs-induced oxidative damage and antioxidant system responses in tobacco cell suspension cultures

Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) are ubiquitous contaminants and can be considerably accumulated by natural plants. In order to elucidate the biochemical and physiological responses of plant to PCDD/Fs, tobacco Bright Yellow-2 (BY-2) cells were selected as model plant and treated with time- and concentration-dependent PCDD/Fs. The toxic effect and oxidative stress caused by PCDD/Fs were evident, which could be indicted by the reduction in fresh mass, the increase in malondialdehyde (MDA) content, and the damage of tobacco cell ultrastructure. PCDD/Fs tolerance was correlated with changes in antioxidant system and hormones of tobacco cells. Superoxide dismutase (SOD) and peroxidase (POD) exhibited peak enzyme activities at the PCDD/Fs concentration of 1000 ng WHO₉₈-TEQ g⁻¹ fresh weight. Glutathione reductase (GR) enzyme activity increased monotonically at high level PCDD/Fs, but the activity of catalase (CAT) was only slightly affected at all treatment. Meanwhile, the exposure to PCDD/Fs resulted in the changes of hormones content. With the increase of exposure concentration of PCDD/Fs, the levels of indole-3-acetic acid (IAA) and abscisic acid (ABA) increased, whereas the concentration of jasmonates (JAs) decreased. The above results suggest that tobacco cells had the ability to cope with the oxidative stress induced by low concentration of PCDD/Fs through increasing the activities of antioxidant enzymes and alternating plant hormones levels. However, oxidative stress and toxicity would burst out when plant cells were exposed to the high levels of PCDD/Fs.     

A study on the effect of deoxynivalenol on serotonin receptor binding in fig brain membranes

Abstract

Central serotoninergic (5‐hydroxytryptamine, 5HT) pathways are believed to be involved in the mechanisms of anorexia and/or emesis evoked by the trichothecene mycotoxin deoxynivalenol (DON). Using an in vitro membrane receptor binding assay, the competitive potency of DON was investigated against several radioactive ligands that have a high affinity for selective 5HT‐receptor subgroups. Receptor site densities and displacement profiles in twelve selected regions of pig brain were investigated. Overall, DON possessed only minimal efficacy to competently block any of the 5HT‐ligands tested. IC₅₀ values (50% inhibitory concentration) of at least 5 mM DON were required to inhibit binding, and in certain regions concentrations of 100 mM were ineffective. In comparison, several standard 5HT‐antagonists showed 10³‐10⁵ times greater capability than DON to displace binding of these ligands. Because these results indicated DON possesses only weak affinity for the 5HT‐receptor subtypes investigated here, this suggested that in vivo, unless relatively high concentrations of the toxin are present, its pharmacological effects may be mediated by mechanisms other than a functional interaction with serotoninergic receptors at the central level.     

Assays of PCB congeners and organochlorine insecticides with the transgenic Arabidopsis and tobacco plants carrying recombinant guinea pig AhR and GUS reporter genes

Certain congeners of polychlorinated biphenyls (PCBs) and organochlorine insecticides are ligands of aryl hydrocarbon receptors (AhRs) in animals. A recombinant guinea pig (g) AhR, XgDV, was constructed by fusing the ligand-binding domain of gAhR, the DNA-binding domain of LexA, and the transactivating domain of VP16. Then, the expression unit of β-glucuronidase (GUS) reporter gene regulated by XgDV was introduced into Arabidopsis and tobacco plants. When the transgenic Arabidopsis XgDV plants were cultured on Murashige–Skoog (MS) medium containing PCB congeners, the GUS activity in the plants increased toxic equivalent (TEQ)-dependently. The GUS activity in the transgenic Arabidopsis XgDV plants cultured on MS medium containing the organochlorine insecticide dieldrin was also induced. On the other hand, in the case of DDT, the GUS activity induced by 3-methylcholanthere in the plants decreased. The transgenic Arabidopsis XgDV plants detected 1000 ng g^?1 PCB126 in 1 g of soils. Thus the XgDV plants seemed to be useful for convenient assays of PCB congeners and organochlorine insecticides, without any extraction and purification steps.