基于RDBMS的海洋溢油生物资源损害评估空间数据库研究

为满足海洋溢油生物资源损害评估数据管理和共享的应用需求,提出构建基于关系数据库(RDBMS)的空间数据库.通过分析电子海图和评估模型数据中的矢量、栅格、时空等空间数据类型及其特征,探讨了RDBMS支持下的空间数据组织、压缩存储、维护管理的实现方法,并建立了基于空间数据库引擎的空间数据访问模式.应用实例表明,基于RDBM...     

环境损害鉴定范围探彘

环境损害鉴定范围在法学、司法领域具有特定法律意义。但是,在行政管理中,环境损害鉴定被环境损害评估所等同、混淆,势必带来环境损害鉴定理论的混乱和环境损害鉴定实践的乱象。如何界定环境损害鉴定范围是环境损害鉴定理论及实践所要回答的基本问题。本文从环境损害鉴定范围界定依据入手,探讨环境损害鉴定范围议题。研究表明,环境损害鉴定范围无论在理论层面还是在实践层面均为缺失状态,环境损害鉴定范围仍未依法确定。其根本原因在于环境损害鉴定理论发育不成熟及环境损害鉴定司法实践匮乏。我国环境损害鉴定实践与环境损害鉴定范围理论界定存在巨大差距。尤其在环境损害鉴定的司法实践中,不可用环境损害评估代替环境损害鉴定。因此。界定环境损害鉴定范围是完善环境损害鉴定理论前提;规范环境损害鉴定范围能促进环境损害鉴定实践展开;界定环境损害鉴定范围可以有效地区分环境损害鉴定与评估。     

黑磷纳米片制备、表征及其对斜生栅藻的毒性效应

黑磷纳米片(Black Phosphorus nanosheets,BPNSs)具有广泛的应用前景,而关于BPNSs的安全性研究还十分匮乏.为探究BPNSs对水生生物的毒性作用,本研究通过液相剥离法制备得到厚度为(58.05±36.48)nm,横向尺寸为(541.25±176.22)nm的BPNSs,选择初级生产者斜生...     

Fe-C合金中辐照缺陷特征的剂量率效应计算模拟

目的尝试采用计算模拟方法探究剂量率对辐照微结构特征的影响,探究常温辐照下剂量率效应的机理。方法采用动力学蒙特卡罗(OKMC)方法,结合近些年第一性原理和分子动力学的计算参数,研究了常温下铁-碳体系中辐照缺陷随剂量率的变化特征。结果在较低的剂量范围(<0.01 dpa)内,间隙型位错环的密度随剂量率的增加而增加;但在较高的剂量范围内,高剂量率辐照呈现较低的间隙型位错环密度、较大的缺陷尺寸。通过比较不同剂量率下的位错线对点缺陷的吸收数目,把剂量率在不同剂量范围内的特征归结于位错吸收与缺陷复合之间的竞争。结论在较低的剂量范围内,位错吸收具有重要影响,随着剂量率的增加,位错吸收的缺陷数目显著减少;而在较高的剂量范围内,基体中间隙-空位缺陷的复合随剂量率的增加而显著增加,以至于高剂量率辐照可能产生较低的辐照硬化。文中的工作对理解剂量率效应的机理提供了一定的科学依据,为离子束模拟中子辐照提供了一定的科学参考。     

环境损害鉴定评估制度发展及黑龙江省建设现状分析研究

随着中国经济高速发展以及工业化进程的不断加快,环境污染事故呈频发态势,环境公益诉讼制度实施和公众环保意识不断觉醒,环境司法诉讼案件数量也呈爆发性增长.环境污染损害鉴定评估工作是环境损害赔偿量化的重要基础性工作,科学的评价环境损害问题已成为环境管理研究的重要课题.基于对环境损害评估制度的调研,介绍了国内外研究现状进展,分析了黑龙江省工作现状,探讨了当前存在的问题,提出了相应的对策建议,为进一步推进环境损害鉴定评估工作发展和完善提供参考.     

壬基酚聚氧乙烯醚暴露下赤子爱胜蚓（Eisenia foetida）的生理损伤

利用急性接触试验和人工土壤试验分别研究了壬基酚聚氧乙烯醚（NPEO）对赤子爱胜蚓（Eisenia foetida）的致死性和氧化损伤.急性接触试验结果显示,NPEO对赤子爱胜蚓的48 h毒性半致死剂量p（48 h,LD50）为0.58 mg·L^-1;人工土壤试验结果显示,NPEO可诱导赤子爱胜蚓CAT酶活力、GST酶活力、GSH含量和氧化产物（MDA）含量上升,暴露28 d时,NPEO浓度与赤子爱胜蚓CAT酶活力、GST酶活力、GSH含量和MDA含量呈正相关,且均存在显著的剂量-效应关系（P＜0.05）,NPEO剂量增加对赤子爱胜蚓SOD酶活性和Cu-Zn SOD酶活性有轻微抑制作用.以上结果表明NPEO在亚致死暴露浓度下＜0.50 mg· kg^-1）会对赤子爱胜蚓产生生理胁迫并导致一定程度的氧化损伤.     

The microcystins-induced DNA damage in the liver and the heart of zebrafish,Danio rerio

Microcystins (MCYST) are the freshwater cyanobacterial toxins, known to induce hepatocellular carcinoma, necrosis, intrahepatic bleeding, as well as human and livestock mortality. Within hepatocytes, MCYST selectively bind to protein phosphatases 1 and 2A, resulting in severe liver damage. The toxicology of MCYST in mice and rats has been well studied, but little is known regarding genotoxicity in aquatic animals. In this study, the zebrafish, Danio rerio was exposed to crude extract of Microcystis aeruginosa bloom. Liver and heart were examined for MCYST-induced toxicity. Light microscopy at 36?h revealed severe, widespread apoptotic necrosis of the majority of hepatocytes, and cytoskeletal deformation in myocardiocytes. Hepatocytes were dissociated with cell shrinkage and margination of nuclear chromatin. Laddering of genomic DNA from the liver and heart of the exposed fish in an increment of 180–200?bp was consistent with apoptosis. Fluorimetric analysis of DNA unwinding was carried out to determine the DNA strand breakage. After 36?h exposure, the % double-stranded DNA was significantly reduced in hepatocytes and myocardiocytes. In conclusion, the results obtained in this study indicate that, the extract of M. aeruginosa bloom is genotoxic to fish. The DNA damage observed in this study may be attributed to the activation of DNA endonucleases. This model of DNA damage may contribute for identifying novel molecular mechanisms of interest for therapeutic application.     

The synergistic interaction of Nickel(II) with dna damaging agents

In this report we present several examples in which nickel(II) in combination with DNA damaging agents caused an enhanced or synergistic biological response using several different endpoints. These examples of Ni(II) toxicity represent several approaches designed to understand the genotoxicity of Ni(II) as well as several other metal ions. They are discussed in this report as a partial basis for our hypothesis that Ni(II) may alter the cellular processing of DNA damage at some common point in the pathway for DNA repair of several different agents. In cultured Chinese hamster cells DNA damage by Ni(II) ions was not readily demonstrated by the method of alkaline elution, but pretreatment of cells with Ni(II) before X‐irradiation produced an enhanced amount of strand breaks compared to the amount produced by X‐rays alone. A synergistic enhancement of cell transformation of Syrian hamster embryo cells was observed for combined treatments of Ni(II) and benzo(a)pyrene. The nickel enhancement of mutagenesis by ultraviolet light was demonstrated for the bacterial gene gpt stably integrated into the Chinese hamster V79 genome.     

考虑孔隙瓦斯劣化作用的煤岩损伤本构模型

矿井瓦斯是煤岩体赋存环境因素之一,同时也是影响煤岩力学性质的主要因素,研究基于煤岩损伤统计特征及Drucker-Prager破坏准则,分析得出了煤岩单轴压缩载荷作用下损伤演化本构模型,基于煤岩弹性波速相关理论建立了孔隙瓦斯对煤岩力学性能劣化损伤力学模型,并在此基础上得出了考虑孔隙瓦斯劣化作用的煤岩损伤本构模型;以原煤及型煤试样为研究对象,开展了不同孔隙瓦斯压力条件下煤岩单轴压缩破坏实验,基于实验研究结果对模型进行了验证。研究结果表明所建立的模型可以很好的反映孔隙瓦斯作用下煤岩单轴压缩载荷条件下的应力-应变关系。     

两种典型氯酚类化合物暴露致稀有鮈鲫肝细胞的损伤效应（Toxicity Effects of Two Kinds of Typical Chlorophenols on Hepatocytes of Gobiocypris Rarus）

为探讨两种典型氯酚类化合物——三氯酚(Trichlorophenol,TCP)、五氯酚(Pentachlorophenol,PCP)单独和混合暴露对稀有鮈鲫(Gobiocyprisrarus)肝脏细胞的毒性效应,实验建立了稀有鮈鲫肝细胞原代培养模型,通过噻唑蓝实验(MTT法)和单细胞凝胶电泳(SCGE)实验分别研究了TCP、PCP及其混合暴露对稀有鮈鲫肝细胞存活率的抑制作用,以及对DNA的损伤作用.结果显示:与对照组相比,TCP和PCP单独和混合暴露均对肝脏细胞的正常生长产生了抑制作用.低剂量暴露时(如0.5、2.5μg·L-1)具有显著的抑制作用(p<0.05);高剂量暴露时(如25、50μg·L-1)具有极其显著的抑制作用(p<0.01).SCGE实验结果显示:与对照组相比,暴露剂量高于12.5μg·L-1的TCP、PCP及其混合暴露均能引起稀有鮈鲫肝细胞DNA的显著损伤(p<0.05,p<0.01).以上结果提示,TCP和PCP具有肝细胞毒性,可以引起稀有鮈鲫肝细胞DNA损伤.