我国环境侵权民事责任制度存在的问题及解决的策略

随着经济的发展环境污染和生态破坏引起的环境侵权问题在我国越来越突出,并逐渐成为环境与资源保护法中最热门的话题,其中构成要件,归责原则,免责事由,民事救济和诉讼时效是其所要探讨的基本问题.     

DIDP通过线粒体-Caspase途径诱导昆明小鼠肝脏损伤的研究

为探究DIDP（Di-iso-decyl phthalate,邻苯二甲酸二异癸酯）对肝脏的影响及其可能的分子机制,以昆明小鼠为研究对象,选用Res（resveratrol,白藜芦醇）为抗氧化剂,分别设置对照组,0.15、1.5、15、150 mg/（kg·d）DIDP组,Res组,150 mg/（kg·d）DIDP+Res组,灌胃染毒9 d后,对小鼠肝脏切片进行HE染色观察,并检测ROS（reactive oxygen,活性氧）、GSH（glutathione,谷胱甘肽）、MDA（malondialdehyde,丙二醛）、Cyt-C（cytochromec,细胞色素C）、Caspase-3和血清中的ALT（alanine aminotransferase,丙氨酸氨基转移酶）含量.结果表明:与对照组相比,15、150 mg/（kg·d）DIDP组小鼠血清中ALT含量极显著上升（P < 0.01）;HE染色结果显示,15、150 mg/（kg·d）DIDP组小鼠出现肝细胞水肿、肝索紊乱、肝窦以及肝中央静脉扩张等现象;15、150 mg/（kg·d）DIDP组小鼠肝脏ROS含量显著上升（P < 0.05）,GSH含量显著下降（P < 0.05）,150 mg/（kg·d）DIDP组小鼠肝脏MDA含量极显著上升（P < 0.01）;1.5、15、150 mg/（kg·d）DIDP组小鼠肝脏中c（Cyt-C）极显著上升（P < 0.01）;15、150 mg/（kg·d）DIDP组小鼠肝脏中Caspase-3表达量极显著上升（P < 0.01）.DIDP染毒剂量的增加对肝脏的各种损伤程度呈上升趋势,Res可减轻上述DIDP对肝脏造成的各种损伤.研究显示,15、150 mg/（kg·d）DIDP可诱导肝脏组织氧化应激水平上升,进而造成线粒体损伤,导致细胞凋亡,造成肝功能受损,因此,线粒体-Caspase途径可能是DIDP诱导肝脏损伤的潜在机制之一.      

邻苯二甲酸二异癸酯对小鼠学习记忆的影响

为研究增塑剂邻苯二甲酸二异癸酯（DIDP）对小鼠学习和记忆能力的影响,以白藜芦醇（Res）作为保护剂,将42只雄性昆明小鼠随机分为6组,每组7只,分别为：生理盐水组、1.5,15,150mg/（kg·d） DIDP组、20mg/（kg·d） Res组、150mg/（kg·d） DIDP+20mg/（kg·d） Res组.连续灌胃染毒9d,期间同时进行Morris水迷宫实验.第10d将小鼠处死,取出脑组织,检测活性氧簇（ROS）、谷胱甘肽（GSH）、丙二醛（MDA）、8-羟基脱氧鸟苷（8-OHdG）、肿瘤坏死因子（TNF-α）、白细胞介素1β（IL-1β）的含量.并对小鼠海马体切片进行H&E染色,观察病理变化.结果显示,15,150mg/（kg·d） DIDP染毒可导致小鼠的学习和记忆能力显著低于对照组,同时可诱发脑组织产生氧化应激,并促进炎症因子释放,而Res能有效减弱脑组织氧化应激水平.由上可得,DIDP致小鼠学习和记忆能力下降可能与其引起的脑组织中海马体的氧化损伤有关,同时Res可能通过降低DIDP引起的氧化应激进而减轻其对小鼠造成的学习记忆损伤.     

机动车排出物对人体健康危害的研究

运用基因、ＤＮＡ、染色体，细胞和整个动物为终点的远期危害测试系统，对各类机动车排出尾气的有机提取物的致突变性及潜在致癌性进行了评估，同时运用流行病学方法对接触人群进行调查，结果表明：（１）柴油车，助动车的颗粒有机提取物包含１００多种化学物，（２）Ａｍｅｓ、ＵＤＳ微核及ＳＨＥ细胞恶性转化试验为阳性结果，具有突变性及致癌性。（３）它们能使人胚细胞形成转化灶并发现其中的ｃ－ｍｙｃ，ｐ２１及ｂｃｌ－２表达     

A new approach to the estimation of the probable number of fatalities in accidental explosions

This paper presents a new methodology for estimating the probable number of fatalities in accidental explosions in fixed installations, as a function of the amount of the flammable substance involved. A review of the procedure proposed by Marshall (1977) (Marshall, V.C., 1977 How lethal are explosions and toxic escapes? The Chemical Engineer, August 1977, 573–577). reveals its limitations, given the great dispersion of ungrouped data. The proposed alternative enables the estimation of the maximum probable number of fatalities and the percentage of cases in which a certain number of fatalities is reached, based on the knowledge of the amount of material presumably involved and through the application of the historical analysis of accidents. It must be pointed out that the proposed method considers not only fatalities derived directly from the overpressure wave but also those due to thermal radiation or missile impact.     

一种处理爆炸多能法的新方法

以多能法中距离－超压关系图为例,介绍了一种运用前馈多层感知器网络对现行多能法中查图步骤进行改进的方法。此法从很大程度上解决了多能法在爆炸灾害评估中手工查图误差大且不方便的缺点。模拟结果表明,该处理方法能够很好的逼近多能法中的超压函数P＝f(R0,C),最后提出了人工神经网络方法在爆炸破坏效应评估中进一步应用的设想。     

回火焊道焊接技术在焦炭塔修复中的应用

为了避免耗时长、费用高的焊后热处理或整体更换筒节,针对铬钼钢焦炭塔内壁环焊缝的裂纹和锥段内壁腐蚀缺陷,提出采用回火焊道焊接技术对内壁缺陷部位进行修复。结果表明,严格按照经评定合格的焊接工艺进行施焊,回火焊道焊接技术可以利用层道间的焊接热循环作用达到焊后热处理的效果,使焊接修复后铬钼钢焦炭塔的母材和复合层的冶金和力学性能满足要求。     

加轴压卸围压下含瓦斯煤岩损伤变形的能量演化机制

采动影响下含瓦斯煤岩的损伤变形是一个极其复杂的非线性过程,单纯依靠传统经典弹塑性力学无法准确分析其破坏机理。针对此情况,通过试验研究了不同初始围压条件下含瓦斯煤岩的损伤变形特征,并分析了损伤变形与能量演化规律之间的内在联系。研究表明:初始围压越高,煤样破坏时强度越大,脆性破坏特征越明显,瓦斯流量急剧增加幅度越大,煤样破坏时积累的总能量和弹性应变能越多,且初始围压与弹性能之间满足对数函数关系。采用累积耗散能定义了煤岩损伤变量,并分析了不同阶段损伤与渗透率之间的演化关系。     

Effect of ambient-level gas-phase peroxides on foliar injury, growth, and net photosynthesis in Japanese radish (Raphanus sativus)

To investigate the effects of ambient-level gas-phase peroxides concurrent with O₃ on foliar injury, photosynthesis, and biomass in herbaceous plants, we exposed Japanese radish (Raphanus sativus) to clean air, 50 ppb O₃, 100 ppb O₃, and 2-3 ppb peroxides + 50 ppb O₃ in outdoor chambers. Compared with exposure to 100 ppb O₃, exposure to 2-3 ppb peroxides + 50 ppb O₃ induced greater damage in foliar injury, net photosynthetic rates and biomass; the pattern of foliar injury and the cause of net photosynthetic rate reduction also differed from those occurring with O₃ exposure alone. These results indicate for the first time that sub-ppb peroxides + 50 ppb O₃ can cause more severe damage to plants than 100 ppb O₃, and that not only O₃, but also peroxides, could be contributing to the herbaceous plant damage and forest decline observed in Japan's air-polluted urban and remote mountains areas.     

Evaluation of protective effects of sulforaphane on DNA damage caused by exposure to low levels of pesticide mixture using comet assay

The objective of the study was to evaluate the potential risk of DNA damage due to exposure to a mixture of the most widely used pesticides, namely endosulfan, chlorpyriphos and thiram at an environmentally relevant concentration (5 μM each) and the DNA protective capacity of sulforaphane (SFN) (10–30 μg/mL). DNA damage in human lymphocytes was ascertained with Single Cell Gel Electrophoresis (SCGE), also called Comet Assay. For positive control, H₂O₂ at 100 mM was used. The pesticide mixture produced DNA damage at the concentration used in the lymphocytes. SFN was able to offer a statistically significant (P < 0.01), concentration-dependant protection to DNA damage between 10–20 μg/mL in both the pre-incubation and co-incubation strategies. The results indicate that exposure to low levels of these pesticide mixtures can induce DNA damage, and the presence of SFN in diet may reduce the incidence of genetic damage, especially in farm workers. However, it is not clear whether SFN is involved in quenching of the free radicals generated by the pesticide mixture or it is involved in DNA repair mechanism.