大气细颗粒物对小鼠T淋巴细胞亚群的影响

大气颗粒物对肺免疫系统有潜在毒性作用,打破免疫系统平衡,大气颗粒物成分中危害首当其冲的是大气细颗粒物(PM_(2.5)),为研究大气细颗粒物引起的机体T淋巴细胞中Th1/Th2免疫失衡方向。本研究通过免疫组化实验方法检测暴露后小鼠肺组织中T淋巴细胞的表达,进一步采用流式细胞术检测大气细颗粒物气管滴注后小鼠肺脏淋巴细胞中Th1/Th2比例。暴露组小鼠肺组织免疫组化研究结果提示浸润细胞区有大量的CD4~+T细胞,中高剂量暴露组小鼠肺组织中淋巴细胞亚群Th1/Th2比例向Th1偏移。大气细颗粒物影响免疫失衡,使T淋巴细胞向Th1漂移。     

潮白河周丛生物群落元素组成与水质变化的生态计量学关系研究

研究了潮白河流域中污染水体对周丛生物群落的碳(C)、氮(N)、磷(P)元素含量以及生态计量组成的影响.结果表明,下游潮白河NH4+-N、NOx--N分别占TN的52%和28%;上游白河则分别占1.6%和38%.潮白河TP含量(0.104 mg.L-1)为白河TP含量(0.005 mg.L-1)的21倍.白河和潮白河周丛生物C、N、P元素的变异系数分别为0.55、0.41、0.62和0.24、0.13、0.18,表明生长于白河周丛生物的元素结构变化更大.无周丛生物的水体NH4+-N和TP的浓度分别为有周丛生物的21倍和11倍.通过对TOC、TN、NOx--N、NH4+-N、TP、pH、氧化还原电位(ORP)和电导率(conductivity)等水质指标进行二元Logistic回归分析得知,水体TP为影响潮白河周丛生物生存的主要因素,其预测正确率为87.3%.周丛生物C、N、P元素间有强相关性,其中N起了"桥梁"作用.生态计量学分析进一步显示周丛生物的N∶P的比值追随水体TN∶TP的变化;并且该比值主要受水体TP浓度影响.周丛生物N∶P可用于水体TN∶TP变化的生态计量学的指示因子.本研究为进一步探究周丛生物群落结构变化,以及对高一级营养级生物群落结构和元素循环的影响奠定了基础.     

基于智能优化算法的河流水质模型参数的优化简

为探索河流水质模型参数新的求解方法，根据有限的实测数据，分别应用免疫进化优化算法和免疫进化优选的捕食搜索算法，对河流水质模型计算公式中的多参数进行优化。将优化得到的计算公式用于国内外若干河流的河段中DO浓度值的拟合，并与实测结果进行了比较。结果表明，将免疫进化优化算法或免疫进化优选的捕食搜索算法优化得到的水质模型参数精度不仅较高，而且相对稳定，从而为河流水质模型参数的优化提供了一种新方法。     

二英类污染物生物分析方法研究进展

二英类物质具有致癌、致畸等毒理及健康效应.我国二英类物质污染源较多,分布较为广泛,因此二英监测任务十分紧迫.但是我国二英实验室相对较少,单纯的仪器分析方法不能满足监测需求,因此急需发展经济、简便、快速的生物检测方法.生物检测方法主要包含免疫类检测方法和基于芳香烃受体(AhR)信号通路的检测方法,本文着重对这两类生物检测方法的原理和进展等进行综述.     

Toxicological effects of mouse diet contaminated with tributyltin on the immune and neurological systems of C57BL/6 mice

Organotin compounds, widely used as antifouling agents, are known to bioaccumulate in the food chain. Among organotin compounds, tributyltin (TBT), a toxic and widespread contaminant, has become a serious factor in environmental pollution and is suspected of being immunotoxic in animals. The purpose of this study was to assess the effects of 80 µg of TBT per kilogram of body weight (kg bw), provided in food, on the immune and neurological systems of C57Bl/6 mice. Data showed that TBT increased the proliferation of T and B lymphocytes in both adult and juvenile female and juvenile male mice, but that it decreased the proliferation of both T and B lymphocytes in adult male mice. The macrophages activity in female and male juvenile mice was higher than in adults of both sexes. The natural killer cytotoxic activity was also increased in juvenile and adult males and females compared to the control groups. In the brain, we observed the presence of TBT in the hippocampus, the striatum, the cortex, and the cerebellum in both the male and female groups. The highest levels were observed in the cortex of females and males, while the lowest levels were found in the cerebellum. TBT also induced an increase in the levels of the antioxidant glutathione (GSH) in the striatum, the hippocampus and in cortical structures but not in the cerebellum where the levels of TBT are lower. Our findings indicate that TBT modulated the immune and nervous systems causing endocrine and nervous perturbations.     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

亚硝酸盐氮胁迫对罗非鱼（GIFTOreoohromisniloticus）血清非特异性免疫酶活性的影响

试验设置了不同浓度亚硝酸盐氮（空白对照、0．75mg·L-1、1．50mg-L-1、3．00mg·L-1和5．00mg·L-1），研究了亚硝酸盐氮胁迫对罗非鱼（GIFTOreochromisniloticus）血清非特异性免疫酶（溶菌酶、碱性磷酸酶、补体c3）活性的影响。结果表明：罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性均呈现出随亚硝酸盐氮浓度升高而降低的趋势，且当亚硝酸盐氮浓度小于1．50mg·L-1时，罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性与对照组相比差异不显著（P〉0．05），说明低于1．50mg·L-1的亚硝酸盐氮不会对罗非鱼机体免疫力产生显著影响；而高于3．00mg·L-1的亚硝酸盐氮胁迫能够显著（P〈O．05）降低罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性，最大下降率分别达到31．75％、27．40％、14．43％，从而显示出高浓度亚硝酸盐氮（〉3．00mg·L-1）能够对罗非鱼机体产生强烈的氧化胁迫和免疫损伤，导致机体免疫力下降，增加罗非鱼对致病菌的易感性。本研究认为，3．00mg·L-1可能是亚硝酸盐氮胁迫引起罗非鱼机体免疫力显著降低的阈值。     

中国农产品虚拟耕地与资源环境经济要素的时空匹配分析

计算出1999~2009年中国各地区农产品虚拟耕地与人口、水资源、耕地资源、水土流失治理以及GDP等要素的基尼系数以及全国8大区域2009年农产品虚拟耕地 资源环境经济要素的不平衡指数。结果表明：(1）我国农产品虚拟耕地与各资源环境经济要素的地域分布匹配程度都不高；其中农产品虚拟耕地与人口、耕地的地域匹配程度相对较高，与水土流失治理之间的地域匹配状况次之，与GDP和水资源的地域匹配程度相对较低；(2）我国农产品虚拟耕地与各资源环境经济要素的外部公平性不高，黄淮海地区为农产品虚拟耕地 资源环境经济要素不公平性最突出地区，其次是华南、西北和东北地区     

基于人工免疫原理的事故预防研究

介绍生物免疫识别模式,分析事故预防过程的实质是抑制潜在危险转化成事故的控制过程,分析比较事故预防与生物免疫识别模式在作用、生存环境、动作触发源等的共性,构建了基于免疫识别模式的事故预防系统并建立了事故预防数学模型;定义事故预防系统的识别率、失效率、误判率并给出了数学表达式,指出监测生产系统各环节状态信息是否符合系统的安全要求就是识别潜在危险的过程,是事故预防的关键,基于人工免疫原理的事故预防数学模型具有较强的健壮性、自适应性和动态防护性等特点。