微电解技术预处理印染废水

印染废水因污染物浓度高、色度大、可生化性差成为难处理的工业废水。本文采用微电解-生化工艺对印染废水进行工程实验,微电解预处理使废水中的COD大幅去除,并显著提高其可生化性;色度问题也得到了有效解决。工程实验结果表明,微电解-生化工艺处理效果好、出水水质稳定、运行费用低,处理后废水能达标排放。     

管道站场基础沉降远程在线监测评价系统设计

为解决部分站场地基承载力不足,经过长期运营部分站场基础沉降不同步,造成的管道弯曲甚至管道破裂问题,提出1种由位置标识物来实现实时准确采集站场基础位移数据的方法,研制1套基于激光测距技术的基础沉降远程在线监测评价系统;系统软件根据实时采集的沉降量与历史监测数据比对,评价站场运行状态,并给出基础沉降安全储备。结果表明:结合历史监测数据可预测站场基础下一检修周期的沉降状况,给出是否需要在检修期内对站场基础进行维护的建议。系统可有效预防基础沉降带来的安全隐患,减小管道破损带来的经济损失。     

RAPD标记鉴别中华绒螯蟹种群的初步研究

用２００个随机引物对中华绒螯蟹（Ｅｒｉｏｃｈｅｉｒｓｉｎｅｎｓｉｓ）辽河种群、长江种群和瓯江种群进行了ＲＡＰＤ遗传标记鉴别研究,其中引物ＨＸ０１和ＨＸ０２检测到瓯江种群和辽河种群所有样品共有的ＨＸ０１０．４和ＨＸ０２０．７扩增片段,Ｍｒ分别为０．４ｋｂ和０．７ｋｂ．这两个扩增片段在模板ＤＮＡ浓度作上下５０％的改变、或在镁离子和引物浓度分别作上下２５％的改变时仍稳定出现,而长江种群样品的ＰＣＲ反应中无这两个扩增片段出现,因而可作为长江种群的鉴别标记．用上述标记检查一些人工养殖的河蟹,发现一些苗种场的蟹苗种质严重混杂．未发现可以区分瓯江种群和辽河种群的标记     

泥炭生化复合肥料田间对比试验

本文介绍了泥炭生化复合肥料与其它几种肥料的田间对比试验。试验结果表明,泥炭生化复合肥料的肥效优于其它几种肥料,且对农业生产的增产效果显著     

渗滤液生化特性在Fenton处理过程中的变化

采用电解呼吸仪分析早、晚期渗滤的生化特性在Fenton过程前后的变化。根据BOD累积曲线 ,由非线性最小二乘法求解出第一阶段生化需氧量BODu 和一级生化动力学常数K。结果表明早期渗滤液易于生化降解 ,经Fenton氧化后 ,由于产生了毒性更强的中间产物 ,渗滤液的驯化时间反面延长 ,K值也略有下降。晚期渗滤液很难生化降解 ,经Fenton处理后其生化特性得到很大的改善。     

Effects of pesticides on soil biochemical characteristics of a paddy soil

IntroductionThemaintenanceofsoilfertilitydependsonthesizeandtheactivityofthesoilmicrobialbiomasswhichisoffundamentalimportanceinbiologicalcyclesofalmostallmajorplantnutrients(Robert,1992 ) .Thereisconsiderableinterestinstudyofsoilbiochemicalcharacteristic…     

Fenton氧化与生化组合技术处理油田采油废水的研究

采用Fenton氧化与生化组合技术处理生物难降解的采油废水的研究结果表明 ,Fenton氧化技术不但对采油废水中有机质有较好的去除率 ,而且大大地改善了废水的可生化性 ,在H2 O2 的投加浓度和Fe2 + 与H2 O2 的摩尔比分别为10mmol/L和 0 .1的条件下 ,经过 30min氧化后可使废水BOD值由原来的 5mg/L上升至 4 0mg/L ;同时随着氧化时间的延长 ,废水中残余的有机物分子量逐渐降低。 30min氧化后的废水经过生物处理 ,其出水COD值为 10 2mg/L ,可以满足国家综合污水外排标准 ,经济分析结果表明 ,该技术处理采油废水的运行成本为 1 4 7元 /t。这一技术在解决石油行业采油废水的外排达标方面具有很好的应用前景。     

DEHP暴露对鲤鱼肾脑生物标志物的影响

为探讨邻苯二甲酸二乙基己酯(DEHP)对鱼类肾、脑组织生物标志物的影响,将鲤鱼分别在浓度为5、20、80、160 mg·L~(-1)的DEHP水体,暴露20 d,以水和吐温-80为对照,测定肾脑组织中多种酶活性和丙二醛(MDA)含量的变化。结果表明:与水对照组相比,吐温-80组所测各项指标,差异均不显著。与水和吐温-80对照组相比,各染毒组,肾脏中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和抗羟自由基、抗超氧阴离子的活力均显著降低(P0.05或P0.01)。谷胱甘肽过氧化物酶(GSH-Px)酶活性呈现先升高后降低,在5、20、80 mg·L~(-1)浓度组显著升高(P0.05)。丙二醛(MDA)含量在80、160 mg·L~(-1)浓度下,显著升高(P0.05),但脑组织中变化不显著。脑中一氧化氮合酶(NOS)在各浓度组显著升高(P0.05或P0.01);乙酰胆碱酯酶(ACh E)在80、160 mg·L~(-1)时降低显著(P0.05);钙调神经磷酸酶(CaN)呈先升高后降低的趋势,在20 mg·L~(-1)下,升高显著(P0.01),在80、160 mg·L~(-1)浓度组,降低极显著(P0.01);抗羟自由基、抗超氧阴离子活性均显著下降(P0.05或P0.01)。可见,在实验浓度范围内,DEHP对鲤鱼具有一定免疫毒性和神经毒性,进一步的机理有待研究。     

Biochemical evaluation of hepatotoxicity in mice due to administration of artemether

Effects of artemether administration on liver and selected biochemical parameters were evaluated. Eighty albino mice were divided into four equal groups. Group 1 was given water which served as control, while groups 2, 3, and 4 were given 1.2, 2.4, or 4.8 mg kg^?1 body weight artemether intramuscularly for five consecutive days. On day 6 all mice were sacrificed by cervical dislocation and blood was collected for analysis of alanine and aspartate transaminases, alkaline phosphatase, copper, and total proteins. Liver tissues were prepared for histological studies. It was found that the serum alanine and aspartate transaminase and alkaline phosphatase activities were higher in groups treated with artemether compared to control. The serum concentrations of copper and total proteins were lower than control. The histological features of liver tissues after administration of artemether showed histopathological alterations. These findings showed that artemether administration may have reversible adverse effects on mouse hepatocytes.     

Biochemical properties of beryllium potentially relevant to its carcinogenicity†

The carcinogenicity of beryllium to several animal species is well established and evidence exists which strongly suggests that this is the case in human exposure. In this review several biochemical properties of the metallocarcinogen are considered including, the causation of cell transformation, and infidelity of DNA synthesis, inhibition of cell division and enzyme induction, and interference with regulatory mechanisms controlling gene expression. These effects are discussed in relation to beryllium chemistry, cellular accumulation mechanisms and distribution to subcellular organdies and molecular targets. It is suggested that the ultimate location and interactions of the metal ion in cell nuclei and its selective inhibition of certain protein phosphorylation reactions in particular are the biochemical effects potentially most relevant to induction of beryllium carcinogenesis.