Relationship between ammonia stomatal compensation point and nitrogen metabolism in arable crops: current status of knowledge and potential modelling approaches

The ammonia stomatal compensation point of plants is determined by leaf temperature, ammonium concentration ([NH4+]apo) and pH of the apoplastic solution. The later two depend on the adjacent cells metabolism and on leaf inputs and outputs through the xylem and phloem. Until now only empirical models have been designed to model the ammonia stomatal compensation point, except the model of Riedo et al. (2002. Coupling soil-plant-atmosphere exchange of ammonia with ecosystem functioning in grasslands. Ecological Modelling 158, 83-110), which represents the exchanges between the plant's nitrogen pools. The first step to model the ammonia stomatal compensation point is to adequately model [NH4+]apo. This [NH4+]apo has been studied experimentally, but there are currently no process-based quantitative models describing its relation to plant metabolism and environmental conditions. This study summarizes the processes involved in determining the ammonia stomatal compensation point at the leaf scale and qualitatively evaluates the ability of existing whole plant N and C models to include a model for [NH4+]apo.     

废水中KMnO4对生物处理效果的影响

为减轻和消除含高浓度KMnO4的牛仔服加工废水对生物处理系统的毒害作用,采用模拟序批式活性污泥法,研究KMnO4对活性污泥微生物生长的影响及COD和NH4+-N的降解规律。结果表明,当处理进水COD浓度500 mg/L,NH4+-N浓度23.5 mg/L,污泥浓度为2 000 mg/L时,曝气时间为4 h,KMnO4质量浓度增加对COD和NH4+-N的降解影响很大;同样条件下曝气时间改为8 h,对NH4+-N的降解影响显著减小,但对COD的降解影响减少不多;并且,高浓度KMnO4对NH4+-N去除效果的抑制作用比对COD的大。因此,处理含高浓度KMnO4的废水需要延长一倍曝气时间,可以获得良好的COD和NH4+-N的降解效果。同时,KMnO4对活性污泥的抑制影响较好地吻合非竞争性抑制机理修正莫若特方程的规律。     

利用13X沸石分子筛净化含NH+4-N废水的实验研究

研究了13X沸石分子筛在静态和动态条件下对中低浓度含NH⁺₄-N废水的吸附性能,包括影响吸附的主要因素、沸石对NH⁺₄-N的吸附效果和沸石的再生等。静态实验结果表明,pH值为6.5～7.5,吸附时间35 min,吸附温度20～30℃的条件下,沸石对50 mL NH⁺₄-N初始浓度（C0）为80 mg/L的废水吸附效果最佳,吸附过程符合Langmuir型吸附等温式,饱和吸附量为8.61 mg/g。动态条件下,随水力停留时间增加,沸石对NH⁺₄-N的吸附量上升,最大饱和吸附量可达24.20 mg/g,吸附过程符合Thomas吸附模型。直接焙烧法对吸附后的沸石进行再生活化处理效果良好。实验证明,利用13X沸石净化中低浓度含NH⁺₄-N废水具有良好的工业化应用前景。     

碱激发胶凝材料及其固化Pb2+的试验研究

对碱激胶凝材料（碱-偏高岭土、碱-矿渣和碱-粉煤灰）与水-水泥体系固化Pb²⁺进行了试验研究,其中水-水泥体系为对比样。结果表明：对于相同稠度的碱激发胶凝材料,即使Pb²⁺含量达到2.4%,除了碱-粉煤灰的抗压强度略低外,其他都达到30 MPa以上,满足填埋或做建筑基材的使用要求;与水泥相比,碱激发胶凝材料能显著降低重金属离子（Pb²⁺）浸出浓度,其规律性与其NH⁺₄交换容量大小的规律性一致,与其固化体的抗压强度的大小没有相关性。     

氧活性粒子氧化NO生成HNO_3

采用强电离介质阻挡放电方法制取高浓度氧活性粒子(O+2、O3)并注入气体外排烟道中,实现O+2、O3氧化NO转化成资源酸(HNO3)的等离子化学反应。描述强电离放电的氧活性粒子产生器,讨论烟道中O+2、O3氧化NO成HNO3等离子体反应机制,分析回收酸液的NO-2、NO-3离子种类及浓度。考察强电离放电等离子体源的输入功率、水体积百分比、气体温度、气体流速对NOx氧化率的影响。氧化率为97.2%的最佳实验条件是:O+2浓度为1.38×1010个/cm3,O3浓度为210 mg/L,烟气温度为65℃,H2O体积浓度为5.6%,停留时间为0.94 s。     

Oral administration of potassium bromate, a major water disinfection by-product, induces oxidative stress and impairs the antioxidant power of rat blood

Potassium bromate (KBrO₃) is a widely used food additive, a water disinfection by-product and a known nephrotoxic agent. The effect of KBrO₃ on rat blood, especially on the anti-oxidant defense system, was studied in this work. Animals were given a single oral dose of KBrO₃ (100 mg/kg body weight) and sacrificed 12, 24, 48, 96 and 168 h after this treatment. Blood was collected from the animals and separated into plasma and erythrocytes. KBrO₃ administration resulted in increased lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased the reduced glutathione content indicating the induction of oxidative stress in blood. Methemoglobin levels and methemoglobin reductase activity were significantly increased while the total anti-oxidant power was greatly reduced upon KBrO₃ treatment. Nitric oxide levels were enhanced while vitamin C concentration decreased in KBrO₃ treated animals. The activities of major anti-oxidant enzymes were also altered upon KBrO₃ treatment. The maximum changes in all these parameters were 48 h after the administration of KBrO₃ and then recovery took place. These results show for the first time that KBrO₃ induces oxidative stress in blood and impairs the anti-oxidant defense system. Thus impairment in the anti-oxidant power and alterations in the activities of major anti-oxidant enzymes may play an important role in mediating the toxic effects of KBrO₃ in the rat blood. The study of such biochemical events in blood will help elucidate the molecular mechanism of action of KBrO₃ and also for devising methods to overcome its toxic effects.