污泥活性炭强化SBR法处理垃圾渗滤液的实验研究

为了进一步处理垃圾渗滤液,试验采用污泥活性炭强化序批式间歇反应器（SBR）法进行处理,通过对比普通SBR法试验,得出投加污泥活性炭强化SBR法处理垃圾渗滤液的效果要远远高于普通SBR法。当污泥活性炭的投加量为1.2 g/L,容积负荷为0.5～1.5 kg BOD₅/(m³·d)时,进水1 h,曝气10 h,沉淀1.5 h,闲置1.5 h,处理效果最好,COD的去除率达到了85%,NH³-N的去除率达到了90%。     

环糊精聚合物对苯胺的吸附和脱附性能研究

以环氧氯丙烷为交联剂,合成和表征了β-环糊精聚合物(β-CDP),从动力学和热力学角度研究了β-CDP对苯胺的吸附性能。研究结果表明,β-CDP对水溶液中的苯胺具有一定的吸附量。用Langmuir, Freundlich和DubininRadushkevich(D-R)吸附等温式拟合了平衡等温数据,并计算出每个模型的参数。苯胺在β-CDP上的吸附符合D-R方程,吸附过程是热力学自发行为。在乙醇中,β-CDP的脱附能力很强,且可循环使用多次。     

酵母菌对厨余垃圾厌氧发酵产乙酸的影响

研究了酵母菌对厌氧发酵过程中垃圾水解速率、挥发性有机酸(VFA)产量、乙酸产量的影响。结果表明：控制反应器中pH值为7时,接种酵母菌后,垃圾的水解速率明显提高,产酸速率和产酸量都明显高于不接种酵母菌的反应器,乙酸浓度能够达到9 458 mg/L,占挥发性有机酸总量的58.2%。垃圾本身含有的微生物对产酸也有促进作用,酵母菌和垃圾本身含有的微生物共同作用才能使得乙酸的产生最大化。     

聚硅酸锌铝的制备及其性能研究

以硅酸钠、硫酸锌、硫酸铝为原料,通过共聚法制备了无机高分子絮凝剂聚硅酸锌铝（PSZAS）,研究了Na₂SiO₃的摩尔浓度、活化时间、Al/Si、Zn/Si 配比及絮凝剂的投加量对絮凝效果的影响,用X-射线衍射（XRD）和电子扫描电镜（SEM）对该絮凝剂的结构及形貌进行了表征。结果表明：当硅酸钠的浓度为0.4 mol/L,硅酸活化时间为2 h,Si∶Al∶Zn=1∶1∶1.5,絮凝剂投加量为20 mL/L废水时,絮凝剂的电中和能力和吸附架桥能力最强,絮凝剂对含H-酸染料模拟废水的絮凝效果最好。     

渗滤液污染包气带中铁的形态变化

从渗滤液场龄和包气带岩性两方面出发,研究了新、老渗滤液对亚粘土和细砂包气带环境中Fe的含量及存在形态的影响。结果表明：新、老渗滤液分别能使细砂包气带介质中除残渣态以外Fe的含量增加16.68%或降低13.82%。亚粘土比细砂作为包气带介质更能缓冲渗滤液对介质中Fe的影响程度,其受影响范围在包气带0～20 cm深度处。当亚粘土为介质的包气带被新渗滤液污染后,其表层介质中碳酸盐结合态Fe的含量会增加15倍之多,为缓冲渗滤液Fe的污染做出了巨大贡献,但这部分Fe的存在也是潜在的二次污染源,在环境pH急剧变化的情况下,它可能会引起地下水高铁污染。     

膜蒸馏技术在石化废水处理领域的应用进展

综述了一种新型分离技术——膜蒸馏技术在石化废水处理领域的应用现状,重点介绍了在高盐度废水处理和挥发性有机物废水处理两个方面的进展;指出膜蒸馏应用过程中存在的主要问题是膜污染;预测了膜蒸馏及其集成技术在废水处理领域的发展前景。     

蒽醌染料中间体溴氨酸降解酶的特性

从污染地分离筛选出的菌株BX26对蒽醌染料中间体溴氨酸有显著的降解脱色作用,降解过程受降解酶的控制,试验结果表明,降解酶为溴氨酸诱导的胞外酶,该酶在温度高于50℃处理后失活,盐度对该酶失活有影响,盐度高于1%会显著降低该酶活力,酶对溴氨酸的催化脱色要有氧参加,氮气气氛中酶活受抑制。     

A mini review of fluoride-induced apoptotic pathways

Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity.     

O／W型乳化液的处理

采用药剂破乳－电解破乳工艺处理Ｏ／Ｗ型乳化液，药剂破乳选用聚合硫酸铁为破乳剂，破乳时最佳ＰＨ为８，聚合硫酸铁的最佳投量为１５００ｍｇ／Ｌ，电解破乳选用铁作阳极，铝作阴极，电流密度０．８６Ａ／ｄｍ＾２，极距２５ｍｍ，电解时间３ｈ。在上述条件下，破乳效果良好，出水清澈透明，ＣＯＤ总去除率可达到９６－９７％。     

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.