有机物对厌氧氨氧化微生物燃料电池脱氮产电性能的影响

通过接种厌氧氨氧化污泥到微生物燃料电池阳极,成功启动厌氧氨氧化微生物燃料电池(ANAMMOX-MFC),研究了葡萄糖和苯酚对ANAMMOX-MFC脱氮产电性能的影响.结果表明,当葡萄糖浓度较低时(100~200 mg·L~(-1))时,对ANAMMOX菌有促进作用,ANAMMOX-MFC脱氮产电性能增强,此时反应器进出水COD浓度变化不大;当葡萄糖浓度高于300 mg·L~(-1)时,产电性能逐渐下降,NH+4-N去除率和去除速率逐渐下降,而NO-2-N去除率和去除速率基本保持不变,此时出水COD浓度也出现降低,说明厌氧氨氧化菌活性受到抑制,反硝化菌活性开始增强.极化曲线拟合程度较低,COD浓度变化对电池内阻影响较小.当苯酚浓度较低时(50~100 mg·L~(-1)),对ANAMMOX-MFC脱氮产电性能影响较低;当苯酚浓度超过200 mg·L~(-1)时,ANAMMOX-MFC脱氮产电性能逐渐被抑制.整个过程进出水COD浓度变化不大,极化曲线拟合程度较低,表观内阻有缓慢升高.     

Association of serum levels of perfluoroalkyl substances with gestational diabetes mellitus and postpartum blood glucose

This study was conducted to examine the association of perfluoroalkyl substance(PFAS)exposure with gestational diabetes mellitus(GDM) risk and postpartum fasting blood glucose.We used a 1:2 matched case–control study with 84 GDM subjects and 168 healthy pregnant women from Beijing, China. The maternal blood was collected at 1–2 days before delivery, and eight linear isomers and fourteen branched isomers were determined in maternal serum.Logistic regression analyses were performed to evaluate the associations after adjusting for potential confounders. The median of the sum of levels of total PFASs was 4.24 ng/m L with a interquartile range(IQR) of 2.82–6.54 ng/m L. Although maternal PFAS exposure was not associated with risk of GDM, significant positive associations were observed between evaluated exposure to specific PFAS congeners and increasing blood glucose. The odds ratio(ORs) of the highest category of postpartum fasting blood glucose for perfluoro-1-metylheptylsulfonat(1 m-PFOS), perfluoro-3/4-metylheptylsulfonat(3 m+4 m-PFOS), perfluoro-5-metylheptylsulfonat(5 m-PFOS), and perfluorohexane sulfonate(PFHx S) were 2.03(95% CI: 1.09–3.77), 1.93(95% CI:1.04–3.58), 2.48(95% CI: 1.33–4.65), and 2.26(95% CI: 1.21–4.21), respectively, suggesting negative effects of maternal exposure to specific PFAS compounds on glucose metabolism.     

应用细胞合成计量关系模型分析鱼腥藻7120的混合营养生长

根据文献中鱼腥藻细胞大分子的含量和组成情况，计算了细胞合成所需要的小分子单体和前体代谢物的量，得到代谢意义上的细胞生物合成计量关系，此计量关系模型，对鱼腥藻7120细胞在气升式光生物反应器中光自养和混合营养生长的对数生长阶段进行了代谢通量分析。结果表明，葡萄糖的利用影响细胞初级碳代谢的流动状况，混合营养生长过程比光自养生长过程磷酸戊糖途径氧化性分支的反应程度明显加强，随着培养的进行，葡萄糖被细胞用作碳源的比例可能减小，而用作能源的比例可能增大。     

Is There a Metabolism of an Urban Ecosystem? An Ecological Critique

The energy and material flows of a city are often described as urban metabolism (UM), which is put forward as a way to link a city's ecology and economy. UM draws parallels to the biology of individual organisms, yet the analogy is misapplied. In striving to be interdisciplinary, UM makes this organismic comparison rather than identifying the city as an ecosystem, thereby ignoring developments in ecological theory. Using inappropriate rhetoric misdirects researchers, which influences scientific investigation-from problem statements to interpretations. UM is valuable in quantifying the city's use of natural resources but does not achieve a comprehensive, integrated analysis of the urban ecosystem. To realize an interdisciplinary, perhaps transdisciplinary, understanding of urban ecology, researchers need to emphasize the essential tenets of material flows analysis, view the city as an ecosystem, and use language that properly reflects current knowledge, theory, and conceptual frameworks in the foundational disciplines.     

资源型城市的“无废城市”建设模式探讨

资源型城市在我国经济发展大局中地位重要而特殊、历史贡献突出,城市发展的生命周期特征和物质代谢的"大进大出"特征明显,固体废物(以下简称固废)治理问题积弊已久、复杂多变。如何建设"无废城市"模式的资源型城市,是当前城市可持续发展和"无废城市"实践亟待破解的难题。本文研究分析了2017年我国资源型城市固废产生、贮存、综合利用、处置环节及管理制度体系建设的主要问题,并从制度设计、产业转型、分类利用、标准建立四个方面提出了"无废"资源型城市建设的政策建议。根据资源型城市所处生命周期发展阶段的不同,提出了基于固废"产、存、用、置、销"的存量、流量挂钩约束的发展模式。同时提出以下建议:快速成长期城市应从产业体系构建、空间布局及准入条件着手控制固废增量;平稳成熟期城市应发展完善高值化资源综合利用产业体系和制度体系;枯竭衰退期城市应注重挖掘和开发存量固废的资源价值;再生发展期城市应加强多源废物协同处置利用产业体系建设。本研究可为资源型城市的"无废城市"建设提供模式参考和政策建议。     

营养限制对厌氧序批操作反应器的影响及其恢复重建过程

研究了在厌氧条件下以葡萄糖为基质的序批操作反应器(ASBR)中营养物浓度限制对基质吸收和储存的影响及其恢复重建过程。结果表明,营养物限制条件下,发酵细菌表现为过量吸收基质并储存为糖原,形成隐性增殖以维持其细胞的正常结构和代谢功能;而甲烷菌由于无储存能力,其表现为活性逐渐降低。短期营养限制条件下(1个周期),基质中无磷时,储存量增加29%;基质中无氮时,储存量增加90%;基质中既无氮也无磷时,储存量增加26%。长期(31个周期)营养限制(基质中氮磷含量减小50%)下,胞内储存糖原量可高达正常状态下的4.8倍,但甲烷活性减少为正常状态下的17.78%。营养物限制对发酵细菌影响较小,对甲烷菌影响较大。将氮磷浓度恢复正常后,反应器的产甲烷能力恢复较快,出水COD经31周期后恢复正常,而胞内糖原在85周期后恢复正常。     

Metabolic effects of diazinon on the European eel

Abstract

Eels were exposed to a sublethal diazinon concentration of 0.042 mg/L for exposure times of 6, 24, 48, 72 and 96 hours. Biochemical analyses of blood composition, such as plasma glucose, total plasma cholesterol and triglycerides, plasma lactate, plasma urea and uric acid, showed significant differences between treated and control animals. Plasma glucose and lactate increased after 6 hours exposure to the insecticide. Plasma cholesterol and triglycerides content decreased during 96 hours treatment. Urea levels increased at 72 hours while uric acid content decreased significantly at 24, 72 and 96 hours exposure to the pesticide.

The observed effects of diazinon on eel metabolism suggested that the treated fish was faced with a serious metabolic crisis, and the fish looked for alternative methods of metabolism to overcome the toxic stress.     

双酚A(BPA)暴露对WHHL家兔糖类和脂类代谢的影响

为利用和人类更为接近的动物模型来研究在高脂血症条件下,BPA暴露是否能促进脂类和糖类代谢异常,并探索潜在的毒性效应机制,选取渡边可遗传高脂血症家兔(WHHL)模型,通过灌胃的方式将其暴露于400μg·kg-1体重的BPA溶液长达12周。在持续暴露第8周,检测了在空腹状态下,家兔血浆中葡萄糖、胰岛素和脂肪含量的变化,并根据所得结果进行了静脉注射胰岛素耐受试验(IVTT)。在暴露第12周,同样对空腹状态下,家兔血浆中的葡萄糖,胰岛素和脂肪含量进行了检测,并测量了血压和心率。然后,将所有的家兔进行解剖,通过苏木精-伊红(HE)及糖原(PAS)染色分别对心脏和肝脏部位的脂肪及糖原蓄积情况进行了病理学切片分析。同时,检测了肝脏中与脂类和糖类代谢相关基因在m RNA水平上的表达变化。结果显示,BPA暴露8周后促使WHHL家兔发生了胰岛素抵抗现象,导致第12周血糖及胰岛素含量升高,同时也促进了高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及游离脂肪酸(NEFA)含量的上升。BPA暴露第12周,暴露组WHHL家兔的冠状动脉粥样硬化损伤程度未发生明显增加,但心肌细胞发生了肿胀,胞质中出现了脂肪的蓄积,同时伴随着心律失常。肝脏重量发生增加,肝细胞中同时出现了脂肪和糖原的蓄积现象,相关基因的表达发生了显著上调。研究结果表明,BPA持续暴露可促进WHHL家兔发生脂类和糖类代谢异常,其毒性效应机制可能和胰岛素抵抗及相关基因的异常表达有关。     

二噁英类化合物的毒性作用机制及其生物检测方法

二噁英类化合物具有高毒性,来源多样且分布广泛,是持久性有机物的典型代表,二噁英类污染物及其对健康的危害已引起了公众的普遍关注。一些二噁英类同系物具有代谢稳定性,其毒性效应主要是通过芳香烃受体介导,而越来越多的研究表明二噁英类毒性作用机制的复杂性。在此背景下,综述了近些年在二噁英类毒性作用机制及其代谢途径的新认识,评价比较了主要二噁英类高通量生物检测方法,以期为该类污染物的环境污染物筛查和风险评估提供参考。     

短链氯化石蜡暴露对HepG2细胞代谢的影响

短链氯化石蜡(short-chain chlorinated paraffins,SCCPs)是一组成分复杂的氯代正构烷烃,在环境中普遍存在。然而有关其毒性机理的信息十分有限,限制了对其健康风险的评估。本研究采用液相色谱–串联质谱(LC-MS/MS)分析技术,研究了不同剂量的SCCPs暴露(0、1.0、10.0和100.0μg·L-1;C13-CPs;55.0%Cl)对人体肝癌细胞Hep G2的糖代谢、氨基酸代谢和脂肪酸代谢的影响。通过偏最小二乘判别分析(PLS-DA)鉴别各组代谢产物谱差异,发现3个SCCPs暴露剂量组均能够与对照组完全分开,表明SCCPs短期暴露能够引起细胞代谢活动的显著改变。SCCPs的低剂量暴露可明显刺激Hep G2细胞对氨基酸的吸收。与对照组相比,SCCPs低剂量暴露组(1.0μg·L-1)培养基中谷氨酰胺、色氨酸和丝氨酸的含量显著(P0.05)降低。而高剂量SCCPs(100.0μg·L-1)暴露抑制了细胞对氨基酸和葡萄糖吸收,但促进了乳酸、丙氨酸、半胱氨酸的生成。氨基酸吸收的抑制不可避免地会影响蛋白质的合成。同时,SCCPs的暴露使饱和脂肪酸代谢紊乱,使不饱和脂肪酸水平上调。为确定SCCPs的毒性作用方式,有必要从转录组和蛋白组层面进一步研究其毒性机制。