Microbial population dynamics during sludge granulation in an anaerobic-aerobic biological phosphorus removal system

The evolution of a microbial community was investigated during sludge granulation using a wide range of micro-scale and molecular biology techniques. Experimental results demonstrate that polyphosphate-accumulating granules were successfully cultured during the anaerobic/aerobic cycle. Improvement in sludge sedimentation performance occurred prior to the formation of granular sludge and was not affected by change in granule size. Rod-shaped and filamentous bacteria appeared to initiate granule formation and generate the structures that supported further granule growth. It was observed that mature granules supported microbial populations that differed from nascent granules and were predominantly packed with coccoid bacteria. It was further observed that the diversity of the granular microbial community increased as the granules grew. Accumulibacter, Nitrosospira and Thauera were mainly responsible for nutrient removal while microorganisms such as Rhodocyclus and Hyphomicrobiaceae appeared to be primarily responsible for forming and maintaining the granule structure.     

pH值和产甲烷抑制剂对两相耦合系统污泥发酵定向产乙酸的影响

采用产氢产乙酸/同型产乙酸两相耦合工艺对剩余污泥进行了半连续式厌氧发酵,主要研究了pH值和产甲烷抑制剂2-bromoethanesulphonate(BES)对耦合系统定向产乙酸的影响.结果表明:碱性pH(pH=10.0)和添加BES都能促进A相乙酸的积累,提高乙酸的产率,同时碱性pH比添加BES更有利于污泥的水解.当...     

胰蛋白酶诱导人脐静脉内皮细胞分泌白细胞介素-8

目的:研究胰蛋白酶对IL-8释放的影响。方法:分离、培养人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)、倒置显微镜观察形态变化,流式细胞术检测内皮细胞标志和蛋白酶活化受体-2(proteinase-activated receptor-2,PAR-2)表达,ELISA检测HUVECs培养上清中IL-8水平。结果:HUVECs表达内皮细胞标志和PAR-2。刺激16 h,1 g/ml胰蛋白酶和100M PAR-2激活肽组HUVECs单层均匀性降低。胰蛋白酶能够显著刺激HUVECs释放IL-8,PAR-2激活肽也诱导IL-8水平升高。蛋白酶抑制剂和PAR-2抑制肽均能够显著抑制胰蛋白酶诱导的IL-8释放。PAR-2激活肽和胰蛋白酶诱导升高的IL-8水平之间成正相关性。结论:胰蛋白酶很可能通过PAR-2激活促进血管内皮细胞释放IL-8。     

The Influence of Soil Properties on the Mobility of Metals Following a Single Application of Polluted Sewage Sludge to Seventy Agricultural Topsoils: A Laboratory Column Study

The main aim of this study was to examine the influence of soil properties on the leaching of Cd, Cr, Cu, Ni, Pb, and Zn following the application of polluted sewage sludge to contrasting topsoils. Seventy agricultural soil samples from different parts of Spain were amended with a single dose of sewage sludge (equivalent to 50 t dry weight ha^?1) and a column study was performed under controlled conditions. After two, four, and six months of incubation, 283 ml of distilled water (equivalent to a rainfall event of 25 l m^?2) was applied. The leachates were then collected and analyzed for metals. For all of the soils considered, the pH was the most important parameter for the control of mobility metals (except for Cu, determined by the sand and soil organic carbon and only to a lesser extent by the soil pH r² = 0.604, p < 0.001) and was negatively related to all of the studied metals. For Pb and Zn, soil pH was the single soil property explaining their mobility (r² = 0.411, p < 0.001 for Pb; r² = 0.713, p < 0.001 for Zn) while for Cd, Cr and Ni, EC, sand and silt also appeared in the statistical models (r² = 0.753, p < 0.001 for Cd; r² = 0.366, p < 0.001 for Cr; r² = 0.784, p < 0.001 for Ni). In the basic soils, soil texture was the most important soil property controlling the mobility of metals (except for that of Pb, which it only weakly predicted). For the acidic-neutral soils, the soil pH was the most important soil property controlling metal mobility (except for that of Cr, which was mainly determined by the pseudo-total Cr content).     

三种接种物启动Anammox-EGSB反应器的性能

为了优选接种物和加速Anammox反应器启动,分别以厌氧产甲烷污泥 (Anaerobic methanogenic sludge,AMS)、新鲜厌氧氨氧化污泥 (Fresh Anammox sludge,FAS) 和储藏厌氧氨氧化污泥 (Stored Anammox sludge,SAS) 作为接种物,研究了厌氧氨氧化膨胀颗粒污泥床 (Anammox-EGSB) 反应器 (R1、R2和R3) 的启动性能。结果表明：3种接种物均能成功启动Anammox-EGSB反应器,启动性能的优劣次序为：R2 (接种物为     

研究报告：骨形态发生蛋白9通过p38激酶途径调控间充质干细胞C3H10T1/2成骨分化

前期研究发现骨形态发生蛋白9(bone morphogenetic protein 9,BMP9)具有较强的诱导间充质干细胞成骨分化的能力.为进一步揭示其诱导和调控间充质干细胞成骨分化的机理,利用BMP9重组腺病毒感染间充质干细胞C3H10T1/2,通过体外细胞实验和体内动物实验,初步分析BMP9是否可通过p38激酶途径调控间充质干细胞成骨分化.结果发现,BMP9可以通过促进p38激酶磷酸化而导致其活化,p38抑制剂SB203580可抑制由BMP9诱导的C3H10T1/2细胞的碱性磷酸酶(alkalinephosphatase,ALP)活性、骨桥蛋白(osteopontin,OPN)表达和钙盐沉积,而且利用抑制剂SB203580抑制p38激酶活性后,BMP9诱导的Smad经典途径的激活也相应受到抑制,RNA干扰导致p38基因沉默同样也可抑制BMP9诱导的ALP活性、OPN表达、钙盐沉积以及裸鼠皮下异位成骨.因此,BMP9可通过活化p38激酶途径调控间充质干细胞C3H10T1/2成骨分化.     

负载型纳米铁制备条件对As(V)吸附的影响

以活性炭为载体,制备了负载型纳米铁除砷吸附剂.以除砷效率为目标,优化了制备过程中活性炭的不同粒径、铁盐种类及浓度、反应温度及速度、铁盐浸泡活性炭时间及反应平衡时间等参数.考虑到除砷效率及工程实际的应用,室温时采取活性炭粒径为20～40目、KBH4的滴加速率为lml·min-1、活性炭经铁盐为质量浓度为6.9％的硫酸亚铁浸泡30 min,反应平衡时间为30 min时所制备的吸附剂综合除砷效果最好(98％).     

Production kinetics of β-carotene from Planococcus sp. TRC1 with concomitant bioconversion of industrial solid waste into crystalline cellulose rich biomass

Cost effective bioprocessing of nutraceuticals in present global scenario is a matter of concern. This study explored Paper mill sludge (PMS) and sugarcane bagasse (SCB) as inexpensive substrate for Planococcus sp. TRC1 mediated valuable β-carotene production and residual treated biomass as value added crystalline cellulose source simultaneously. Both biomass supported significant bacterial growth reaching highest yield 38.54 ± 1.4 mg/g on PMS (36 h) and 47.13 ± 1.9 mg/g (48 h) on SCB in solid state fermentation. Luedeking-Piret model revealed growth associated production with α and much lower β values of 5.18 and 0.24 for PMS and 4.5 and 0.165 for SCB. Cost analysis exhibited decrementation of pigment cost/mg by 84 % compared to synthetic media. Optimum production conditions were 30 °C temperature, pH 7, 10 % inoculum and initial moisture content 80 % (PMS) and 85 % (SCB). TLC (R_f = 0.9), HPLC (RT = 7.646) and lambda max (465 nm) confirmed pigment’s β-carotene nature with significant antioxidant and antimicrobial activity. It showed stability at varied temperature, pH and light conditions along with negligible phytotoxicity on Vigna radiata. Planococcus sp. TRC1 delignified PMS (41 %) and SCB (38 %) and FT-IR, FESEM and XRD suggested crystalline nature of residual cellulose rich fraction shedding light on a biorefinery approach for valorization of industrial solid wastes.     

Dracorhodin perchlorate inhibits osteoclastogenesis through repressing RANKL-stimulated NFATc1 activity

Osteolytic skeletal disorders are caused by an imbalance in the osteoclast and osteoblast function. Suppressing the differentiation and resorptive function of osteoclast is a key strategy for treating osteolytic diseases. Dracorhodin perchlorate (D.P), an active component from dragon blood resin, has been used for facilitating wound healing and anti-cancer treatments. In this study, we determined the effect of D.P on osteoclast differentiation and function. We have found that D.P inhibited RANKL-induced osteoclast formation and resorbed pits of hydroxyapatite-coated plate in a dose-dependent manner. D.P also disrupted the formation of intact actin-rich podosome structures in mature osteoclasts and inhibited osteoclast-specific gene and protein expressions. Further, D.P was able to suppress RANKL-activated JNK, NF-κB and Ca²⁺ signalling pathways and reduces the expression level of NFATc1 as well as the nucleus translocation of NFATc1. Overall, these results indicated a potential therapeutic effect of D.P on osteoclast-related conditions.     

Metformin attenuates trauma‐induced heterotopic ossification via inhibition of Bone Morphogenetic Protein signalling

AMP‐activated protein kinase (AMPK) is an intracellular sensor of energy homoeostasis that is activated under energy stress and suppressed in energy surplus. AMPK activation leads to inhibition of anabolic processes that consume ATP. Osteogenic differentiation is a process that highly demands ATP during which AMPK is inhibited. The bone morphogenetic proteins (BMPs) signalling pathway plays an essential role in osteogenic differentiation. The present study examines the inhibitory effect of metformin on BMP signalling, osteogenic differentiation and trauma‐induced heterotopic ossification. Our results showed that metformin inhibited Smad1/5 phosphorylation induced by BMP6 in osteoblast MC3T3‐E1 cells, concurrent with up‐regulation of Smad6, and this effect was attenuated by knockdown of Smad6. Furthermore, we found that metformin suppressed ALP activity and mineralization of the cells, an event that was attenuated by the dominant negative mutant of AMPK and mimicked by its constitutively active mutant. Finally, administration of metformin prevented the trauma‐induced heterotopic ossification in mice. In conjuncture, AMPK activity and Smad6 and Smurf1 expression were enhanced by metformin treatment in the muscle of injured area, concurrently with the reduction of ALK2. Collectively, our study suggests that metformin prevents heterotopic ossification via activation of AMPK and subsequent up‐regulation of Smad6. Therefore, metformin could be a potential therapeutic drug for heterotopic ossification induced by traumatic injury.