The degradation of selected chlorinated aliphatic hydrocarbons(CAHs)exemplified by trichloroethylene(TCE),1,1-dichloroethylene(DCE),and chloroform(CF)was investigated with Fenton oxidation process.The results indicate...The degradation of selected chlorinated aliphatic hydrocarbons(CAHs)exemplified by trichloroethylene(TCE),1,1-dichloroethylene(DCE),and chloroform(CF)was investigated with Fenton oxidation process.The results indicate that the degradation rate was primarily affected by the chemical structures of organic contaminants.Hydroxyl radicals(·OH)preferred to attack the organic contaminants with an electron-rich structure such as chlorinated alkenes(i.e.,TCE and DCE).The dosing mode of Fenton’s reagent,particularly of Fe^(2+),significantly affected the degradation efficiency of studied organic compound.A new“time-squared”kinetic model,C=C_(oexp)(-k_(obst)^(2)),was developed to express the degradation kinetics of selected CAHs.This model was applicable to TCE and DCE,but inapplicable to CF due to their varied reaction rate constants towards·OH.Chloride release was monitored to examine the degree of dechlorination during the oxidation of selected CAHs.TCE was more easily dechlorinated than DCE and CF.Dichloroacetic acid(DCAA)was identified as the major reaction intermediate in the oxidation of TCE,which could be completely removed as the reaction proceeded.No reaction intermediates or byproducts were identified in the oxidation of DCE and CF.Based on the identified intermediate,the reaction mechanism of TCE with Fenton’s reagent was proposed.展开更多
背景:程序性细胞死亡受体1(programmed death receptor-1,PD-1)在高糖环境下影响骨髓间充质干细胞成骨分化的作用机制尚不清楚。目的:探讨高糖环境中PD-1对大鼠骨髓间充质干细胞成骨分化的影响及其调控机制。方法:将大鼠骨髓间充质干细...背景:程序性细胞死亡受体1(programmed death receptor-1,PD-1)在高糖环境下影响骨髓间充质干细胞成骨分化的作用机制尚不清楚。目的:探讨高糖环境中PD-1对大鼠骨髓间充质干细胞成骨分化的影响及其调控机制。方法:将大鼠骨髓间充质干细胞随机分为正常糖组(5.6 mmol/L)、高糖组(30 mmol/L)、PD-1过表达组、PD-1过表达空载组、PD-1敲低组、PD-1敲低空载组、PI3K/AKT通路抑制剂组(PD-1敲低+5μmol/L LY294002)。通过在高糖培养基中培养大鼠骨髓间充质干细胞来模拟体外糖尿病环境,采用qRT-PCR检测大鼠骨髓间充质干细胞中PD-1及其配体PD-L1和成骨标志物Runx2、OSX的mRNA表达,采用碱性磷酸酶染色和茜素红S染色观察成骨分化能力,采用CCK-8检测细胞增殖情况,采用Western blot检测PD-1、PD-L1、p-PI3K、p-AKT的蛋白表达。结果与结论:①高糖组PD-1及PD-L1表达显著高于正常糖组,高糖组骨髓间充质干细胞的成骨分化能力较正常糖组显著下降;②敲低PD-1表达可以促进骨髓间充质干细胞的成骨分化、增加细胞增殖活性,同时激活PI3K/AKT通路;③加入PI3K/AKT通路抑制剂LY294002后,骨髓间充质干细胞成骨分化能力显著下降。结果表明:PD-1依赖于PI3K/AKT信号通路抑制高糖环境下大鼠骨髓间充质干细胞的成骨分化。展开更多
基金The authors greatly appreciate the financial support from the Department of Energy,USA(Grant No.DE-FG07-96ER14716)This study was also supported by the National Key Technologies R&D Program funded by the Ministry of Science and Technology of China(Grant No.2006BAJ08B02).
文摘The degradation of selected chlorinated aliphatic hydrocarbons(CAHs)exemplified by trichloroethylene(TCE),1,1-dichloroethylene(DCE),and chloroform(CF)was investigated with Fenton oxidation process.The results indicate that the degradation rate was primarily affected by the chemical structures of organic contaminants.Hydroxyl radicals(·OH)preferred to attack the organic contaminants with an electron-rich structure such as chlorinated alkenes(i.e.,TCE and DCE).The dosing mode of Fenton’s reagent,particularly of Fe^(2+),significantly affected the degradation efficiency of studied organic compound.A new“time-squared”kinetic model,C=C_(oexp)(-k_(obst)^(2)),was developed to express the degradation kinetics of selected CAHs.This model was applicable to TCE and DCE,but inapplicable to CF due to their varied reaction rate constants towards·OH.Chloride release was monitored to examine the degree of dechlorination during the oxidation of selected CAHs.TCE was more easily dechlorinated than DCE and CF.Dichloroacetic acid(DCAA)was identified as the major reaction intermediate in the oxidation of TCE,which could be completely removed as the reaction proceeded.No reaction intermediates or byproducts were identified in the oxidation of DCE and CF.Based on the identified intermediate,the reaction mechanism of TCE with Fenton’s reagent was proposed.
