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Bingsheng Zhou - One of the best experts on this subject based on the ideXlab platform.
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the adverse effect of tcipp and TCEP on neurodevelopment of zebrafish embryos larvae
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
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The adverse effect of TCIPP and TCEP on neurodevelopment of zebrafish embryos/larvae.
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
Hengqi Wang - One of the best experts on this subject based on the ideXlab platform.
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the adverse effect of tcipp and TCEP on neurodevelopment of zebrafish embryos larvae
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
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The adverse effect of TCIPP and TCEP on neurodevelopment of zebrafish embryos/larvae.
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
Wilhelm Püttmann - One of the best experts on this subject based on the ideXlab platform.
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Behavior of organophosphates and hydrophilic ethers during bank filtration and their potential application as organic tracers. A field study from the Oderbruch, Germany.
Science of The Total Environment, 2013Co-Authors: D.k. Stepien, J Regnery, C Merz, Wilhelm PüttmannAbstract:The behavior of organophosphates and ethers during riverbank filtration and groundwater flow was assessed to determine their suitability as organic tracers. Four sampling campaigns were conducted at the Oderbruch polder, Germany to establish the presence of chlorinated flame retardants (TCEP, TCPP, TDCP), non-chlorinated plasticizers (TBEP, TiBP, TnBP), and hydrophilic ethers (1,4-dioxane, monoglyme, diglyme, triglyme, tetraglyme) in the Oder River, main drainage ditch, and anoxic aquifer. Selected parameters were measured in order to determine the hydro-chemical composition of both, river water and groundwater. The results of the study confirm that organophosphates (OPs) are more readily attenuated during bank filtration compared to ethers. Both in the river and the groundwater, TCPP was the most abundant OP with concentrations in the main drainage ditch ranging between 105 and 958 ng L(-1). 1,4-dioxane, triglyme, and tetraglyme demonstrated persistent behavior during bank filtration and in the anoxic groundwater. In the drainage ditch concentrations of 1,4-dioxane, triglyme, and tetraglyme ranged between 1090 and 1467 ng L(-1), 37 and 149 ng L(-1), and 496 and 1403 ng L(-1), respectively. A positive correlation was found for the inorganic tracer chloride with 1,4-dioxane and tetraglyme. These results confirm the possible application of these ethers as environmental organic tracers. Both inorganic and organic compounds showed temporal variability in the surface- and groundwater. Discharge of the river water, concentrations of analytes at the time of infiltration and attenuation were identified as factors influencing the variable amounts of the analytes in the surface and groundwater. These findings are also of great importance for the production of drinking water via bank filtration and natural and artificial groundwater recharge as the physicochemical properties of ethers create challenges in their removal.
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Temporal concentration changes of DEET, TCEP, terbutryn, and nonylphenols in freshwater streams of Hesse, Germany: possible influence of mandatory regulations and voluntary environmental agreements
Environmental Science and Pollution Research, 2009Co-Authors: Kristin Quednow, Wilhelm PüttmannAbstract:Background, aim, and scope The present study focuses on the temporal concentration changes of four common organic pollutants in small freshwater streams of Hesse, Germany. The substances (tris(2-chloroethyl)phosphate (TCEP), the technical isomer mixture of 4-nonylphenol (NP), 2-( t -butylamino)-4-(ethylamino)-6-(methylthio)- s -triazine (terbutryn), and N , N -diethyl- m -toluamide (DEET)) are subject to differing regulations. Whereas the use of NP and the related nonylphenolethoxylates (NPEOs) are almost completely banned under EU directive 2003/53/EC, the herbicide terbutryn is only restricted for use as a herbicide in the majority of member states of the European Union (EU). In contrast, TCEP and DEET are not regulated by legislation, but have been replaced in some products through consumer pressure. The impact of regulation on the environmental concentrations of these pollutants is discussed. Materials and methods The substances were monitored in small freshwater streams in the Hessisches Ried region, Germany, during the period September 2003 to September 2006. The samples were extracted with solid phase extraction (SPE) and analyzed by coupled gas chromatography–mass spectrometry (GC–MS). Results All target compounds were detected frequently within the fresh water streams of the study area. Monitoring in the study area revealed a significant concentration decrease only for NP. For the other three compounds, no significant concentration decrease was observed. Terbutryn concentrations and loads showed a seasonal trend with higher levels in summer and autumn, but were also present in winter and spring. Concentrations of TCEP and DEET were in the range of prior investigations. Discussion The decrease of NP concentrations and loads during the sampling period indicates that the regulation of NP and NP ethoxylates has led to a significant improvement in reducing the occurrence of this compound in the aquatic environment. Furthermore, the ban on agricultural use of terbutryn at the end of 2003 had no discernable influence on terbutryn concentrations in the following years. Conclusions The benefits of national bans or self-regulations by manufacturers on several chemicals appear to be limited. In contrast, the European-wide ban (of NP) revealed to be effective in preventing the substance from entering the aquatic environment on a large scale and reduced the NP concentration to an acceptable level (i.e., below the PNEC). Recommendations and perspectives Further research is needed to investigate diffuse sources and point sources of terbutryn not related to agriculture. Further research is required to find an explanation for the ongoing high concentration of TCEP in river water despite of the supposed replacement of TCEP by TCPP already in the 1990s.
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Monitoring of the three organophosphate esters TBP, TCEP and TBEP in river water and ground water (Oder, Germany)
Journal of Environmental Monitoring, 2003Co-Authors: Elke Fries, Wilhelm PüttmannAbstract:The behaviour of the three organophosphate esters tributyl phosphate (TBP), tris(2-chloroethyl)phosphate (TCEP) and tris(2-butoxyethyl)phosphate (TBEP) during infiltration of river water to ground water has been investigated. The monitoring site is the Oder River and the adjacent Oderbruch aquifer. From March 2000 to July 2001, 76 ground water samples from monitoring wells located close to the Oder River and nine river water samples were collected. Additionally, influent and effluent samples from local waste water treatment plants, one sample of rain water and samples of roof runoff were collected. All samples were analysed by solid-phase-extraction followed by gas chromatography/mass spectrometry. TBP, TCEP and TBEP were detected at mean values of 622 ng l(-1), 352 ng l(-1), and 2955 ng l(-1), respectively in municipal waste water effluents. This points to a major input of these compounds into the Oder River by municipal waste water discharge. The concentrations of TBP and TBEP decreased downstream the Oder River possibly due to aerobic degradation. TBP, TCEP and TBEP were detected in ground water influenced predominantly by bank-filtered water. This demonstrates a transport of organic compounds by river water infiltration to ground water. TBP, TCEP and TBEP were also detected in rain water precipitation, roof runoff and ground water predominantly influenced by rain water infiltration. This hints to an input of these compounds to ground water by dry and wet deposition after atmospheric transport. Organophosphate esters were also detected in parts of the aquifer at 21 m depth. This demonstrates low anaerobic degradation rates of TBP, TCEP and TBEP.
John Kim - One of the best experts on this subject based on the ideXlab platform.
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TCEP traffic consolidation for energy proportional high radix networks
International Symposium on Computer Architecture, 2018Co-Authors: Gwangsun Kim, Hayoung Choi, John KimAbstract:High-radix topologies in large-scale networks provide low network diameter and high path diversity, but the idle power from high-speed links results in energy inefficiency, especially at low traffic load. In this work, we exploit the high path diversity and non-minimal adaptive routing in high-radix topologies to consolidate traffic to a smaller number of links to enable more network channels to be power-gated. In particular, we propose TCEP (Traffic Consolidation for Energy-Proportional high-radix networks), a distributed, proactive power management mechanism for large-scale networks that achieves energy-proportionality by proactively power-gating network channels through traffic consolidation. Instead of naively power-gating the least utilized link, TCEP differentiates links with the type of traffic (i.e., minimally vs. non-minimally routed traffic) on them since the performance impact of power-gating on minimal traffic is greater than non-minimal traffic. The performance degradation from the reduced number of channels is minimized by concentrating available links to a small number of routers, instead of distributing them across the network, to maximize path diversity. TCEP introduces a shadow link to quickly reactivate an inactive link and Power-Aware progressive Load-balanced (PAL) routing algorithm that incorporates the link power states in load-balancing the network. Our evaluations show that TCEP achieves significantly higher throughput across various traffic patterns while providing comparable energy savings for real workloads, compared to a prior approach proposed for the flattened butterfly topology.
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ISCA - TCEP: traffic consolidation for energy-proportional high-radix networks
2018 ACM IEEE 45th Annual International Symposium on Computer Architecture (ISCA), 2018Co-Authors: Gwangsun Kim, Hayoung Choi, John KimAbstract:High-radix topologies in large-scale networks provide low network diameter and high path diversity, but the idle power from high-speed links results in energy inefficiency, especially at low traffic load. In this work, we exploit the high path diversity and non-minimal adaptive routing in high-radix topologies to consolidate traffic to a smaller number of links to enable more network channels to be power-gated. In particular, we propose TCEP (Traffic Consolidation for Energy-Proportional high-radix networks), a distributed, proactive power management mechanism for large-scale networks that achieves energy-proportionality by proactively power-gating network channels through traffic consolidation. Instead of naively power-gating the least utilized link, TCEP differentiates links with the type of traffic (i.e., minimally vs. non-minimally routed traffic) on them since the performance impact of power-gating on minimal traffic is greater than non-minimal traffic. The performance degradation from the reduced number of channels is minimized by concentrating available links to a small number of routers, instead of distributing them across the network, to maximize path diversity. TCEP introduces a shadow link to quickly reactivate an inactive link and Power-Aware progressive Load-balanced (PAL) routing algorithm that incorporates the link power states in load-balancing the network. Our evaluations show that TCEP achieves significantly higher throughput across various traffic patterns while providing comparable energy savings for real workloads, compared to a prior approach proposed for the flattened butterfly topology.
Ling Zhang - One of the best experts on this subject based on the ideXlab platform.
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the adverse effect of tcipp and TCEP on neurodevelopment of zebrafish embryos larvae
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
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The adverse effect of TCIPP and TCEP on neurodevelopment of zebrafish embryos/larvae.
Chemosphere, 2019Co-Authors: Hengqi Wang, Chenglian Feng, Ling Zhang, Lihua Yang, Bingsheng ZhouAbstract:Tris (1-chloro-2-propyl) phosphate (TCIPP) and tris (2-chloroethyl)phosphate (TCEP) are two widely used chlorinated organophosphate flame retardants (ClOPFRs), and have been frequently detected in various environmental media. Concern is now growing whether TCIPP and TCEP can cause neurotoxicity since they have similar chemical structure with organophosphorus pesticide. Therefore, in this study, zebrafish embryos (2-120 h post-fertilization [hpf]) were exposed to TCIPP or TCEP (0, 100, 500 or 2500 mu g/L) or a model neurotoxicant, chlorpyrifos (CPF, 100 mu g/L) to investigate the adverse effects and possible mechanisms of TCIPP and TCEP on neurodevelopment. Our results showed that CPF exposure resulted in developmental toxicity including decreased hatching, survival rates and increased malformation rates (e.g., spinal curvature) as well as behavior changes such as decreased locomotive activity in dark stimulation. In contrast, TCIPP and TCEP showed no significant effects on developmental parameters, but caused similar effects on locomotive activity at high concentration, indicating that although not as potent as CPF. TCIPP and TCEP may still cause adverse effects on neurodevelopment. Furthermore, our results suggest that TCIPP and TCEP showed no effects on acetylcholine content or AChE activity, which were considered as the main targets of CPF. However, TCIPP and TCEP exposure can significantly down regulate the expression of selected genes and proteins related to neurodevelopment (e.g., mbp, syn2a, and alpha 1-tubulin) similar as CPF did. Besides that, TCIPP and TCEP can also affect the transcription of shha and gap43, which were not affected by CPF, pointing out a complex mechanism underlying TCIPP and TCEP's neurodevelopmental toxicity. Overall, our results demonstrated that TCEP and TCIPP may have adverse effect on the neurodevelopment of zebrafish embryos/larvae, but the underlying mechanism is not via the inhibition of acetyl cholinesterase activity. (C) 2018 Published by Elsevier Ltd.
