Using lightly polluted water of WenYu River in Beijing as the research object and making use of electrochemistry method to treat it,the effects of the changes of the chloride concentration in the water and cell voltag...
Using lightly polluted water of WenYu River in Beijing as the research object and making use of electrochemistry method to treat it,the effects of the changes of the chloride concentration in the water and cell voltage on removing pollutants were *** results revealed that electrochemical oxidation method could partly remove ammonia NH-N,TN and COD,the highest removal rate of the NH-N,TN and COD were able to achieve 95%,89%and 68%*** the higher the chloride concentration in the water,the higher the removal rate to pollutants,along with the increase of cell voltage,the removal rates of pollutants increased *** the addition of the chloride concentration and the increase of cell voltage both have their limitations,in this way,the removal rates of the pollutants could be guaranteed. Considering the power consumption and other factors,the optimal running conditions of this experiment were the electrolysis time 20 min,the cell voltage 7 V,the chloride solution concentration of the addition 5.0mol/L and the dosing amount 2 L/*** the course of chemical reaction of electrochemical process was expressed too.
Experimental research was performed on the multiple current peaks (MCP) in atmospheric pressure glow dielectric barrier discharge in helium. In a MCP discharge sequence, the next discharge pulse is always affected by ...
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Experimental research was performed on the multiple current peaks (MCP) in atmospheric pressure glow dielectric barrier discharge in helium. In a MCP discharge sequence, the next discharge pulse is always affected by the previous one. The accumulated charges on the dielectric plate play an important role in the MCP formation. In addition, two discharge modes, glow and Townsend discharge modes, can be observed in a MCP discharge sequence. The discharge mode tends to convert from glow to Townsend discharge mode when increasing the applied voltage, decreasing the gas gap and reducing driving frequency, respectively. (C) 2008 Elsevier B.V. All rights reserved.
High pressure microwave assisted extraction (HPMAE) was applied to extract the ginsenosides from Panax ginseng root. The influences of extraction solvent, extraction pressure and extraction time were individually inve...
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High pressure microwave assisted extraction (HPMAE) was applied to extract the ginsenosides from Panax ginseng root. The influences of extraction solvent, extraction pressure and extraction time were individually investigated. HPMAE has been compared with other extraction methods, including Soxhlet extraction, ultrasound-assisted extraction and heat reflux extraction. The determination of ginsenosides was performed by HPLC-ESI-MS. The results indicated that the HPMAE not only took a shorter time but also afforded higher extraction yields of ginsenosides, especially ginsenoside Rb-1, Rc, Rb-2 and Rd. Furthermore, the neutral ginsenosides and malonyl ginsenosides in Panax ginseng root extracts by HPMAE were investigated. The malonyl ginsenoside m-Rb-1, m-Rc, m-Rb-2 and m-Rd degraded in HPMAE at 400 kPa (109-112 degrees C) in 70% (v/v) ethanol-water and at 600 kPa (112-115 degrees C) in methanol, and transformed into corresponding neutral ginsenoside Rb-1, Rc, Rb-2 and Rd. Using water as extraction solution, tile neutral ginsenosides degraded under HPMAE at 400 kPa (135-140 degrees C), and transformed into less polarity rare ginsenosides. (c) 2008 Elsevier Ltd. All rights reserved.
We previously reported that ischemic postconditioning with a series of mechanical interruptions of reperfusion reduced infarct volume 2 days after focal ischemia in rats. Here, we extend this data by examining long-te...
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We previously reported that ischemic postconditioning with a series of mechanical interruptions of reperfusion reduced infarct volume 2 days after focal ischemia in rats. Here, we extend this data by examining long-term protection and exploring underlying mechanisms involving the Akt, mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) signaling pathways. Post-conditioning reduced infarct and improved behavioral function assessed 30 days after stroke. Additionally, postconditioning increased levels of phosphorylated Akt (Ser473) as measured by western blot and Akt activity as measured by an in vitro kinase assay. Inhibiting Akt activity by a phosphoinositide 3-kinase inhibitor, LY294002, enlarged infarct in postconditioned rats. Postconditioning did not affect protein levels of phosphorylated-phosphatase and tensin homologue deleted on chromosome 10 or -phosphoinositide-dependent protein kinase-1 (molecules upstream of Akt) but did inhibit an increase in phosphorylated-glycogen synthase kinase 3 beta, an Akt effector. In addition, postconditioning blocked beta-catenin phosphorylation subsequent to glycogen synthase kinase, but had no effect on total or non-phosphorylated active beta-catenin protein levels. Furthermore, postconditioning inhibited increases in the amount of phosphorylated-c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 in the MAPK pathway. Finally, postconditioning blocked death-promoting delta PKC cleavage and attenuated reduction in phosphorylation of survival-promoting epsilon PKC. In conclusion, our data suggest that postconditioning provides long-term protection against stroke in rats. Additionally, we found that Akt activity contributes to postconditioning's protection;furthermore, increases in epsilon PKC activity, a survival-promoting pathway, and reductions in MAPK and delta PKC activity;two putative death-promoting pathways correlate with postconditioning's protection.
Dephosphorylated and activated glycogen synthase kinase (GSK) 3 beta hyperphosphorylates beta-catenin, leading to its ubiquitin-proteosome-mediated degradation. beta-catenin-knockdown increases while beta-catenin over...
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Dephosphorylated and activated glycogen synthase kinase (GSK) 3 beta hyperphosphorylates beta-catenin, leading to its ubiquitin-proteosome-mediated degradation. beta-catenin-knockdown increases while beta-catenin overexpression prevents neuronal death in vitro;in addition, protein levels of beta-catenin are reduced in the brain of Alzheimer's patients. However, whether beta-catenin degradation is involved in stroke-induced brain injury is unknown. Here we studied activities of GSK 3 and beta-catenin, and the protective effect of moderate hypothermia (30 degrees C) on these activities after focal ischemia in rats. The results of Western blot showed that GSK 3 beta was dephosphorylated at 5 and 24 h after stroke in the normothermic (37 degrees C) brain;hypothermia augmented GSK 3 beta dephosphorylation. Because hypothermia. reduces infarction, these results contradict with previous studies showing that GSK 3 dephosphorylation worsens neuronal death. Nevertheless, hypothermia blocked degradation of total GSK 3 beta protein. Corresponding to GSK 3 activity in normothermic rats, beta-catenin phosphorylation transiently increased at 5 h in both the ischemic penumbra and core, and the total protein level of-catenin degraded after normothermic stroke. Hypothermia did not inhibit beta-catenin phosphorylation, but it blocked beta-catenin degradation in the ischemic penumbra. In conclusion, moderate hypothermia can stabilize beta-catenin, which may contribute to the protective effect of moderate hypothermia. (c) 2008 Elsevier B.V. All rights reserved.
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