Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life ...Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.展开更多
The thermally activated persulfate （PS） degradation of carbon tetrachloride （CT） in the presence of formic acid （FA） was investigated. The results indicated that CT degradation followed a zero order kinetic mode...The thermally activated persulfate （PS） degradation of carbon tetrachloride （CT） in the presence of formic acid （FA） was investigated. The results indicated that CT degradation followed a zero order kinetic model, and CO2^- was responsible for the degradation of CT confirmed by radical scavenger tests. CT degradation rate increased with increasing PS or FA dosage, and the initial CT had no effect on CT degradation rate. However, the initial solution pH had effect on the degradation of CT, and the best CT degradation occurred at initial pH 6. Cl^- had a negative effect on CT degradation, and high concentration of Cl^- displayed much strong inhibition. Ten mmol·L^-1HCO3^- promoted CT degradation, while 100mmol·L^-1NO3^- inhibited the degradation of CT, but SO4^2- promoted CT degradation in the presence of FA. The measured Cl^- concentration released into solution along with CT degradation was 75.8% of the total theoretical dechlorination yield, but no chlorinated intermediates were detected. The split of C-Cl was proposed as the possible reaction pathways in CT degradation. In conclusion, this study strongly demonstrated that the thermally activated PS system in the presence of FA is a promising technique in in situ chemical oxidation （ISCO） remediation for CT contaminated site.展开更多
Trichloroethene （TCE） degradation by Fe（III）- activated calcium peroxide （CP） in the presence of citric acid （CA） in aqueous solution was investigated. The results demonstrated that the presence of CA enhanced...Trichloroethene （TCE） degradation by Fe（III）- activated calcium peroxide （CP） in the presence of citric acid （CA） in aqueous solution was investigated. The results demonstrated that the presence of CA enhanced TCE degradation significantly by increasing the concen- tration of soluble Fe（III） and promoting H202 generation. The generation of HO· and O2^-· in both the CP/Fe（III） and CP/Fe（III）/CA systems was confirmed with chemical probes. The results of radical scavenging tests showed that TCE degradation was due predominantly to direct oxidation by HO·, while O2^-· strengthened the generation of HO· by promoting Fe（III） transformation in the CP/Fe （III）/CA system. Acidic pH conditions were favorable for TCE degradation, and the TCE degradation rate decreased with increasing pH. The presence of Cl·-, HCO3·-, and humic acid （HA） inhibited TCE degradation to different extents for the CP/Fe（III）/CA system. Analysis of Cl·- production suggested that TCE degradation in the CP/Fe （III）/CA system occurred through a dechlorination process. In summary, this study provided detailed information for the application of CA-enhanced Fe（III）-activated calcium peroxide for treating TCE contaminated groundwater.展开更多
基金supported by the National Natural Science Foundation of China,Nos.81730033,82171193(to XG)the Key Talent Project for Strengthening Health during the 13^(th)Five-Year Plan Period,No.ZDRCA2016069(to XG)+1 种基金the National Key R&D Program of China,No.2018YFC2001901(to XG)Jiangsu Provincial Medical Key Discipline,No.ZDXK202232(to XG)。
文摘Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.
基金This study was financially supported by a grant from the National Natural Science Foundation of China （Grant Nos. 41373094 and 51208199）.
文摘The thermally activated persulfate （PS） degradation of carbon tetrachloride （CT） in the presence of formic acid （FA） was investigated. The results indicated that CT degradation followed a zero order kinetic model, and CO2^- was responsible for the degradation of CT confirmed by radical scavenger tests. CT degradation rate increased with increasing PS or FA dosage, and the initial CT had no effect on CT degradation rate. However, the initial solution pH had effect on the degradation of CT, and the best CT degradation occurred at initial pH 6. Cl^- had a negative effect on CT degradation, and high concentration of Cl^- displayed much strong inhibition. Ten mmol·L^-1HCO3^- promoted CT degradation, while 100mmol·L^-1NO3^- inhibited the degradation of CT, but SO4^2- promoted CT degradation in the presence of FA. The measured Cl^- concentration released into solution along with CT degradation was 75.8% of the total theoretical dechlorination yield, but no chlorinated intermediates were detected. The split of C-Cl was proposed as the possible reaction pathways in CT degradation. In conclusion, this study strongly demonstrated that the thermally activated PS system in the presence of FA is a promising technique in in situ chemical oxidation （ISCO） remediation for CT contaminated site.
基金This study was financially supported by the National Natural Science Foundation of China （Grant Nos. 41373094 and 51208199）, China Postdoctoral Science Foundation （No. 2015M570341） and the Fundamental Research Funds for the Central Universities （No. 22A2015 14057）. The contributions of Dr. Mark Brusseau were supported by the NIEHS Superfund Research Program （P42 ES04940）.
文摘Trichloroethene （TCE） degradation by Fe（III）- activated calcium peroxide （CP） in the presence of citric acid （CA） in aqueous solution was investigated. The results demonstrated that the presence of CA enhanced TCE degradation significantly by increasing the concen- tration of soluble Fe（III） and promoting H202 generation. The generation of HO· and O2^-· in both the CP/Fe（III） and CP/Fe（III）/CA systems was confirmed with chemical probes. The results of radical scavenging tests showed that TCE degradation was due predominantly to direct oxidation by HO·, while O2^-· strengthened the generation of HO· by promoting Fe（III） transformation in the CP/Fe （III）/CA system. Acidic pH conditions were favorable for TCE degradation, and the TCE degradation rate decreased with increasing pH. The presence of Cl·-, HCO3·-, and humic acid （HA） inhibited TCE degradation to different extents for the CP/Fe（III）/CA system. Analysis of Cl·- production suggested that TCE degradation in the CP/Fe （III）/CA system occurred through a dechlorination process. In summary, this study provided detailed information for the application of CA-enhanced Fe（III）-activated calcium peroxide for treating TCE contaminated groundwater.
