第九分会环境与健康风险

[e-mail]207030100875,[e-mail][e-mail][e-mail][e-mail]/T4633-1997WS/T88-199650ml5%90.3%107.6%0.456.75mg/kg710062,[e-mail]273(X1)(X2)(X3)(X4)(X5)(r)r1=0.850r2=0.414r3=-0.632r4=-0.802r5=-0.582.(F=257.90)^Y1=151.0+0.006923X1-1.143X4+0.006789X522.3^Y(g/L)X1(m)X4()X5(mm)[e-mail][e-mail];2;3;4;5Budd-ChiariSyndromeB-CS700B-CS128128,98.44%150g/L150300g/L27.35%300g/L71.09%1.56%1.02.0mg/L75.0%2.04.0mg/[e-mail]----NH4+-NDPNH4+-ND[e-mail]2330029Non-pointsource,NPS97.5%.1,[e-mail](4162771mg/L)(P0.01)[e-mail][e-mail]1,[e-mail]2100039200456364820SPSS11.5p0.05(p0.05)[e-mail]21400061.6%(98/159)47.6%(50/105)[e-mail]150km5~[e-mail]0.84=V/[e-mail]HsDDTsPCBsOCPs-HCH-HCH-HCH-HCHp,p-DDEo,p-DDTp,p-DDTp,p-DDD-HCH-HCH-HCH-HCHp,p-DDEo,p-DDTp,p-DDDp,[e-mail]198828,51.6%100g/L,1999838.8%1030%80%;;,,1LTPLTDLTPLTDLTP34%LTD28%2Ca++,Ca++Pb++Ca++Ca++Pb++Ca++PKCPKC-cAMP-,K+K+K+3NMDANMDA(),K+()5c-fosc-jun,mRNADNA,,,DNAcAMPPKACREB6,,,,LTPLTPCa2+-GlsNMDA100101sunx.03s@igsnrr..ac.cnAsAsAsAs,130026,[e-mail](nAChRs)modulatestheinductionoflong-termpotentiation(LTP),oneofthepossiblecellularmechanismsforlearning.Toinvestigatetheeffectofnicotine(NIC)onsynapticplasticityinchroniclead-exposedrat,fieldexcitatorypostsynapticpotentials(fEPSP)andpaired-pulsefacilitation(PPF)wererecordedintheCA1areaofhippocampalslicesexposedtolead.Theresultsshowedthat:(1)NIC(1M)facilitatedtheinductionofLTPinCA1areaofthehippocampusbyaweaktetanicstimulation(100Hz,20Pulses),whichdoesnotbyitselfproduceLTPinlead-exposedrats.Thiseffectwassignificantlysuppressedbymecamylamine(MEC;5M),anonselectivenicotinicantagonist,suggestingthatloweredthethresholdforLTPinthechroniclead-exposedratbynicotineisthroughnAChRs.(2)Thenicotine-mediatedLTPwasblockedbydihydro--erythroidine(DhE1M),astrongantagonistofthenAChRscontaining42subunits.Whilelong-termdepression(LTD)wasproducedbythecombinationofNICandmethyllycaconitine(MLA;10nM),anantagonistofnAChRscontaining7subunits;neitherLTPnorLTDwasobservedbythecombinationofNIC,MLAandDHE.ItimpliesthatseveralnAChRssubtypesareinvolvedinthenicotine-mediatedsynapticplasticity.(3)NICapplicationenhancedpaired-pulsefacilitation(PPF)inhippocampalCA1region,andthenicotine-mediatedLTPinlead-exposedratswasreversedbytheapplicationofeitherD-(-)-2-amino-5-phosphonopentanoicacid(D-AP5;50M)£¬theNMDAreceptorantagonist,or(PTX;50M),anantagonistof-aminobutyricacid(GABA)Areceptor.Theseresultssuggestedthatnicotine-mediatedsynapticplasticityisduetotheenhancementofNMDARresponsesbydisinhibitionofpyramidalcellsthroughpresynapticnAChRs.Thismayrepresentthecellularbasisofnicotine-mediatedcognitiveenhancementobservedinchroniclead-exposedrats.ThisworkwassupportedbyTheNationalBasicResearchProgramofChina(No.2002CB512907),AcademiaSinica(No.KZCX3-SW-437).13131,[e-mail]2.1000393.162650()932050X34235024.5116.87g/g1.120.48g/ml4.441.71g/ml6.021.79mg/L1.351.01g/g0.0950.047g/ml2.291.70g/ml2.991.11mg/L5.802.14g/g0.230.10g/ml2.191.34g/ml1.311.06g/g0.0330.008g/ml0.610.39g/mlX86.361111,[e-mail]2430070/@yahoo.com.cn2,[e-mail][e-mail]/510405,[e-mail],1.52.01,[e-mail]@[e-mail]8844.7%P0.0585.7%P0.01SO275%(P0.05)[e-mail]2100053280320nmB(UVB)sdisort19471UVB1km2111320%ICNIRP30J/m2