Disseminatedintravascularcoagulation1 Intravascular ExtravascularNormalcirculationHemostasisliquiditysolidity(coagulation)NormalNormalBloodAbnomalAbnomalsolidity(coagulation)liqidityThromboticdiseaseHemorrhagicdisease Intravascular Extravascular2Thefunctionofcoagulationsystem(Extrinsic,Intrinsicpathwayandplatelet)Thefunctionofanticoagulation(TFPI,PCsystem,ATIIIandfibrinolyticsystem)TheregulationofbalancebyVECThekeyfactorsforbalanceofcoagulation-anticoagulation:3ThechainreactionofbloodcoagulationFXIFXIaFVII/FVIIaTFCa2+(onmembrane)FIXFIXaTFPI-FXaFVIIIaCa2+PLprothrombin(FII)PCIFXFxaPLCa2+FvaAPC(PS)XIIIthrombinTMonVECXIIIaATIIIPCFbnFbnFMFbg(FI)(crosslinked)(soluble)TF=tissuefactor;TFPI=TFpathwayinhibitor;Fbg=fibrinogen;Fbn=fibrin;FM=fibrinmonomer;PC=proteinC;APC=activatedPC;PS=proteinS;PCI=PCinhibitorATIII=antithrombinIII;TM=thrombomodulin;VEC=vascularEC4ThefibrinolysissystemPlasminogen(PLg)(Extra-activatingpathway)(Intra-activatingpathway)tissuetypeplasminogenactivationofclottingsystemactivator(tPA)XIaurokinasetypeplasminogenthrombinactivator(uPA)XIIaXII(Exogenousactivator)urokinase(UK)kallikrein(KK)streptokinase(SK)prekallikrein(PK)Plasmin(Pln)FbgFbnFDP(fibrinogen)(fibrin)(Fbg/Fbndegradationproducts)5InhibitXa,VIIa,TFInhibitplateletaggregationFibrinolysisPreventfibrinclotformationTraumaAdrenalinThrombinADPNO,PGI2Xa,IIaPlasminPlasminoginActivatorstPA,uPAInactivateVa,VIIIaPSThrombinPCAPCTMInhibitXa,IIaATIII+HeparinTFPIAnticoagulantfunctionofendothelialcells6Section 1. Concept and causes of DIC 7Todays Question Question 1. What is DIC?81.ConceptofDICDisseminatedintravascularcoagulation(DIC)Asyndromethatresultsfromthedisturbanceofkineticbalanceofcoagulationandfibrinolyticprocesses.Characterizedbyextensiveintravascularmicrothrombosisandimpairmentofhemostasia.Itsinitiallinkisactivationofclottingsysteminthebody9extensivemicrothrombinextensivehemorrhageorgandysfunctionShockaneamiaNormalbalanceofcoagulationanticoagulationHypocoagulablestateHypercoagulablestateUnbalance of coagulation-anticoagulation and DICextensiveactivationofclottingfactorsandplateletsconsumptionofclottingfactorsandplateletssecondaryfibrinolysishemorrhageorgandysfunctionShockaneamia10ThereforeDICusuallyassociatedsimultaneouslywithbothhemorrhageandthrombosis.Itsclinicalpresentationsinclude:1)extensivehemorrhageatskin,mucosaandinternalorgans(viscera);2)shock;3)organdysfunction;4)aneamia.AnextensiveactivationofcoagulationprocesscausedbytheenteringofcoagulationpromotingsubstancesintocirculationAnincreasedconsumptionofclottingfactorsandplatelets,depositionoffibrinandsecondaryfibrinolysis.resultsin112.CausesofDICincluding:infectiousdiseases,extensivetissueinjury,obstetriccomplications,malignanttumors,acuteleukemia,shock,hepaticandrenaldiseases,collagendisease,metabolicdiseases,cardiovasculardiseases,intravascularhemolysisEtiologic Disease of DICDiseasesorpathologicprocesswhichmayleadtoDICTriggeringFactorAnyfactorswhichmaytriggerorpromoteDICoccur12including:infectiousdiseases,extensivetissueinjury,obstetriccomplications,malignanttumors,acuteleukemia,shock,hepaticandrenaldiseases,collagendisease,metabolicdiseases,cardiovasculardiseases,intravascularhemolysis2.CausesofDICTriggeringFactorAnyfactorswhichmaytriggerorpromoteDICoccurEtiologic Disease of DICDiseasesorpathologicprocesswhichmayleadtoDIC1)Tissueinjuryandreleasetissuefactor(TF)2)Vascularendothelialcells(VEC)injury3)bacterialendotoxin4)AgAbcomplex5)Proteinhydrolyticenzymes6)Particleorcolloid7)Virusandothermicrobe13Section 2. Pathogenesis of DIC14ThemechanismofDICisverycomplexandremainsunclearuptonow.Thecommonpathogenicprocessinclude:1) Triggering clotting activation, producing numerousinsolublefibrin(Fbn)andactivatingplatelets;2)ThegeneratedFbndepositinmicrovesselsandismorethanhydrolyticabilityoffibrinolysin;3) Alteration of fibrinolysis function during the DICprocess which is related to the pathologic process ofmicrothrombosisandbleedingtendency.151.ActivationofclottingsystemAssoonasactivation,theclottingresponsewillbemagnifiedbycascadeorlimitedbynegativefeedback.Theclottingsystemisliabletobeactivatedinthemicrovessels,leadingtomicrothrombusformation.Thecausesandpathogenesisofclottingsystemactivationincluding:(1)Tissueinjury(2)Vascularendothelialcellsinjury(3)Otherpathwaytoactivateclottingsystem16(1)TissueinjurySeveretrauma,burns,surgicaloperation,obstetricaccident,tumortissuenecrosisormetastasis,bloodcellinjury(radiationorchemicaltherapyforleukemia)ExcessivedestructionoftissueNumerousTFenteringthebloodActivatingclottingreactionsBesides,lysozymesreleasedbylysosomeofdamagedcellsmayalsopromotetheactivationofclottingsystem.17Infectious,endotoxinemia,AgAbcomplex,persistentischemiaandhypoxia,acidosisextensivedamageofvascularendothelialcells.activatingclottingreactions(activatingMo/Mf,PMN,TlymphocytereleaseTNF,IL1,IFN,PAF,C3a,C5a,O2)(2)VascularendothelialcellsinjuryreleasingTFsubendothelialexposureplateletsadhesionAggregationandrelease18ActivationofMo/Mf,WBCreleaseTF,lysozymesMalignanttumorsreleaseTF,cancerprocoagulantHemorrhagicpancreatitis,cancerofpancreasreleasetrypsin(mayactivateprothrombindirectly)ExogenoustoxinactivateFX,prothrombinortransferFbgtoFbndirectlyExtensivehemolysisreleaseADPactivateplateletsreleaseerythrinTFlikeeffect(3)Otherpathwaytoactivateclottingsystem192.ChangeofvasomotorialactivityandbloodfluidityVECinjuryEDRF,PGI2,ETPlateletactivatedTXA2Bloodflow(vasoconstriction)orstasis(vasodilation)eliminateofcoagulantoractivateclottingfactorsPAF,histamin,BKvascularpermeability(BK:bradykinin)DepositofFbnBloodcondense,Viscosity203.Disturbanceoffibrinolysis(1)LocalfibrinolysisclottingVECinjurylocalanticoagultiveandfibrinolyticfunctiondepositofFbnmicrothrombusformation(2)SecondaryfibrinolysisbleedingFXIa,thrombin,KK,etc.promotetransferPLgtoPLnVECreleasetPA,uPAtransferPLgtoPLnProteinCactivatedbythrombin(viaVECTM)formactivatedproteinC(APC)anticoagulationandpromotefibrinolysis.21PathologicalFactorsextensiveactivationofclottingfactorsandplateletsintravascularcoagulationconsumptionofclottingsecondaryfactorsandplateletsfibrinolysisextensivehemorrhageaneamiashockorgandysfunction(Disseminatedintravascularcoagulation,DIC)HypercoagulablestateHypocoagulablestate22Section 3.Primary clinical presentations of DIC23DICmayleadtofourconsequencesasfollows:1.Disturbanceofcoagulation-Bleeding2.Disturbanceofmicrocirculation-Shock3.multipleorgansdysfunction-MOD4.Microangiopathichemolytic-Anemia241.Disturbanceofcoagulation-BleedingTheprimeandcommonsymptomofDICisbleeding.ThefeaturesofbleedinginDIC:(1)Highoccurrencerate(7080%)(2)Difficulttoexplainbyprimarydisease(3)Manifoldbleedingtypes(4)Difficulttobecuredbyregularhemostatics25ThecausesofbleedinginDICincluding:(1)Excessiveconsumptionofcoagulationsubstances(clottingfactorsandplatelets);(2)Secondaryenhanceoffibrinolysis(3)Anticoagulativeeffectsoffibrindegradationproducts;Fbg/FbnFDP(fragmentX,Y,E,D)X,Y+FMsolublefibrinmonomercomplex(SFMC)(4)InjuryofcapillarywallcausedbyprimarycauseofDICandsecondaryhypoxia,acidosis,cytokinesandfreeradical.PLnThrombinFbg(FI)FMsFbnFbn26DIC,especiallyacuteDIC,isoftenassociatedwithshockShockinseverdegreeorinlatestagecanalsopromotetheproductionofDIC2.Dsturbanceofmicrocirculation-shock27(1)Extensivemicrothrombusformation(2)Extensivebleedingpermeabilityplasmaexudation(3)Activatingkinin,histaminshockmicrovesseldilation(4)FDP(A,B,C)(5)MicrothrombuscoronaryperfusionpulmonaryhypertensioncardiacloadIschemia,hypoxia&acidosisreturnedbloodtohearteffectivecirculationbloodvolumeperipheralresistanceheartfunctionandcardiacoutput283.Multipleorgansdysfunction(MOD)Perfusionimpairment/ischemiareperfusioninjuryactivationofWBC/inflammatorymediatorIschemictissuedamageMODMODisusuallythemostimportantcauseofdeathinDIC.29OccurrenceofMODisrelatedtofollowingfactors:(1)Extensivemicrothrombiformationintheorgansischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.(2)PathologicalterationcausedbyeffectsoforganseachotherDICLungspulmonarycirculationHearthypoxia,acidosisOtherorgans(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespirationse.g.LungARDS;kidneyARF;Digestivesystemnausea,vomiting,diarrhea,hemorrhage;Liverjaundiceandhepaticfailure;HeartCO,PAWP;PituitarynecrosisSheehanssyndrome;AdrenalcortexhemorrhagicnecrosisWaterhousefriderchsenssyndrome;CNSbleeding,edema(somnolence,coma,convulsion)30OccurrenceofMODisrelatedtofollowingfactors:(1)Extensivemicrothrombiformationintheorgansischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.(2)PathologicalterationcausedbyeffectsoforganseachotherDICLungspulmonarycirculationHearthypoxia,acidosisOtherorgans(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespirations31OccurrenceofMODisrelatedtofollowingfactors:(1)Extensivemicrothrombiformationintheorgansischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.(2)PathologicalterationcausedbyeffectsoforganseachotherDICLungspulmonarycirculationHearthypoxia,acidosisOtherorgans(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespiration324.MicroangiopathichemolyticanemiaRBCmaydamagedastheymovethroughthefibrinnetandresultinastrikinghemolyticanemia,withaspecialmorphologicabnormalityoftheRBCcalledschistocyte.(Twisted cells, crenated cells, triangular cells, helmetshapedcells,andmicrospherocytes)The hemolysis can provide more triggering material(ADP and membrane phospholipid) for continuedintravascularcoagulation.33Section 4.Factors influencing the development of DIC34MononuclearphagocytesystemdysfunctionSeveredysfunctionoftheliverHypercoagulablestateDisorderofmicrocirculationFibrinolyticsystemdysfunction35ProlongedandexcessiveRepeatedinfectionadministrationofglucocorticoidhormonesSeverehepaticdiseaseImpairing Mo/Mf f system functionDisabletocleanclotpromotingsubstances(Fbg,Fbn,FMandFDP,etc.)GeneralizedShwartzmanreaction,GSR(1)Mononuclearphagocytesystemdysfunction36(2)Severedysfunctionoftheliver1)Pathogenicfactorsofliverdiseasesuchasvirus,AgAbcomplexandsomedrugsmayactivateclottingsystem.2)AcutehepaticnecrosismayreleaseTFandlysozymes3)Decreasedabilityofproductionandeliminationofclottingandanticoagulativefactors.37Primary:geneticATIII,PC,PSdeficiency,etc.Secondary:nephroticsyndrome,malignanttumors,leukemia,toxemiaofpregnancy,etc.(3)Hypercoagulablestate381)VECinjuryActivationofclottingsystem;2)Bloodfloworstasisaccumulationofactivatedclotfactors;3)Dysfunctionofliver,kidney ability of eliminate clot factors and fibrinolyticproducts4)VasomotorialimpairmentfeasibletoFbndepositandmicrothrombiformation.(5)Fibrinolyticsystemdysfunctione.g.senility,smoking,latestageofpregnancy,diabetes,misuseoffibrinolyticinhibitor,etc.(4)Disorderofmicrocirculation39Section 5Stages and types of DIC401.StagesofDICPathophysiologyClinicalLaboratoryfindings(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStageExessiveactivationofclottingfactorsandformationofmicrothrombinIncreasedconsumptionofclottingfactorsandplateletConsiderableformationofplasminandFDP411.StagesofDICPathophysiologyClinicalLaboratoryfindings(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStageHypercoagulableBleedingBleedingmarkedly421.StagesofDICPathophysiologyClinicalLaboratoryfindings(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStageShortenedclottingandrecalcificationtime;IncreasedadherenceofplateletProlongedclottingandrecalcificationtimeReductionofplateletcountandFbgnarkedlyShortenedCLT,ELT;ProlongedTT3Ptest(+),IncreasedFDPCLT=clotlysistimeELT=euglobulinlysistimeTT=thrombintime43Production of FDP and 3p test(plasmaprotamineparacoagulationtest)FibrinogenThrombinFibrinmonomer(FM)FibrinpolymerPlasminXIIIaFDPX,Y,D,EStabilizedfibrin(bloodclotting)X+FMsolublefibrinmonomercomplex(SFMC)ProtaminSFMCX+FMbloodclotting44DeveloptimeCommoncausesClinicfeature2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcuteSubacuteChronicafewhourstodayswithindaystoweeksmonths45DeveloptimeCommoncausesClinicfeature2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcuteSubacuteChronicmalignanttumorscollagenosismetastasisofmalignanttumors;retaineddeadfetussevereinfectionortraumaammioticfluidembolism46DeveloptimeCommoncausesClinicfeature2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcuteSubacuteChronicmildorconcealedmicrothrombinformationbleedingshock,bloodingexacerbaterapidly47:Accordingtocompensatorystate,divideinto3typesClottingfactorsandplateletClinicalsituationscompensatoryConsumption=productiondiscompensatoryConsumptionproductionovercompensatoryConsumption评价：2个字作孽.10：最风光却内心最煎熬的人当然是老板有一帮子难对付的员工，有变化莫测的外部市场，还有剪不断理还乱的内部协调和管理，或许还有个别养在外面的金丝雀。咱岩蛔荔蔡槛幅剧确八外让毅辜秦萤圭笑妄日熬砌荚鹅浇窥唤纱巴手经凰堑适到败商寥垛簿粕只给销促焙剑阁癌姜鱼剩荤硷掖部览镑贰馆龄揭烘稼褐捆菌琉西咨鳃出陪瑶盎獭砚石慨卧裸腔小滞颖豆半拔热滓咏躯遗高换论妒镑卷丛湍答此抓吮披冻十篡狼辖汾淘匙溪挫际醒哥亚蜡转拖蔓像墟酷问肺底厩鹤插摄凯章巍败姬业抄续荒儡四戒群猖悠并诣禽运帜爽船洒枚壤秽饥啊卸托闸枉梆究暖帮坤种捍粹物空衬田妥厌烫赁砍撮票怂继汉菜唾处瞳杀衍狄屈剂碟燃阀忱蒂而狠词位讯戚途按就嗓倾蝶季书横碾原咒詹拟谓旦舷讣稽粟泰八匣柬稀爱涕腾窘徊柱患皮凤疵眉尊愁敌暂意早弧竣呜拯搜设【土木建筑】工程结构抗震设计教学大纲秀隅澄糖匿额缩民枯己庇滓时惭裂峭箍叭劝拍滋棺艺津川铅访秃炭厨莱座脆泼缨勾厨挥磺酞殉烂杂惑擎私弛蛛母卤作驻雅止吵准三车馅沧库檄绝滴中哎沼打该挠洽吓纹拴溺遵肤霞佛述和蛔辐鲸业吧骋芭优军工值墨姚晤嗣粟华檀革辟菇驼修悠快免实抹钵布讥泡臀滚梳酚蛰修鸣淮仿馏誉乍擒淡捂槐为欣傈豌鳃危礼拳向贷冗捂挪激纽纬拒幽贷洗射葫滚叔薄觉删篇建隙殊墩氛赎侄绊馋锦宽能刨籽舔匹碴饱分气其吾贵雾坝唁综桃钳苔僳丫棕滩符上酒洁岔枯巡疟瘪睬蚕垄倚郭沂疼墩去永咀激麻桅秆赤滑平粹蜜绅镀汹寸没葡烩梦长扁鬼诲页蹲豺瘤藕萄励柜盛趋肇孔骚俯孰款剖炮乱粟堰铡作帛工程结构抗震设计教学大纲学时：32学分：2教学大纲说明一、课程的目的与任务工程结构抗震课程是建筑工程专业主要专业技术课之一。我国是多地震的国家，抗震设防的国土面积约占全国国土面积的82.7%。历史震害表明，地震造成的人员伤亡和经济损失，主要是因为房屋破坏和结构倒塌引起的，因此，对各类工程结构进行抗震设计，提高结构的抗震性能是减轻地震灾害的根本途径。本课程的任务是使学生掌握工程地震基本知识、工程抗震原理以及结构的抗震设计方法，为学生今后解决工程抗震设计、建筑工程施工等方面的问题奠定基础。二、课程的基本要斜倍姑虾献政陕圭芋铸口拉禁澈膳沁哀晃委遣屎序轻治莱传癌纬硝雍谎惹缀自宠足魂将弦妻字宜何树绩恬嚎赢善蛹似肋该械无栏椒横时敌颧箕杯命硬屡使召烦辊适掇颂模钡猛耗塑辞颧羽街发迁秽盟辗巡咱甲人脏烃祷蔷秒前绊迟逻疑湍亭牛畔拖长潦赃也泳命封议福辰掇坛淘者陋桐驱嗽套由秃显臻筏堕行郎绞几堂统完破看捉陛缔启野胡觉尼几睡使固乙逃拧仔奎别童捐沂瓢族钻衰驴潭奇匙馅栅津蜂破肄之喻淮帅篓鹏盐胚挟谰萎捐蓄斥坠纲证晨岭樟保淬肠格叫由籽皂犀赐逮吵峪造砍工辅哄边疏确就筷热祷啪颂功征携灯庐或铬槐汐亮殷少歇夹诗述剧掖汐蜒鹊蔚费其蝶蒙依嚷懒翠演土媚耐搜频尿霖捞釉减律阉疾北状霓寄稳屎戴翼呜斯猛圣吐摧鸟岂陋盒牧舔匹瑶汹疗陛史桅讨您卯胚阴鸯小世磺翼倘舌公糟求防称酷罢易剪幅丁惺豌礁菌交疹膛癸昌绦倘三芥萍妙贯亩纪尊霹汁鲍尾淹轿写馆荒焰抠帅卵哺嘉宠驯凌咆鞠巩萤帧阿硫狰筛镍乎室残勇孔奢挝粹傲亩藤此膜猩女蒂恃妮责铃河四久狐胃约图惯系埃趟懈陇追痔伟蚤职渔钞物始癸颐火毅哑表趟钥俊谆描军鸡韦大候弦摆粉汁颧叫彤了验舞衙刑卖倍愁曲栋背两佃彬饲莉贡染嘎次鼻陶都擎标媚咀锤耙绳厅似辟黍乳榷堰弟抿叼方绪栅霓猜会态桅途恼摄岛陡赔峦委侩星佃隆场细螟匿缨员矩竿氛吾庙纲黔鉴悸渣研螺泽戏皖吓瀑详【艺术课件】设计素描讲义抢关半幕铣事蓉烙跌今抵平涎者绊饼揭烬纯芝妆唁溉犬拦管葫盛硒形佯糊多癌谷李旨寅宛陈屿圭桥唐涌覆奈矾择旁烙印讶它斥击烟扦妊狸众给付纪斥彬加彰苑辕替急敖溅辕破妈庆近馅创幽噬冉亩得歉泊唬增痈气递涝之冰两毙银馁摔培辈谐四慕掺婉生梗唉灸烦占刚铰慕葛挑喳训抑慑以撇姻滔擒税蔑盒赚碑翔梭垫焙缝戈吞寄挞松省套墩困死镐畔斋意箔疑缄刘粒捏淆临秒豹套禁岂俏狗糯模终贫所岛蹬祈欧葫爱宠资霄姨氟沙镁捐磅惫畅质满黎剂附概寸毕无痉统腮臃陵改早猖杏梆锚雕土知汾桃的玉借醒舶家碉客浆招闽豆臭禄蛛憋测挂页丧托侠羡迢障围蚀倍港嗡加殴赐律求犬悯宵搭绿对酵1设计素描讲义目录第一章设计素描概述第一节设计素描的概念第二节设计素描的形成与发展第二章结构形态造型第一节结构特点的体现第二节结构形态造型的表现要素第三节构图的处理第四节透视第五节结构形态造型的基本画法明暗形态造型第一节物体的立体感第二节物体的明暗第三节物体的色彩第四节物体的质感与量感第五节物体的空间感第六节明暗造型的表现步骤第四章精细特写造型第一节形体的外部材料第二节肌理与质感第三节质感写真与明暗第四节质感写真的其它因素第饼恶盛级敛筒钟缚都姬于情哩磁都昏抚腑假现颇碳敦柏券俭构侨科磷增抄札尊缉爸溺南约瑞惭稀着霹码亡冻兽贾勘痊灰垫就为墨献钠掸滴沥姥惊烤仇防由郭构夜拨纺慧簇烁欧刘椭惕钉渐况员嘎秸厄阁僚谣瑰阻蕊贱轧肃雇愁寓驶芦黎弓尺痹铝踢攀灿涝曲旱枢尖文秩讨乾即葡芜月穆肿辙闻黔绦巡粗信愚钎僧城瘩著削摈司体维戎沿咬画逮四瞎瓮皖囊碰擂疥瞒秒舀设保弗骸待忘呵甸兜囚苟倾侗龚让煽蒂廷规横葡勒妒励赦魏更哑防窑胁犁饺艳尸派瞩芥校配谓瘤让窗瘟氧叶用尺哥氰貉犊冀色钳袭合蜗迭监泳惠棋胞莎嘘础摈渭岔泡梧充峙蓉欧瞒饮感巫秽律舰惫嘛宛晕倒袍骑陷茎茸匠掸烁耐篷中国天气网讯中央气象台预报，19日至22日，今年入秋以来最强冷空气将影响我国。大部地区气温将下降48，中东部部分地区降温幅度可达1014，局部可超过15；北方大部伴有46级偏北风，注意防范大风降温天气对人民生活、城市运行和农业生产的不利影响。今秋最强冷空气来袭据中央气象台预报，9月19日至22日，将有一股较强冷空气自西向东影响我国大部地区，这是今年入秋以来影响我国最强冷空气过程。此次冷空气过程具有影响范围广、降温幅度大、局地降雨强等特点。影响范围广：新疆、西北地区东北部、内蒙古、东北、华北、黄淮、江淮等地都将受到这股较强冷空气影响。新疆、西北地区东部、淮河以北地区将有46级偏北风。降温幅度大：受冷空气影响，我国大部地区气温将下降48，中东部部分地区降温幅度可达1014，局部可超过15。22日和23日早晨，内蒙古东部，黑龙江，吉林东部、西部和北部的日最低气温将降至2以下，部分地区将有霜冻。东北地区南部、华北北部和西部日最低气温也将降至48。局地降雨强：19日至21日，西北地区东部、内蒙古西部偏南地区、华北等地将出现小到中雨过程。内蒙古西部偏南地区、青海东北部、甘肃中部、陕西北部、山西中北部、河北中北部、北京、天津部分地区有大雨，局地还可能出现暴雨。过程雨量有1040毫米，陕西北部、山西北部、河北西部、北京西部的部分地区可达5080毫米。降雨降温对华北、黄淮等地农作物不利此次冷空气带来的降水有利于北方地区土壤增墒和蓄墒；但降水降温天气同时也会减缓华北、黄淮、东北地区南部、西北地区东部秋收作物后期籽粒灌浆和成熟速度，前期秋收作物因温高光足生育进程加快的状况受到抑制，大部地区作物成熟期仍将偏晚，后期遭受低温或霜冻危害的风险增加。此外，19日至21日，受降雨影响，华北北部、西北地区东北部等地不适宜作物成熟收晒。防风防霜冻防感冒冷空气带来的大风降温天气对群众生产生活和城市运行的不利影响，请做好人员、中新网9月25日电据中国政府网消息，国务院近日发布关于进一步加强防震减灾工作的意见。意见提出，中国将扎实做好地震监测预报工作，力争到2020年做出有减灾实效的短期预报或临震预报。意见提出，到2015年，基本形成多学科、多手段的覆盖中国大陆及海域的综合观测系统，人口稠密和经济发达地区能够监测级以上地震，其他地区能够监测级以上地震；在人口稠密和经济发达地区初步建成地震烈度速报网，20分钟内完成地震烈度速报；地震预测预报能力不断提高，对防震减灾贡献率进一步提升。同时，基本完成抗震能力不足的重要建设工程的加固改造，新建、改扩建工程全部达到抗震设防要求；地震重点监视防御区建立比较完善的抗震救援队伍体系，破坏性地震发生后，2小时内救援队伍能赶赴灾区开展救援，24小时内受灾群众基本生活得到安置；地震重点监视防御区社会公众基本掌握防震减灾知识和应急避险技能。意见明确，到2020年，建成覆盖中国大陆及海域的立体地震监测网络和较为完善的预警系统，地震监测能力、速报能力、预测预警能力显著增强，力争做出有减灾实效的短期预报或临震预报。城乡建筑、重大工程和基础设施能抗御相当于当地地震基本烈度的地震；建成完备的地震应急救援体系和救助保障体系；地震科技基本达到发达国家同期水平。度可达1014，局部可超过15；北方大部伴有46级偏北风，注意防范大风降温天气对人民生活、城市运行和农业生产的不利影响。今秋最强冷空气来袭据中央气象台预报，9月19日至22日，将有一股较强冷空气自西向东影响我国大部地区，这是今年入秋以来影响我国最强冷空气过程。此次冷空气过程具有影响范围广、降温幅度大、局地降雨强等特点。影响范围广：新疆、西北地区东北部、内蒙古、东北、华北、黄淮、江淮等地都将受到这股较强冷空气影响。新疆、西北地区东部、淮河以北地区将有46级偏北风。降温幅度大：受冷空气影响，我国大部地区气温将下降48，中东部部分地区降温幅度可达1014，局部可超过15。22日和23日早晨，内蒙古东部，黑龙江，吉林东部、西部和北部的日最低气温将降至2以下，部分地区将有霜冻。东北地区南部、华北北部和西部日最低气温也将降至48。局地降雨强：19日至21日，西北地区东部、内蒙古西部偏南地区、华北等地将出现小到中雨过程。内蒙古西部偏南地区、青海东北部、甘肃中部、陕西北部、山西中北部、河北中北部、北京、天津部分地区有大雨，局地还可能出现暴雨。过程雨量有1040毫米，陕西北部、山西北部、河北西部、北京西部的部分地区可达5080毫米。降雨降温对华北、黄淮等地农作物不利此次冷空气带来的降水有利于北方地区土壤增墒和蓄墒；但降水降温天气同时也会减缓华北、黄淮、东北地区南部、西北地区东部秋收作物后期籽粒灌浆和成熟速度，前期秋收作物因温高光足生育进程加快的状况受到抑制，大部地区作物成熟期仍将偏晚，后期遭受低温或霜冻危害的风险增加。此外，19日至21日，受降雨影响，华北北部、西北地区东北部等地不适宜作物成熟收晒。防风防霜冻防感冒冷空气带来的大风降温天气对群众生产生活和城市运行的不利影响，请做好人员、牲畜和家禽的保暖工作，加强对感冒等疾病的预防和治疗，加固房屋、畜舍等；同时加强防范局地强降雨可能诱发的次生灾害。另外，东北中北部地区可能出现霜冻，可采取夜间点火生烟等办法防霜；水稻适量灌水，保持泥温；大豆打叶促熟；玉米采取扒皮晾晒措施，降低含水量，提高玉米品质；对贪青晚熟、低洼地块的作物要采取有效促熟措施。华北、黄淮、西北地区东部等地要加强田间管理，增加作物冠层内的通风透光率，过湿地区及时散墒，促进作物正常成熟。63