简介：一种爆炸强风缓解选择由使用接球手系统增加了结构的安全。这些系统从弹道的碎片或碎片抓住或排斥窗口或填入墙保护生活和性质的失败。他们能被设计在新建设独立并且结构翻新或过去常扩充结构的变硬的技术。电报，织物，和薄计量器表钢是在过去使用的接球手系统的例子。接球手系统的一个新、演变的范畴基于能被用于墙和窗口升级的聚合材料。这些产品和设计原则为甚至更大的在里面使用性能创造设计系统的Sherwin威廉(SW)使用KCPT强风工程能力和SW材料是一个证明强风缓解概念和K&C保护的技术Pte有限公司(KCPT)。

简介：基于传统的弄平的粒子水动力学(SPH)算法，连接表搜索算法与可变变光滑长度结合了，方形的支持领域被提出改进计算效率并且保证计算精确性。一个舷侧液体舱上的高速度碎片影响的物理过程为模拟被规划。数字结果一般软件ANSYSAUTODYN与那些同意了很好，它验证数字方法的有效性和可行性。从液体舱，液体舱的宽度，和碎片的事件角度的外部板厚度的观点，保护的机制上的这些参数的影响被分析为一个舷侧液体舱的保护的设计提供一个基础。结果证明外部板厚度的影响不是明显的；因此，常规设计能在外部板的设计被采用。液体舱的宽度在碎片和液体舱的宽度的剩余速度上有大影响应该被设计在满足另外的要求的房屋下面尽可能宽。有碎片的速度变细是很明显的某个事件在角度，并且内部板附近的高压的地区是不对称的。液体舱的内部板应该根据壳形式，主要尺寸，和脆弱的点被加强。

简介：ObjectivesToinvestigatetheprotectiveeffectofthrombopoietin(TPO)onmyocardialcellsinvitro.MethodsH9C2celllinewasmaintainedinIscove’smodifiedDulbecco’smedium(IMDM)supplementedwith10%calfserum.Beatingcellsfromheartventriclesofneonatalheartwereculturedataninvitrosystem.Apoptosisofthecelllineabovewasinducedbytreatmentofdoxorubicin(DOX)andwasblockedbyTPO.CellsurvivalrateofH9C2cellwasmeasuredbytheMTTassay.Changesofbeatingrateofneonatalmyocardialcellswerecapturedbydigitalcameraandbeatingratewascalculated.Flowcytometrywasemployedtostudyanti-apoptoticeffectofTPObystainingJC-1proteintoH9C2cell.ResultsMTTassaydemonstratedthatdoxorubicinreducedcellsurvivalrateby73.8%±1.1%,50ng·mL-1and100ng·mL-1TPOincreasedcellsurvivalrateby84.6%±3.6%(P<0.05),86%±4%(P<0.01)atadose-dependentmanner.Beatingrateofprimaryneonatalmyocardialcellsalsodecreasedto15%±8%at48h,100ng·mL-1TPOimprovedbeatingrateto48%±11%(P<0.01).TPOdecreasedapoptoticratefrom19%±9%to11%±6%(P<0.05).ConclusionsTPOhasprotectiveeffectonmyocardialcellsinvitro.Anti-apoptosisisoneofthemechanismsbywhichTPOprotectsinjuredheart.

简介：Propofolcaninhibittheinflammatoryresponseandreducethesecretionandharmfuleffectsofastrocyte-derivedproinflammatorycytokines.Inthisstudy,afterpropofolwasinjectedintotheinjuredsciaticnerveofmice,nuclearfactorkappaBexpressionintheL4-6segmentsofthespinalcordintheinjuredsidewasreduced,apoptosiswasdecreased,nervemyelindefectswerealleviated,andthenerveconductionblockwaslessened.Theexperimentalfindingsindicatethatpropofolinhibitstheinflammatoryandimmuneresponses,decreasestheexpressionofnuclearfactorkappaB,andreducesapoptosis.Theseeffectsofpropofolpromoteregenerationfollowingsciaticnerveinjury.

简介：Astrategyforthesynthesisofpolymer-protectivebimetallicsolsisproposedwhichhastheadvantageofthestrongprotectiveeffectofthepolymeragentononeofthecompositestostabilizethebimetalliccolloidalparticles.Thisstrategyiscertifiedtobeusefultothepredicationoftheformationofstablebimetalliccolloidsprotectedbypolymerandtothecontroloftheparticlesizetoacertainextent.AseriesofnewPVP-protectivebimetalliccolloidaldispersionscontainingnoblemetalelement(Pt,Rh,Pd),lighttransitionmetalelement(Co,Fe),andboronareobtainedfromthecorrespondingsaltsbythemethodsofreductionbystageandcoreduction,usingtheNaBH4asreductant.TheTEM,XRDandEPMAmeasurementsindicatetheformationofbimetalliccolloids.AninterestingkindofcoilaggregationisobservedinthesystemsofPVP-Pt-CoandPVP-Rh-Copreparedbythemethodofreductionbystage.

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简介：Tostudytheinsecticidalactivityandtoxicitymechanismofspinosad,weassayedbioactivityofspinosadbyleafmembranemethodanditseffectsontheactivitiesofdetoxifyingandprotectiveenzymesinMalacosomaneustriatestacealarvaebyspectrophotometry.Theresultsshowedthatspinosadhadanextremelyhightoxicityagainstthe4thand5thinstarlarvae.TheglutathioneS-transfer(GST)activityin4thand5thinstarlarvaewasfirstlyinhibited,theninduced,andfinallyinhibited,whilethemixed-functionaloxidase(MFO)activitywasinhibitedandthenenhanced.Theinducedeffectoncarboxylesterase(CarE),theinducedandinhibitedeffectonacetylcholinesterase(AchE)andperoxidase(POD),andthecomplicatedeffectsonsuperoxidedismutase(SOD)andCatalase(CAT)weredeterminedin4thinstarlarvaewithspinosadtreatment.However,theobviousinhibitioneffectswerefoundontheactivitiesofCarE,AchE,SODandPODinthe5thinstarlarvaewhereasthecatalase(CAT)activitywasinhibited,thenincreased,andinhibitedfinally.Therefore,spinosadcouldeffectivelydisruptandinterferenotonlythedetoxifyingandprotectiveenzymesbutalsonormalphysiologicalmetabolismofM.neustriatestaceaandshowextremelyhightoxicityagainstthispest.

简介：AbstractSevere fever with thrombocytopenia syndrome (SFTS), caused by a novel identified bunyavirus SFTS virus (SFTSV), was an emerging viral infectious disease that was firstly reported in China. There are no licensed vaccines and therapeutics against SFTSV currently. B-Propiolactone (BPL) inactivated whole virions of SFTSV strain AH12 were prepared as experimental vaccine in different antigen dose with or without Al(OH)3 adjuvant. The experimental SFTS vaccine was a satisfying immunogen, which could efficiently trigger the development of high levels of SFTSV NP-specific IgG antibodies and neutralizing antibodies against SFTSV Strain HB29 in BALB/c and C57/BL6 mice, and could induce SFTS virus-specific cellular immune responses to a certain extent. A single dose of vaccine was immunogenically insufficient in BALB/c mice; the second and third dose resulted in significant boost in antibody response. The use of Al(OH)3 adjuvant resulted in higher antibody titers. The mediate-dose of vaccine could induce as high and equivalent level of antibody titer as that of high-dose. The experimental SFTS vaccine in mediate-and high antigen dose with adjuvant resulted in solid protection of C57/BL6 mice against wild-type SFTSV challenge with markedly accelerated virus clearance from blood and spleen compared with controls. The experimental SFTS vaccine prepared in this study could efficiently elicit virus specific humoral and cellular immune responses in both BALB/c and C57/BL6 mice, and could protect C57/BL6 mice against SFTS virus challenge. These results supplied evidence that inactivated vaccine was a promising vaccine candidate for the prevention of SFTSV infection.

简介：ObjectiveToinvestigatetheprotectiveeffectsofsoundconditioningagainstsubsequenthigh-levelnoisetraumainrats.MethodRatswereexposedtoa4kHzoctavebandnoiseat95dBSPLfor10hours,thentoatraumaticexposuredose(105dBSPLfor13hours)delivered12hlater.Controlanimalswereexposuredtothetraumaticdoseonly.ABRthresholdswereobtainedbeforeandafternoiseexposure.ResultAnimalsthathadbeensoundconditioneddemonstratedlessABRthresholdshiftcomparedtothosethathadnot.ConclusionModeratelevelsoundexposureappearstohaveatougheningeffectontheratcochlea(or'conditioning')leadingtodecreasedhearinglossfromsubsequenttraumaticexposure.

简介：IntroductionLightningcancausegreatdestruction.AccordingtotherecordinthenorthernChina,morethan150lightningstrokesoccuronapowersystemannually.Highvoltage(millionsofvolts)andlargecurrent(hundredsof-kA)associatedwithlightning,willdamagepropertyandevenkillpeopleandlivestocks.Itwillbeverydangerousifalightningstrokestrikesoildepotofpowerplantorsubstation.Inaddition,thehighvoltageinducedbytheelectrostaticchargegeneratedduetooilflowingwillprobablycausedamageunlesstheelectrificationhasbeenlimitedanddrainedoff.

简介：BACKGROUND:Ithasbeensuggestedthatmelatonin(MT)canprotectsecondaryneuronalinjury.However,theprotectiveeffectofMTonneuronalinjuryinischemia/reperfusionmodelsinvitrostillhasnotbeenproved.OBJECTIVE:ToinvestigatetheprotectiveeffectofMToncentralischemicinjuryofnervecellsandanalyzeitspossiblemechanism.DESIGN:Contrastobservationalstudy.SETTING:DepartmentofBiochemistryandMolecularBiology,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology.MATERIALS:Ratsaged7-8daysandweighing10-12gwereprovidedbyMedicalExperimentalAnimalCenter,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,MTwasprovidedbySigmaCompany,USA.METHODS:TheexperimentwascarriedoutintheLaboratoryofBiochemistryandMolecularBiology,TongjiHospital,HuazhongUniversityofScienceandTechnologyfromOctober2002toMarch2004.TheeffectsofMTontheneurodegenerationinducedbyoxygen-glucose-deprivation(OGD)weretestedinculturedratcerebellargranulecells.NeurondamagewasquantitativelyassessedbyTypanBlueexclusionandMTTassayatdifferenttimepointsafteroxygen-glucose-deprivation(90minutes).DNAgelelectrophoresisandacridineorangestainwereperformedtodeterminethenatureofcelldamage.Andfluorescencespectrophotometerwasusedforquantificationofintracellularmalondialdehyde(MDA)atvarioustimeintervals.MAINOUTCOMEMEASURES:Correlationbetweendegreesofneuronalinjuryandreperfusiontimes,apoptosis,andproductionofMDAincells.RESULTS:①Theneuroninjurywasaggravatedwithreperfusiontime.②TheprotectiveeffectofMTwastime-anddose-dependentwhenitsconcentrationwasnothigherthan10μmol/L.⑧WhenneuronswereexposedtoOGDfor90minutes.partofthecellsexhibitedtypicalfeaturesofapoptosis:internucleosomalDNAcondensationandDNAladderonagarosegelelectrophoresis.MTaddedtocellsrecoveringfromOGDexertedneuroprotectiveactionagainstOGD-inducedapoptosis.④InOGDexposedculture

简介：Objective:Tostudytheclinicaltherapeuticeffectofanisodamineonrespiratoryfunctionafterseverebraininjury.Methods:Ninetypatientswithrespiratorydysfunctionfollowingseverebraininjuryweredividedintotwogroups:atreatmentgroup(n=45,treatedwithroutinetherapyplusanisodamine)andacontrolgroup(n=45,treatedwithroutinetherapyonly).Thepulmonaryventilationfunctionandoxygenationfunctionwerecomparedbetweenthetwogroups.Results:Inthetreatmentgroup,12hoursaftertreatmenttherespiratoryratereduced,thepartialpressureofcarbondioxide(PCO2),thepartialpressureofoxygeninarterialblood(PaO2)andoxygenationexponentincreased,thedeadspaceventilationdoseandthepulmonaryalveolus-partialpressureofarterialoxygendifferencedecreased,andtheventilationfunctionoftherespiratorytractandpulmonaryoxygenationfunctionimproved.Therewasasignificantdifferencebetweenthetwogroups(P<0.01).Noside-effectwasfoundexceptaslightincreaseofintracranialpressureandheartrate.Conclusions:Anisodaminecanimprovepulmonaryventilationfunctionandoxygenationfunctionanddecreasetheincidenceofhypoxemiamarkedly.Itiseffectiveintreatingrespiratorydysfunctionafterseverebraininjury.

简介：这研究的目的是决定包括伪-ketoacids(伪-ketoglutarate和pyruvate)，抗氧化剂的效果喂奶并且glutamate/malate联合，对老鼠精子上的氧化应力。我们的结果显示出那H2O2(250渭molL?1)导致的损坏例如损害活动性，腺苷triphosphate(ATP)弄空，精子蛋白质phosphorylation的抑制，减少的acrosome反应和减少的生存能力，能被精子的孵化显著地与伪-ketoglutarate阻止(4mmolL?1)或pyruvate(4mmolL?1)。没有在媒介的外长的H2O2，pyruvate的增加(4mmolL?1)显著地增加了superoxide阴离子(O2?在精子暂停的路)水平(P鈮?0.01)，而伪-ketoglutarate的增加(4mmolL?1)并且喂奶(4mmolL?1)有95kDa的尺寸的显著地提高的tyrosine-phosphorylated蛋白质(P鈮?0.04)。同时，伪-ketoglutarate，pyruvate，喂奶，在媒介补充的glutamate和malate能为精子活动性被用作重要精力来源和供应ATP。在结论，现在的结果证明伪-ketoacids能是为保护老鼠精子免受H2O2攻击的伤害的有效抗氧化剂并且能是有效部件改进Biggers，Whitten和Whittingham媒介的抗氧化剂能力。

简介：二indica米饭(OryzasativaL.)材料，XieqingzaoB(对热应力敏感)并且082(对热应力容忍)，被用来从热应力在稻秧的保护学习brassinolide(BR)的角色。幼苗受到高温(38degC/30degC)并且与0.005喷洒了BR的mg/L。分析在叶绿素，蛋白质和malondialdehyde(MDA)的内容上被进行，电解质，过氧化物酶(邮政部门)的活动和超级氧化物dismutase(草皮)和他们的isozymes表示的漏在叶子铺平。在高温处理下面，BR的申请显著地增加了叶绿素和蛋白质的内容，和邮政部门和草皮的活动，并且在热敏感的材料XieqingzaoB的叶子减少了MDA和电解质的漏的内容，而BR热容忍的材料在那些上有更少的效果082相对。BR处理在两材料的叶子提高了邮政部门isozymes的表示。在高温压力和BR处理下面，在082减少的四草皮isozymes的表示，而是二草皮isozymes的表示在XieqingzaoB增加了。这建议BR由在叶子提高这些活动或防御性酶的表示水平从热应力在稻秧的保护起一个重要作用。有各种各样的热忍耐的材料可能在反应的机制不同用BR申请加热应力。

简介：Somefactorssuchascontinuouspricefallingofrareearthconcentrates,increaseinproductioncostandincreasinginvestmentinsafetyandenvironmentalprotectionpreventedthedevelopmentofminingindustry.Tosafeguardtheinterestsofminingcompaniesandfacilitatethehealthydevelopmentofrareearthindustry,REMiningSocietyofMianningCountyheldageneralmeetingrecently.FollowingresolutionswerepassedonJuly13th:1.SinceJuly14th2005,thelowestprotectivemarketpricesofrareear...

简介：Theaimofthisstudyistoexpressthereceptor-bindingdomainofBacillusanthracisprotectiveantigeninE.coli.SignalsequenceoftheoutermembraneproteinA(OmpA)ofE.coliwasattachedtothe5'endofthegeneencodingprotectiveantigenreceptor-bindingdomain(the4^thdomainofPA,PALM).TheplasmidcarryingthefusiongenewasthentransformedintoE.coliandinducedtoexpressrecombinantPAlMbyIFFG.TherecombinantproteinwaspurifiedbychromatographyandthenidentifiedbyN-terrainalsequencingandWesternblot.Therecombinantprotein,about10%ofthetotalbacterialproteininvolume,wassecretedtotheperiplasmicspaceofthecell.Afterapurificationprocedureincludingionexchangechromatographyandgelfiltration,about10mgofhomogenousrecombinantPAD4wasobtainedfrom1Lculture.DatafromN-terminalsequencingsuggestedthattheaminoacidsequenceofrecombinantPAD4wasidenticalwithitsnaturalcounterpart.AndtheresultofWesternblotshowedtherecombinantproteincouldbindwithanti-PAserumfromrabbit.HighlevelsecretedexpressionofPAD4wasobtainedinE.coli.TheresultsreportedherearepartsofacontinuingresearchtoevaluatePAD4asapotentialdrugforanthraxtherapyoracandidateofnewvaccine.

简介：Propofolpreconditioninghasbeenshowntoprovideneuroprotectionagainstspinalischemia/reperfusioninjury.Inthisstudy,spinalcordischemia/reperfusioninjurywasinducedbyblockingtheabdominalaortainrabbitsfor40minutes.Resultsshowedthattheco-applicationofpropofolpreconditioningandpostconditioningregimenamelioratedpathologicalinjuryoftheischemicspinalcordandsuppressedtheelevationofmalondialdehydelevelsandincreasedsuperoxidedismutaseactivitiesinthespinalcordtissues.Co-applicationofpropofolpreconditioningandpostconditioningresultedinpotentprotectiveeffectsagainstspinalcordischemia/reperfusioninjuryandprolongedthespinalcord'stolerancetoischemia.Thisprotectionwasassociatedwiththeanti-lipidperoxidationcapacityofthespinalcordtissues.

简介：ObjectivesToinvestigatetheeffectoftelmisartanonhumanumbilicalveinendothelialcells(HUVEC)exposedtohighglucoseinvitroandtherelatedmechanism.MethodsHUVECswereincubatedwithtelmisartanandglucose(5mmol/L,30mmol/L)at0h,12h,24h,36h,48h,respectively.Thelevelofmalondialdehyde(MDA)andsuperoxidedismutase(SOD)inthesupernatantofculturedendothelialcellswasmeasuredbythiobarbituricacidtestandxanthineoxidasetest.TheexpressionofPPAR-γwasdeterminedat24hourwithWesternblottechnique.ResultsWhentheendothelialcellswereculturedinhighglucoseenvironment,theMDAlevelwassignificantlyincreased,buttheSODactivityandtheproteinexpressionofPPAR-γweremarkedlydecreased.However,thehighglucose-inducedeffectswereinhibitedbytelmisartanintervention.ConclusionTelmisartancandecreaseoxidativestressandincreasePPAR-γexpressionofendothelialcellsinhighglucoseenvironment.

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

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