简介：Thesubsea动态起床人底(SDRB)是为漂浮的生产站台绳索系统的设备的一重要的片。一结束被连接，带热扩大负担和其它结束的一条僵硬管道，带灵活起床人的动态负担僵硬管道被连接到一个灵活起床人，它的功能因此是在灵活起床人和在海床上修理灵活起床人的僵硬管道之间的一个转变连接。作为一个典型subsea产品，在另一方面，设计将为subsea产品满足标准的要求。由学习尖的干舷和subsea管道的压力analysisphilosophy，为SDRB的尖压力分析的一个物理模型和过程被建立了。负担被考虑了的不利设计的条件，和从僵硬管道和动态负担灵活性的静态的负担的联合也被优化了。并且在为有检查规则的尖应力的AMSE，DNV和API标准之间的比较分析被做了。因为SDRB属于subsea管道终端产品，DNV标准的使用尖应力被推荐检查它的进程。最后，这个过程SDRB的尖应力被计算了，并且结果证明夹克衫管子和SDRB的搬运人管子压力处理尖当whole.The舱壁不能被在详细分析使用FEA软件ANSYS的AutoPIPE软件精确地模仿，满足DNV标准，但是检查结果将仍然满足DNV标准的要求。

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简介：Theapplicabilityandlimitationofseveralquadraticstrengththeorieswereinvestigatedwithrespectto2D-C/SiCand2.5D-C/SiCcomposites.Akindofdamage-basedfailurecriterion,referredtoasD-criterion,isproposedfornonlinearceramiccomposites.Meanwhile,thenewlydevelopedcriterionispreliminarilyvalidatedundertension-shearcombinedloadings.ThepredictionshowsthatthefailureenvelopegivenbyD-criterionislowerthanthatfromTsai–HillandHoffmancriteria.Thisrevealsthatthedamage-basedcriterionisreasonableforevaluationofdamage-dominatedfailurestrength.

简介：TheGermanwaltzingguineapigisastrainofanimalsexpressingdeafnessandseverebalancedisordersatbirth.ThemutationarosespontaneouslyinabreedingfacilityinGermanyandastheaffectedanimalsshowacharacteristicwaltzingbehavior,thestrainisnamedtheGermanwaltzingguineapig.ThestrainispresentlybredonlyatKarolinskaInstitutet.Thehereditaryinnerearimpairmenthasarecessivemodeofinheritanceandthestrainthusproducesnotonlyaffectedhomozygotesbutalsosymptom-freeheterozygotesandfullynormaloffspring.Theoutcomedependssolelyonthegenotypeoftheparents.Theheterozygotes,whichhaveobtainedthe'waltzing'genefromoneparentonly,havenormalhearingandnobalancedysfunction.Theheterozygousanimalsappearnormalbutwill,inturn,carrythegeneticdefecttothenextgeneration.Thepresentthesisisfocusedontheseanimals.Noiseandototoxicdrugsarewellknownstressfactorsthatinterferenegativelywiththehearingorganinbothhumansandanimals,causinghearingimpairment.However,theinter-individualvariabilityinsusceptibilitytoauditorystressfactorsissurprisinglylarge,mostlikelyduetodifferentgeneticpredisposition.Inthisstudy,heterozygousanimalsoftheGermanwaltzingguineapig,animalscarryingageneticdefectknowntocauseseverehearingimpairment,wereusedtostudyhowanunexploredgenefordeafnessinteractswithauditorystressagents,i.e.noiseexposureandtheototoxicdrugsgentamicinandcisplatin.AnimalswereexposedtobothnarrowbandaswellasbroadbandnoiseatdifferentagesandhearingthresholdsweremeasuredusingABRs.HeterozygotesoftheGermanwaltzingguineapigshowedlessthresholdshiftscomparedtocontrolstrains.Olderanimalswerelessaffectedbythenoisetraumathanyoungeranimals.Totestthehypothesisthattheefferentsystemcontributestoprotectionoftheinnerearagainstnoisetrauma,measurementsusinganewmethodofpostonsetadaptationofDPOAEsandmaximumadaptationmagnitudewereconducted.T

简介：现在的工作解释限制为长棱柱的堆的自我重量传播的静电干扰在休息的一个角度倾向了并且相称性地在一个僵硬的底上形成了。有沿着斜坡表面的应力的动员状态的极化的主要的轴的闭合被在平衡方程上强加主要压力的取向采用。比较用一个有弹性的模型基于有限元素方法随计算被做。而且，在一个矩形的僵硬的底上扔的沙堆的实验被进行验证理论学习。测量压力侧面通常与理论结果同意了很好。

简介：Themicrostructureofstress-inducedmartensite(SIM)inthenanocrystallineNiTialloywasinvestigatedbymeansoftransmissionelectronmicroscopy(TEM).Theresultshowsthatthemulti-variantstructureofthemartensiteissuppressedandonlysingle-variantmartensitictwinsformaftertensiledeformationwhenthegrainsizeissmallerthan80nm.Thenormaldirectionsofthe(001)B190twinplanesareallwithintherangeof45°fromtheaxialdirectionofthewire.Theanglebetweentwincrystals(1'11)Mand(111)ToftheSIMisalsofoundtobesmallerthanthatofthermallyinducedmartensiteinnanocrystallineNiTi.

简介：ThispapercalculatesthestaticCoulombstresschangesgeneratedbyfourearthquakesintheYutianareaduring2008~2014separately,thendiscussesthetriggeringinfluence,theiraccumulatedCoulombstresschangesandtheirinfluenceonnearbyfaults.TheresultsindicatethattheMS5.5earthquakein2011andtheM_S7.3earthquakein2014arebothintheregionswheretheCoulombstresschangeispositive,thestresschangesare0.004MPaand0.021MPa,respectively,meaningtheyaretriggeredbypriorearthquakes.TheMS6.2earthquakein2012occurredintheplacewhereCoulombstresschangewasnegative,soitispostponedbythepriorearthquakes.TheimageofCoulombstresschangesoftheMS7.3earthquakein2014isinaccordwithaftershocks(ML≥3.0)distribution,butsomeregionsonthefaultwheretheCoulombstresschangeispositivehavefewaftershocks,andstrongaftershocksmayoccuratthesedistrictsinfuture.Inaddition,thispapercalculatestheCoulombstresschangeonnearbyfaults,andfindsthattheCoulombstresschangesofdifferentelementsintheGGCfaultareverydifferent,andmustreceivestrongtriggered-influence,thoughtheresultmaybeinfluencedbytheinputfinitefaultmodel,sothereisstillalargeearthquake-risk.TheGGN,PLC,PLWandLBWfaultswerealsotriggeredbythefourearthquakesoccurringbetween2008~2014.TheirmaximumCoulombstresschangesallexceed0.002MPa,sotheyalsohaveastrongearthquakehazard.

简介：Oxidativestressiscloselyassociatedwithsecondarycelldeathinmanydisordersofthecentralnervoussystemincludingstroke,Parkinson’sdisease,Alzheimer’sdisease.Amongmanyaberrantoxidativestress-associatedproteins,DJ-1hasbeenassociatedwiththeoxidativestresscelldeathcascadeprimarilyinParkinson’sdisease.Althoughprincipallyexpressedinthecytoplasmandnucleus,DJ-1canbesecretedintotheserumunderpathologicalcondition.Recently,aclosepathologicalassociationbetweenDJ-1andoxidativestressinstrokehasbeenimplicated.Tothisend,weandothershavedemonstratedtheimportantroleofmitochondriainneuroprotectionforstrokebydemonstratingthatthetranslocationofDJ-1inthemitochondriacouldpotentiallymitigatemitochondrialinjury.Here,wediscussourrecentfindingstestingthehypothesisthatDJ-1notonlyfunctionsasaformofintracellularprotectionfromoxidativestress,butthatitalsoutilizesparacrineand/orautocrinecuesinordertoaccomplishextracellularsignalingbetweenneighboringneuronalcells,resultinginneuroprotection.ThisarticlehighlightsrecentevidencesupportingthestatusofDJ-1askeyanti-oxidativestresstherapeutictargetforstroke.

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简介：Residualstressevolutionregularityinthermalbarrierceramiccoatings(TBCs)underdifferentcyclesofthermalshockloadingof1100℃wasinvestigatedbythemicroscopicdigitalimagecorrelation(DIC)andmicro-Ramanspectroscopy,respectively.Theobtainedresultsshowedthat,asthecyclenumberofthethermalshockloadingincreases,theevolutionoftheresidualstressundergoesthreedistinctstages:asharpincrease,agradualchange,andareduction.TheextensionstressneartheTBCsurfaceisfasttransformedtocompressiveonethroughjustonethermalcycle.Afterdifferentthermalshockcycleswithpeaktemperatureof1100℃,phasetransformationinTBCdoesnothappen,whereasthegeneration,development,evolutionofthethermallygrownoxide(TGO)layerandmicro-cracksarethemainreasonscausingtheevolutionregularityoftheresidualstress.

简介：Thedynamicmicrocosmswereusedtoevaluatetheeffectofoilspillsonmicrobialecologicalsysteminmarinesedimentandtheenhancementofnutrientontheoilremoval.ThefunctionandstructureofmicrobialcommunitycausedbytheoilpollutionandphosphatedosageweresimultaneouslymonitoredbydehydrogenaseactivityassayandPCR-denaturinggradientgelelectrophoresis(DGGE)techniques.Theresultsindicatedthattheamountoftotalbacteriainalldynamicmicrocosmsdeclinedrapidlywithincubationtime.Thenumberofpetroleum-degradingbacteriaandtheactivityofsedimentdehydrogenaseweregraduallyenhancedbypetroleumintheoil-treatedmicrocosms,whiletheybothshowednoobviousresponsetophosphatedosage.Incomparison,phosphatespikedheterotrophicbacteriaandtheyshowedasignificantincreaseinamount.DGGEprofilesindicatedthatpetroleumdosagegreatlychangedcommunitystructure,andthebacteriabelongedtoclassDeltaproteobacteria,andphylaBacteroidetesandChlorobiwereenriched.Thisstudydemonstratedthatpetroleuminputgreatlyimpactedthemicrobialcommunitystructureandconsequentlythemarinesedimentpetroleum-degradingactivitywasenhanced.Phosphatedosagewouldmultiplyheterotrophicbacteriabutnotsignificantlyenhancethepetroleumdegradation.

简介：Basedonatomicforcemicroscopytechnique,wefoundthatthechondrocytesexhibitsstressrelaxationbehavior.Weexploredthemechanismofthisstressrelaxationbehaviorandconcludedthattheintracellularfluidexudingoutfromthecellsduringdeformationplaysthemostimportantroleinthestressrelaxation.Weappliedtheinversefiniteelementanalysistechniquetodeterminenecessarymaterialparametersforporohyperelastic(PHE)modeltosimulatestressrelaxationbehaviorasthismodelisprovencapableofcapturingthenon-linearbehaviorandthefluid-solidinteractionduringthestressrelaxationofthesinglechondrocytes.ItisobservedthatPHEmodelcanpreciselycapturethestressrelaxationbehaviorofsinglechondrocytesandwouldbeasuitablemodelforcellbiomechanics.

简介：Vibrationfatigueisthemainfailuremodeofcompressorblade.Evaluatingthevibrationstressofbladethatleadstocrackingisveryusefulforanalysisofvibrationfatigue.Inthispaper,fatiguestressestimationmethodsbyquantitativefractographywerestudiedthroughexperimentalbladeandin-servicefirst-stagecompressorbladeinordertoevaluatetheinitiationvibrationstressofin-serviceblade.Theanalysisprocessofinitiationvibrationstresswasestablished.Theevaluatingresultofvibrationstressofin-servicebladesubjectedtocentrifugalforceandbendingvibrationstressagreeswithaeroenginetestresult.Itisshownthattheevaluationmethodcannotonlyevaluatetheequivalentfatiguestressesofdifferentcrackdepthsbutalsoyieldtheinitiationequivalentfatiguestress.

简介：我们在单轴的弯曲负担下面在Ｔ形榫眼和松开的雄榫(M<)家具关节在应力和紧张分布上学习了松开的雄榫尺寸的效果，并且决定了松开的雄榫长度的效果(30，45，60，并且90公里)并且把M<关节的时刻能力弄弯上的松开的雄榫厚度(6和8公里)与聚乙烯化合物的醋酸盐(PVAc)构造了粘合剂。在联合元素的压力和紧张分布然后为每个联合使用ANSYS有限元素(FE)被估计软件。关节的弯曲时刻能力与雄榫的厚度和长度显著地增加了。基于FE分析结果，在单轴的弯曲下面，最高砍压力价值在雄榫的中间的部分被获得，当时最高砍有弹性的紧张价值在在雄榫表面和榫眼的墙之间的胶水线被估计。砍强调在联合元素的有弹性的紧张价值通常与雄榫尺寸和相应弯曲时刻能力增加了并且砍。在预言的最大值之间有一致性砍关节的压力价值和失败模式。

简介：Zygosaccharomycesrouxiiisasalt-tolerantyeastspeciescapableofremovingcadmium(Cd)pollutantfromaqueoussolution.Presently,thephysiologicalcharacteristicsofZ.rouxiiunderthestressofsodiumchloride(NaCl)andCdarepoorlyunderstood.ThisstudyinvestigatedtheeffectsofNaClandCdonthegrowth,oxidativestressandantioxidantenzymeactivitiesofZ.rouxiiafterstresstreatmentfor24h.ResultsshowedthatNaClorCdalonenegativelyaffectedthegrowthofZ.rouxii,butthegrowth-inhibitingeffectofCdonZ.rouxiiwasreducedinthepresenceofNaCl.FlowcytometryassayshowedthatunderCdstress,NaClsignificantlyreducedtheproductionofreactiveoxygenspecies(ROS)andcelldeathofZ.rouxiicomparedwiththoseintheabsenceofNaCl.Theactivitiesofsuperoxidedismutase(SOD),catalase(CAT),andperoxidase(POD)ofZ.rouxiiweresignificantlyenhancedby2%–6%NaCl,whichlikelycontributedtothehighsalttoleranceofZ.rouxii.ThePODactivitywasinhibitedby20mgL-1CdwhiletheSODandCATactivitieswereenhancedby8mgL-1Cdandinhibitedby20mgL-1or50mgL-1Cd.Theinhibitoryeffectofhigh-levelCdontheantioxidantenzymeactivitiesofZ.rouxiiwascounteractedbythecombineduseofNaCl,especiallyat6%.ThisprobablyaccountedforthedecreaseinCd-inducedROSproductionandcelldeathofZ.rouxiiafterincubationwithNaClandCd.OurworkprovidedphysiologicalcluesastotheuseofZ.rouxiiasabiosorbentforCdremovalfromseawaterandliquidhighlysaltyfood.

简介：Inthepresentstudy,artificialneuralnetwork(ANN)approachwasusedtopredictthestress–straincurveofnearbetatitaniumalloyasafunctionofvolumefractionsofaandb.Thisapproachistodevelopthebestpossiblecombinationorneuralnetwork(NN)topredictthestress–straincurve.Inordertoachievethis,threedifferentNNarchitectures(feed-forwardback-propagationnetwork,cascade-forwardback-propagationnetwork,andlayerrecurrentnetwork),threedifferenttransferfunctions(purelin,Log-Sigmoid,andTan-Sigmoid),numberofhiddenlayers(1and2),numberofneuronsinthehiddenlayer(s),anddifferenttrainingalgorithmswereemployed.ANNtrainingmodules,theloadintermsofstrain,andvolumefractionofaaretheinputsandthestressasanoutput.ANNsystemwastrainedusingthepreparedtrainingset(a,16%a,40%a,andbstress–straincurves).Aftertrainingprocess,testdatawereusedtochecksystemaccuracy.Itisobservedthatfeed-forwardback-propagationnetworkisthefastest,andLog-Sigmoidtransferfunctionisgivingthebestresults.Finally,layerrecurrentNNwithasinglehiddenlayerconsistsof11neurons,andLog-Sigmoidtransferfunctionusingtrainlmastrainingalgorithmisgivinggoodresult,andaveragerelativeerroris1.27±1.45%.Intwohiddenlayers,layerrecurrentNNconsistsof7neuronsineachhiddenlayerwithtrainrpasthetrainingalgorithmhavingthetransferfunctionofLogSigmoidwhichgivesbetterresults.Asaresult,theNNisfoundedsuccessfulforthepredictionofstress–straincurveofnearbtitaniumalloy.

简介：Ingeneral,earthquakecyclerelatedtoearthquakefaultingcouldincludefourmajorprocesseswhichcouldbedescribedby(1)faultlocking,(2)self-accelerationornucleation(possibleforeshocks),(3)coseismicslip,and(4)post-stressrelaxationandafterslip.Asuddenstaticstresschange/perturbationinthesurroundingcrustcanadvance/delaythefaultinstabilityorfailuretimeandmodifyearthquakerates.Basedonasimpleone-dimensionalspring-sliderblockmodelwiththecombinationofrate-and-statedependentfrictionrelation,inthisstudy,wehaveapproximatelyderivedthesimpleanalyticalsolutionsofclockadvance/delayoffaultfailurescausedbyasuddenstaticCoulombstresschangeappliedinthedifferenttemporalevolutionperiodsduringanearthquakefaulting.Theresultshavebeenusedinthephysics-basedexplanationofdelayedcharacteristicearthquakeinParkfieldregion,California,inwhichthenextcharacteristicearthquakeofM6.0after1966occurredin2004insteadofaround1988accordingtoitscharacteristicreturnperiodof22years.Atthesametime,theanalyticalsolutionsalsoindicatethatthetimeadvance/delayinCoulombstresschangederivedbythedislocationmodelhasacertainlimitationandfundamentalflaw.Furthermore,wediscussedtheessentialdifferencebetweenrate-andstate-variableconstitutive(R–S)modelandCoulombstressmodelusedcommonlyincurrentearthquaketriggeringstudy,anddemonstratedthat,infact,theCoulombstressmodelcouldbeinvolvedintheR–Smodel.Theresults,wehaveobtainedinthisstudy,couldbeusedinthedevelopmentoftime-dependentfaultinteractionmodelandtheprobabilitycalculationrelatedtothetime-dependentandrenewalearthquakepredictionmodel.

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简介：Freeradicalsinducedbytraumaticbraininjuryhavedeleteriouseffectsonthefunctionandantioxidantvitaminlevelsofseveralorgansystemsincludingthebrain.Melatoninpossessesantioxidanteffectonthebrainbymaintainingantioxidantenzymeandvitaminlevels.Weinvestigatedtheeffectsofmelatoninonantioxidantabilityinthecerebralcortexandbloodoftraumaticbraininjuryrats.Resultsshowedthatthecerebralcortexβ-carotene,vitaminC,vitaminE,reducedglutathione,anderythrocytereducedglutathionelevels,andplasmavitaminClevelweredecreasedbytraumaticbraininjurywhereastheywereincreasedfollowingmelatonintreatment.Inconclusion,melatoninseemstohaveprotectiveeffectsontraumaticbraininjury-inducedcerebralcortexandbloodtoxicitybyinhibitingfreeradicalformationandsupportingantioxidantvitaminredoxsystem.