简介：Mostmigrainepatientssufferfromcutaneousallodynia;however,theunderlyingmechanismsareunclear.Calcitoningene-relatedpeptide(CGRP)playsanimportantroleinthepathophysiologyofmigraine,anditistherefore,apotentialtherapeutictargetfortreatingthepain.Inthepresentstudy,aratmodelofconsciousmigraine,inducedbyrepeatedelectricalstimulationofthesuperiorsagittalsinus,wasestablishedandtreatedwithelectroacupunctureatFengchi(GB20)(depthof2–3mm,frequencyof2/15Hz,intensityof0.5–1.0mA,15minutes/day,for7consecutivedays).ElectroacupunctureatGB20significantlyalleviatedthedecreaseinhindpawandfacialwithdrawalthresholdsandsignificantlylessenedtheincreaseinthelevelsofCGRPinthetrigeminalganglion,trigeminalnucleuscaudalisandventroposteriormedialthalamicnucleusinratswithmigraine.NoCGRP-positivecellsweredetectedinthetrigeminalnucleuscaudalisorventroposteriormedialthalamicnucleusbyimmunofluorescence.Ourfindingssuggestthatelectroacupuncturetreatmentamelioratesmigrainepainandassociatedcutaneousallodyniabymodulatingthetrigeminovascularsystemascendingpathway,atleastinpartbyinhibitingCGRPexpressioninthetrigeminalganglion.

简介：Asingeniousasnature'sinventionofmyelinsheathswithinthemammaliannervoussystemis,asfatalcanbedamagetothisspecializedlipidstructure.Long-termlossofelectricalinsulationandoffurthersupportivefunctionsmyelinprovidestoaxons,asseenindemyelinatingdiseasessuchasmultiplesclerosis(MS),leadstoneurodegenerationandresultsinprogressivedisabilities.Multiplelinesofevidencehavedemonstratedtheincreasinginabilityofoligodendrocyteprecursorcells(OPCs)toreplacelostoligodendrocytes(OLs)inordertorestorelostmyelin.Muchresearchhasbeendedicatedtorevealpotentialreasonsforthisregenerationdeficitbutdespitepromisingapproachesnoremyelination-promotingdrugshavesuccessfullybeendevelopedyet.InadditiontoOPCsneuralstemcellsoftheadultcentralnervoussystemalsoholdahighpotentialtogeneratemyelinatingOLs.Thereareatleasttwoneuralstemcellnichesinthebrain,thesubventricularzoneliningthelateralventriclesandthesubgranularzoneofthedentategyrus,andanadditionalsourceofneuralstemcellshasbeenlocatedinthecentralcanalofthespinalcord.Whileasubstantialbodyofliteraturehasdescribedtheirneurogeniccapacity,stilllittleisknownabouttheoligodendrogenicpotentialofthesecells,evenifsomeanimalstudieshaveprovidedproofoftheircontributiontoremyelination.Inthisreview,wesummarizeanddiscussthesestudies,takingintoaccountthedifferentniches,theheterogeneitywithinandbetweenstemcellnichesandpresentcurrentstrategiesofhowtopromotestemcell-mediatedmyelinrepair.

简介：Therewasasurgeinpublishedresearchrelatedtobarefootrunninginthepast2decades,andespeciallyinthepast5years.Forexample,thenumberofreturnsfor'barefootrunning'inGoogleScholarincreaseddramaticallyrelativetothesearchreturnsfor'running'(Fig.1).'Running'relatedreturnsstartedatabout220,000in1997andpeakedatabout376,000in2007(a0.7timesincrease)andgraduallydecreasedtolessthan

简介：这篇文章介绍黑暗的事的搜索的地位的广泛的评论。开始的八节在黑暗中被奉献给话题物质和它的试验性的搜索，和剩余的到在天体物理学和宇宙论选择了话题，它被打算在粒子物理为学生供应一些需要的背景。节9和13是介绍的宇宙论。三个天体物理学的话题，大巨响nucleosynthesis节10，Boltzmann搬运方程并且都从巨大的粒子节11，和CMBanisotropy节12罐头结冰当合理近似被做时，在分析途径被学习。他们的原来的经分解形式，这篇文章很仔细列在后面到，被粒子物理学家给。黑暗物质是要求及时更改保持当前的一个演变题目。当它出现在出版时，因此如此的一个主题的评论将无疑有一些东西想要。这评论能为想追求黑暗物质的题目的那些研究生形成一个谦卑基础，这被希望。读者能使用广泛的目录看见材料在文章盖住的insomedetails。

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简介：Inthispaper,theperformancecharacteristicsofASTMA19QS31803andASTMA1S2F51duplexstainlesssteelwereintroduced,andtheweldabilitieswereanalyzed.Theweldingrepairproceduresofthickwallduplexstainlesssteelweredevelopedbyweldingprocedurequalification.Researchshowsthattherepairweldinghaslesseffectonmechanicalpropertiesofweldedjointsandgreatinfluenceonphaseproportionsandpittingcorrosionresistance.Thetestresultsmeettherequirementsofprojectspecifications.Therepairweldingprocedurecanbeusedinproject,andonlyonetimerepairshallbeused.

简介：Thereliabilityoftheproductsoldunderawarrantyisusuallymaintainedbythemanufacturerduringthewarrantyperiod.Aftertheexpiryofthewarranty,however,theconsumerconfrontsaproblemabouthowtomaintainthereliabilityoftheproduct.Thispaperproposes,fromtheconsumer’sperspective,areplacementpolicyaftertheextendedwarranty,undertheassumptionthattheproductissoldundertherenewablefreereplacementwarranty(RFRW)policyinwhichthereplacementisdependentontherepair-costthreshold.Theproposedreplacementpolicyisthereplacementaftertheextendedwarrantyisperformedbytheconsumerbasedontherepair-costthresholdorpreventivereplacement(PR)age,whicharedecisionvariables.Theexpectedcostratemodelisderivedfromtheconsumer’sperspective.Theexistenceanduniquenessoftheoptimalsolutionthatminimizestheexpectedcostrateperunittimeareoffered.Finally,anumericalexampleispresentedtoexemplifytheproposedmodel.

简介：

简介：Inthisstudy,threerapidrepairtechniquesareproposedtoretrofitcircularbridgepiersthatareseverelydamagedbytheflexuralfailuremodeinmajorearthquakes.Thequasi-statictestsonthree1:2.5scaledcircularpierspecimensareconductedtoevaluatetheefficiencyoftheproposedrepairtechniques.Forthepurposeofrapidrepair,therepairprocedureforallthespecimensisconductedwithinfourdays,andthebehavioroftherepairedspecimensisevaluatedandcomparedwiththeoriginalones.Afiniteelementmodelisdevelopedtopredictthecyclicbehavioroftherepairedspecimensandthenumericalresultsarecomparedwiththetestdata.Itisfoundthatalltherepairedspecimensexhibitsimilarorlargerlateralstrengthanddeformationcapacitythantheoriginalones.Theinitiallateralstiffnessofalltherepairedspecimensislowerthanthatoftheoriginalones,whiletheyshowahigherlateralstiffnessatthelaterstageofthetest.Nonoticeabledifferenceisobservedfortheenergydissipationcapacitybetweentheoriginalandrepairedpierspecimens.Itissuggestedthattherepairtechniqueusingtheearly-strengthconcretejacketconfinedbycarbonfiberreinforcedpolymer(CFRP)sheetscanbeanoptimalmethodfortherapidrepairofseverelyearthquake-damagedcircularbridgepierswithflexuralfailuremode.

简介：Inflammationafterstrokeisthemaincauseofcerebralischemia/reperfusioninjury.Cascadingeventsafterinjurycanleadtocelldeath.Heatshockprotein70andotherendogenousinjury-signalingmoleculesarereleasedbydamagedcells,whichcanleadtosystemicstressreactions.Protectingthebrainthroughrepairbeginswiththestress-injury-repairsignalingchain.Thisstudyaimedtoverifywhetheracupunctureactsthroughthischaintofacilitateeffectivetreatmentofischemicstroke.Ratmodelsofcerebralischemia/reperfusioninjurywereestablishedbyZeaLonga'smethod,andinjurysiteswereidentifiedbyassessingneurologicalfunction,2,3,5-triphenyltetrazoliumchloridestaining,andhematoxylin-eosinstaining.ElectroacupunctureatacupointsBaihui(DU20)andZusanli(ST36)wasperformedinthemodelratswithdilatationalwaves,deliveredfor20minutesadayat2–100Hzandanamplitudeof2mA.Weanalyzedthebloodserumfromtheratsandfoundthatinflammatorycytokinesaffectedthelevelsofadrenotrophinandheatshockprotein70,eachofwhichfollowedasimilarbimodalcurve.Specifically,electroacupunctureloweredthepeaklevelsofadrenocorticotrophichormoneandheatshockprotein70.Thus,electroacupuncturewasabletoinhibitexcessivestress,reduceinflammation,andpromotetherepairofneurons,whichfacilitatedhealingofischemicstroke.

简介：Thepapergivesananalysisontechnicalcharacteristicsofrepairtechniquesforfrictionstirweldingdefects.Toovercomethedefects,anewrepairtechnique,inertiafrictionpullplugwelding(IFPPW),wasresearchedanditsequipmentwasdevelopedaswell.ElementarydatumwasachievedbyinvestigatingtheinfluencesoftechnologicalparametersonmechanicalpropertiesandbyanalyzingthestructuralcharacteristicsofrepairjointwithIFPPW.ThestudyshowsthatthestabilityandreliabilityofweldingprocessofIFPPWcanbeguaranteedthroughtheconstantenergyfromtheflywheel.Integratedwiththeadvantagesoffrictionpullplugwelding,theIFPPW,freefrombackanvil,isconsideredasapromisingtechniqueinrepairofterminationkeyholeofbobbintoolfrictionstirweldingandpoint-likedefectsinaluminumalloywelding.

简介：AIMTo鉴别在透明婴儿透镜和先天的cataract.METHODSLens相关的miRNAs的中央上皮的透镜相关的microRNAs(miRNAs)的表示从PubMed被检索数据库。在透明婴儿透镜和先天的奔流的这些miRNAs的表示层次被茎环颠倒抄写聚合酶链反应(RT-PCR)决定。人权保护的算法被用来预言这些差别的目标基因表示了miRNAs。目标mRNA是validated.RESULTSSix透镜相关的miRNAs从屏蔽PubMed被检索数据库。在透明婴儿透镜的最丰富的miRNA根据茎环RT-PCR是miR-184。miR-182在先天的奔流是起来调整的。相反地，miR-204和miR-124是下面调整的。miR-204比miR-124在表示展出了更重要的减少。另外，Meis2被预言是用人权保护的算法的miR-204的目标。miR-204mimic/antagomirtransfection实验建议了在miR-204的表示之间的否定关联，建议他们在先天的奔流的致病的参与并且miR-182，miR-204和miR-124的Meis2.CONCLUSIONThe表示层次在透明婴儿透镜和先天的奔流的中央上皮之间不同。miR-204可以经由silencingMeis2行动调整透镜开发和先天的奔流形成。

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简介：Leber'scongenitalamaurosis(LCA)andrecentgenetherapyadvancementfortreatinginheritedretinopathieswereextensiveliteraturereviewedusingMEDLINE,PubMedandEMBASE.Adeno-associatedviralvectorswerethemostutilisedvectorsforoculargenetherapy.Conephotoreceptorcellsmightuseanalternatepathwaywhichwasnotreliantoftheretinalpigmentepithelium(RPE)derivedretinoidisomerohydrolase(RPE65)toaccessthe11-cisretinaldehydechromophore.Researcheffortsdedicatedontheprogressionofagene-basedtherapyforthetreatmentofLCA2.Suchgenetherapyapproacheswereextremelysuccessfulincanine,porcineandrodentLCA2models.TherecombinantAAV2.hRPE65v2adenoassociatedvectorcontainedtheRPE65cDNAandwasreplicationdeficient.ItsinvitroinjectionintargetcellsinducedRPE65proteinproduction.Thegenetherapytrialsthatweresofarconductedforinheritedretinopathieshavegeneratedpromisingresults.PhaseIclinicaltrialstocureLCAandchoroideremiademonstratedthatadeno-associatedviralvectorscontainingRPEgenesandphotoreceptorsrespectively,couldbesuccessfullyadministeredtoinheritedretinopathypatients.AphaseIIItrialispresentlyongoingandifsuccessful,itwillleadthewaytoadditionalgenetherapyattemptstocuremonogenic,inheritedretinopathies.

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简介：Brownplanthopper(BPH)isaninsectspeciesthatfeedsonthevascularsystemofriceplants.ToexaminethedefencemechanismofriceplantsagainstBPH,thepathogenesis-relatedgenes(PR1a,PR2,PR3,PR4,PR6,PR9,PR10a,PR13,PR15andPRpha),signalingmoleculesynthesisgenes(AOS,AXR,ACOandLOX),antioxidant-relatedgenes(CAT,TRX,GSTandSOD)andligninbiosynthesis-relatedgenes(CHS,CHIandC4H)wereinvestigatedinaresistantricevariety.AOS,PR6,PR9andPR15genesshowedsignificantlyincreasedrelativeexpressionlevelsat24.38-,19.17-,14.71-,and12.74-foldcomparedtothecontrol.Moderateincreasedrelativeexpressionlevelsofligninbiosynthesis-relatedgene(C4H),pathogenesis-relatedgenes(PR4,PR10aandPRpha),andantioxidant-relatedgene(GST)werefound,whileCHI,LOX,SOD,TRX1andAXRshoweddecreasedrelativeexpressionlevels.Itwasthusclearlyshownthatwound-inducedresponsegeneswereactivatedinriceplantsafterBPHattacksthroughAOSactivation.JasmonicacidsignalingmoleculemayactivatePR6,PR15,GSTandCATsubsequentlyincreasingtheirexpressionforH2O2detoxification.PR6wereexpressedatthehighestrelativelevelamongthePRgenes.ThesegenesthereforehavealsoaconsiderablesynergisticrolewiththeothergenesagainstBPHbyinterferedtheirdigestiontractsystem.

简介：LetT_1beasingularintegralwithnon-smoothkernelor±I,letT_2andT_4bethelinearoperatorsandletT_3=±I.DenotetheToeplitztypeoperatorbyT~b=T_1M~bI_αT_2+T_3I_αM~bT_4,whereM~bf=bf,andI_αisthefractionalintegraloperator.Inthispaper,weinvestigatetheboundednessoftheoperatorT~bontheweightedMorreyspacewhenbbelongstotheweightedBMOspace.

简介：AIMTo调查反脉管的上皮的生长的效果在normoxic和hypoxic条件下面的纤维变性相关的煽动性的调停人的表示上的因素(VEGF)代理人，并且进一步澄清在anti-VEGFtherapy.METHODSHuman以后位于纤维变性下面的机制网膜的颜料上皮(RPE)细胞在normoxic和hypoxic条件下面被孵化。为组织缺氧处理，在200楲敭瑮??杧獥整?桴?敮慧楴敶挠牯敲慬楴湯戠瑥敷湥琠敨攠灸敲獳潩?景洠剩木?愠摮?楥?的CoCl2?乏?单佉呎敨攠灸敲獳潩?敬敶獬漠?業???洠剩木?愠摮洠剩??搠晩敦?敢睴敥?桴?散瑮慲?灥瑩敨楬浵漠?牴湡灳牡湥?湩慦瑮氠湥?湡?潣杮湥瑩污挠瑡牡捡?猠杵敧瑳湩?桴楥?湩潶癬浥湥?湩琠敨瀠瑡潨敧敮楳?景挠湯敧楮慴?慣慴慲瑣

简介：Objective:Congenitalauditoryneuropathy(AN)affectshearingandspeechdevelopment.ThedegreeofhearingdifficultyincongenitalANvariesasafunctionofpathologyattheinnerearhaircell(IHC)synapsesortheauditorynerve.WereportacaseofaChinesegirlwithANrevealedbyOTOF(otoferlin)genemutationanalysiswhohadonlyamildhearingloss.Patient:A13-year-oldChinesegirlwasdiagnosedashavingcongenitalANonthebasisofOTOFgenemutationanalysis.Shemanifestamildsensorineuralhearinglosswith50%maximummonosyllablespeechdiscriminationrate,normalDPOAEs(distortionproductotoacousticemissions)beyondambientnoiselevels,onlySPs(summatingpotentials)evokedduringECoG(electrocochleography)andabsentABRs(auditoryevokedbrainstemresponses)bilaterallytoclickspresentedat100dBnHL.Shewasabletoeffectivelycommunicatewithothersbyspeechreadingowingtohermildhearingloss.Moreover,bilateralhearingaidshelpedhertocommunicate.Conclusions:OurpatientwasdemonstratedtohaveamutationontheOTOFgene.Nevertheless,shewasabletocommunicateusingauditoryvisualspeechreadinginspiteofamildauditorythresholdelevationprobablyduetopartialpathologyattheIHCsynapsesorintheauditorynerve.

简介：Age-relatedmaculardegeneration(AMD)causesirreversiblelossofcentralvisionforwhichthereisnoeffectivetreatment.IncipientpathologyisthoughttooccurintheretinaformanyyearsbeforeAMDmanifestsfrommidlifeonwardstoaffectalargeproportionoftheelderly.Althoughgeneticaswellasnon-genetic/environmentalrisksarerecognized,itscomplexaetiologymakesitdifficulttoidentifysusceptibility,orindeedwhattypeofAMDdevelopsorhowquicklyitprogressesindifferentindividuals.HerewesummarizetheliteraturedescribinghowtheAlzheimer's-linkedamyloidbeta(Aβ)groupofmisfoldingproteinsaccumulateintheretina.ThediscoveryofthiskeydriverofAlzheimer'sdiseaseinthesenescentretinawasunexpectedandsurprising,enablinganaltogetherdifferentperspectiveofAMD.WearguethatAβfundamentallydiffersfromothersubstanceswhichaccumulateintheageingretina,anddiscussourlatestfindingsfromamousemodelinwhichphysiologicalamountsofAβweresubretinally-injectedtorecapitulatesalientfeaturesofearlyAMDwithinashortperiod.OurdiscoveriesaswellasthoseofotherssuggestthepatternofAβaccumulationandpathologyindonoraged/AMDtissuesarecloselyreproducedinmice,includinglate-stageAMDphenotypes,whichmakesthemhighlyattractivetostudydynamicaspectsofAβ-mediatedretinopathy.Furthermore,wediscussourfindingsrevealinghowAβbehavesatsingle-cellresolution,andconsiderthelong-termimplicationsforneuroretinalfunction.WeproposeAβasakeyelementinswitchingtoadiseasedretinalphenotype,whichisnowbeingusedasabiomarkerforlatestageAMD.