简介:目的:开发一个新奇方法由DHPLC检测CpGmethylation。方法:在DNA与钠重亚硫酸盐被对待以后,失配修理基因hMLHl倡导者被聚合酶链反应(PCR)放大。DHPLC被用来在他们的部分使中毒的温度分开PCR产品。BstUI消化试金也为比较学习被使用。结果:A294bp乐队被PCR在结肠癌房间线RKO和胃的癌症房间线PACM82的每件DNA样品以后获得。这二个乐队能被DHPLC在53掳C(为RKO的保留时间6.7min对为PACM82的6.2min)完全分开。当PACM82不是methylated时,自从methylation能保护C的变换到T并且在重亚硫酸盐治疗以后使更高的C/G满意,我们断定在RKO房间的hMLHl倡导者是methylated,导致推迟的时间。从BstUI消化试金的与那些一致的这些结果。结论:在hMLHl的CpG岛的Methylation能被DHPLC在重亚硫酸盐修正以后方便地检测。
简介:AIM:Toanalyzethemismatchrepair(MMR)statusandtheARID1Aexpressionaswellastheirclinicopathologicalsignificanceingastricadenocarcinomas.METHODS:WeexaminedtheexpressionsofMMRproteinsandARID1Abyimmunohistochemistryinconsecutive489primarygastricadenocarcinomas.Theresultswerefurthercorrelatedwithclinicopathologicalvariables.RESULTS:ThelossofanyMMRproteinexpression,indicativeofMMRdeficiency,wasobservedin38cases(7.8%)andwassignificantlyassociatedwithanolderage(68.6±9.2vs60.4±11.7,P<0.001),afemalesex(55.3%vs31.3%,P=0.004),anantrallocation(44.7%vs25.7%,P=0.021),andadifferentiatedhistology(57.9%vs39.7%,P=0.023).AbnormalARID1Aexpression,includingreducedorlossofARID1Aexpression,wasobservedin109cases(22.3%)andwassignificantlycorrelatedwithlymphaticinvasion(80.7%vs69.5%,P=0.022)andlymphnodemetastasis(83.5%vs73.7%,P=0.042).ThetumorswithabnormalARID1AexpressionmorefrequentlyindicatedMMRdeficiency(47.4%vs20.2%,P<0.001).AmultivariateanalysisidentifiedabnormalARID1Aexpressionasanindependentpoorprognosticfactor(HR=1.36,95%CI:1.01-1.84;P=0.040).CONCLUSION:OurobservationssuggestthattheAIRD1Ainactivationisassociatedwithlymphaticinvasion,lymphnodemetastasis,poorprognosis,andMMRdeficiencyingastricadenocarcinomas.
简介:Deareditor,Itiswithgreatinterestthatwereadthearticle“Relationshipofcalcitoningene-relatedpeptidewithdiseaseprogressionandprognosisofpatientswithseveretraumaticbraininjury”(Chenetal.,2018).Inthisstudy,theauthorsevaluated121patientswhoweredividedintomild/moderatetraumaticbraininjury(TBI)(n=61),severeTBI(n=35)andcontrol(n=25)groups,andmeasuredserumlevelsofcalcitoningene-relatedpeptide(CGRP)andserumendothelin-1(ET-1).TheyfoundthatlowlevelsofCGRPandhighlevelsofET-1wereassociatedwithhighmortalityat6months.IdentificationofmorphologicalabnormalitiesonCTscansisveryimportantforevaluatingpatientswithTBIbecausedifferentdiagnosesaremadebasedondifferentimagingfindings(Maasetal.,2005).
简介:三个米饭变化,Zhonghan3,Shanyou63和Aizizhan,当在检测微分活跃甲基的材料骑车并且响应干旱应力转移相关基因表示,被使用。实验被在干旱的条件下面的微分显示器技术与10%PEG6000答案模仿了的基因薄片和mRNA执行。结果显示甲基周期能在Zhonghan3和Shanyou63的叶子被激活,但是在干旱应力下面在Aizizhan的叶子禁止了。而且,干旱应力能导致很多methyltransferase基因的表示,特别Rubisco蛋白质methylation的抄写联系了基因,它是有益的因为Rubisco蛋白质氧化和降级的预防,和干旱应力能禁止DNAmethyltransferase基因和histonemethyltransferase基因的抄写。这结果证实活跃甲基骑车并且转移相关基因涉及米饭干旱抵抗。
简介:Theχcalculusisamodelofconcurrentandmobilesystems.Itemphasizesthatcommunicationsareinformationexchanges.Inthepaper,twoconstructionsareincorporatedintotheframeworkofthechicalculus,whichareasymmetriccommunicationandmismatchconditionwidelyusedinapplications.Sincethebarbedbisimilarityhasproveditsgeneralityandgaineditspopularityasaneffectiveapproachtogeneratingareasonableobservationalequivalence,westudyboththeoperationalandalgebraicpropertiesofthebarbedbisimilarityinthisenrichedcalculus.Theinvestigationsupportsanimprovedunderstandingofthebisimulationbehaviorsofthemodel.Italsogivesageneralpictureofhowthetwoconstructionsaffecttheobservationaltheory.
简介:thermo感觉迟钝的苍白的绿叶异种(pgl2)从T-DNA被孤立米饭的插入的转基因的线(OryzasativaL。subsp。装饰用的梨树cv。Nipponbare)。基因分析显示显型被一个后退的变化在单个原子编码基因引起。印射PGL2基因,一张F2人口被与Longtefu穿过异种构造(OryzasativaL。subsp。indica)。PGL2地点粗略地在染色体8上被连接到SSR标记RM331。细微地印射基因,14个新InDel标记在标记,和PGL2附近被开发进一步被印射到2.37Mbcentromeric区域。叶子的叶绿素内容上的分析证明在全部的叶绿素(Chl)异种和野类型之间没有明显的差别当在异种的Chla/Chlb的比率仅仅是大约1时,满足,它在野类型是比那显然低的,建议PGL2基因与在Chl之间的变换有关是andChlb。而且,在centromeric区域附近的教材设计的方法被讨论,它将提供卓见进在工厂着丝点的功能的基因的好印射。
简介:BACKGROUND:ThedetectionofdifferentialgeneexpressioninbrainispossiblebycDNAmicroarraytechnology,andthescreeningofdifferentiallyexpressedgenesmightprovideabiologicalbasisforgene-targetedtherapyfortumors.OBJECTIVE:TodetectthedifferentialexpressionofgenesamongastrocytomaSHG-44(WHOgradeIV),CHG-5(WHOgradeII),andATRA-treatedSHG-44celllinesbycDNAmicroarray.DESIGN:Laboratoryexperimentsinvitro.SETTING:DepartmentofNeurobiology,theThirdMilitaryMedicalUniversity.MATERIALS:TheexperimentwasperformedattheDepartmentofNeurobiologyintheThirdMilitaryMedicalUniversityoftheChinesePLAfromJanuarytoOctober2007.TheSHG-44cellline(WHOgradeⅣ)wasestablishedbyProf.ZiweiDu,andtheCHG-5cellline(WHOgradeII)wassetupbyProf.XiuwuBianfromtheThirdMilitaryMedicalUniversityoftheChinesePLA.ThecDNAmicroarraycontaining9182knowngeneswaspreparedandprovidedbyDr.YangZhongattheCityUniversityofHongKong.METHODS:ToscreendifferentiallyexpressedgenesfromthegeneexpressionprofilesdetectedbycDNAmicroarraycomparisonsweremadebetweenCHG-5andSHG-44cellsandbetweenSHG-44cellswithorwithouttreatmentwith10μmol/LATRA.SomedifferentiallyexpressedgeneswereselectedrandomlyforNorthernBlotanalysistoconfirmtheresultsofthemicroarray.Thedeterminationcriteriafordifferentialgeneexpressionwereasfollows.①TheratioofCy5signaltoCy3wasgreaterthan2.0orlessthan0.5.②Theresultsofthetriplicatemicroarrayhybridizationsshowedthesametrendinthreeexperiments.③Ageneappearedatleasttwotimesonthetriplicatemicroarrayhybridizations,andthe3rdvaluedidnotshowacontradictorytrend.AnormalizedratioofCy5intensitytoCy3greaterthan2.0orlessthan0.5wasconsideredtorepresentup-regulatedordown-regulatedgeneexpression,respectively.MAINOUTCOMEMEASURES:Theidentificationofgenesthatweresimilarlyregulated(overlapping)dur
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:A Chronology of the Repair of the Potala PalaceAChronologyoftheRepairofthePotalaPalace¥byWangMingxing1989October1-7:ThePotala...
简介:Unbalancedregionaldevelopmentcanbeexaminedbylookingatthemismatchbetweendemographicdistributionandeconomicdistributionacrosstheregions.UsingtheindicatorsmeasuringthedegreeofmismatchbetweendemographicandeconomicdistributionoftheregionsinChina,thispaperrevisitsthedisparitiesandtheirchangesinregionaldevelopment,indentifyingaconvergingtrendintheregionaldifferencesafter2003.Bydecomposingtheregionaldifferencesintocontributionsofdemographicandeconomicconcentrations,thispaperalsoexploresthemechanismsofchangingregionaldifferences,andconcludesthatthechangesofregionaldifferencesaremoreattributabletotheeffectsofeconomicgatheringthantothoseofdemographicgathering.Demographicconcentrationisplayinganincreasinglyimportantroleinreducingtheregionaldifferenceswithreducingbarrierstopopulationmobility.ThepaperalsodiscussespolicyapproachesaddressingbalancedregionaldevelopmentinChina.
简介:Immunobiologicalstudyisakeytorevealingtheimportantbasisoffacialnerverepairandregenerationforbothresearchanddevelopmentofclinictreatments.Themicroenvironmentalchangesaroundaninjuriedfacialmotoneuron,i.e.,theaggregationandexpressionofvarioustypesofimmunecellsandmoleculesinadynamicequilibrium,impenetratefromthestarttotheendoftherepairofaninjuredfacialnerve.Theconceptof'immunemicroenvironmentforfacialnerverepairandregeneration',mainlyconcernswiththedynamicexchangebetweenexpressionandregulationnetworksandavariatyofimmunecellsandimmunemoleculesintheprocessoffacialnerverepairandregenerationforthemaintenanceofaimmunemicroenvironmentfavorablefornerverepair.Investigationonmicroglialactivationandrecruitment,Tcellbehavior,cytokinenetworks,andimmunologicalcellularandmolecularsignalingpathwaysinfacialnerverepairandregenerationarethecurrenthotspotsintheresearchonimmunobiologyoffacialnerveinjury.Thecurrentpaperprovidesacomprehensivereviewoftheabovementionedissues.Researchoftheseissueswilleventuallymakeimmunologicalinterventionspracticabletreatmentsforfacialnerveinjuryintheclinic.