简介:Colorectalcarcinoma(CRC)isacommoncauseofmorbidityandmortalityworldwide.TwopathogenicpathwaysareinvolvedinthedevelopmentofadenomatoCRC.ThefirstpathwayinvolvesAPC/β-catenincharacterizedbychromosomalinstabilityresultingintheaccumulationofmutations.ThesecondpathwayischaracterizedbylesionsinDNAmismatchrepairgenes.AberrantDNAmethylationinselectedgenepromotershasemergedasanewepigeneticpathwayinCRCdevelopment.CRCscreeningisthemostefficientstrategytoreducedeath.SpecificDNAmethylationeventsoccurinmultistepcarcinogenesis.EpigeneticgenesilencingisacausativefactorofCRCdevelopment.DNAmethylationshavebeenextensivelyexaminedinstoolfromCRCandprecursorlesions.ManymethylatedgeneshavebeendescribedinCRCandadenoma,althoughnodefiniteDNAmethylationbiomarkerspanelhasbeenestablished.MultipleDNAmethylationbiomarkers,includingsecretedfrizzled-relatedprotein2,secretedfrizzled-relatedprotein1,tissuefactorpathwayinhibitor2,vimentin,andmethylguanineDNAmethyltransferase,havebeenfurtherinvestigated,andobservationshaverevealedthatDNAmethylationbiomarkersexhibitwithhighsensitivityandspecificity.ThesemarkersmayalsobeusedtodiagnoseCRCandadenomainearlystages.Realtimepolymerasechainreaction(qPCR)issensitive,scalable,specific,reliable,timesaving,andcosteffective.Stoolexfoliatedmarkersprovideadvantages,includingsensitivityandspecificity.AstoolqPCRmethylationtestmayalsobeanenhancedtoolforCRCandadenomascreening.
简介:摘要现阶段,机载电子信息系统当中较为普遍的热源之一就是机载电子芯片,这两者之间有着十分紧密的关联,其次,在进行系统产热量的估算时,机载电子芯片上产生的热量也是最为重要的参数,当然,它也是不能缺少的一部分。但是目前为止,在电子芯片制造的过程中,部分制造商制造出来的芯片发热参数并不是十分的完美,这就导致芯片发热的参数无法达到相应的标准,一旦在运行专用程序时出现非满负载的情况,那么芯片就会受到一定的影响,比如芯片发热量过大,而芯片额定的发热量不够,这就导致芯片的发热量无法达到额定的发热量。针对以上问题,我们应该尽可能的减小散热冷却系统的规模,所以,本篇论文中主要研究的内容就是芯片发热的机理以及芯片的封装特性。
简介:Aminoglycosides(AmAn)arewidelyusedfortheirgreatefficiencyagainstgram-negativebacterialinfections.However,theycanalsoinduceototoxichearingloss,whichhasaffectedmillionsofpeoplearoundtheworld.Aspreviouslyreported,individualsbearingmitochondrialDNAmutationsinthe12SrRNAgene,suchasm.1555A>Gandm.1494C>T,aremorepronetoAmAn-inducedototoxicity.Thesemutationscausehumanmitochondrialribosomestomorecloselyresemblebacterialribosomesandenableastrongeraminoglycosideinteraction.Consequently,exposuretoAmAncaninduceorworsenhearinglossintheseindividuals.Furthermore,awiderangeofseverityandpenetranceofhearinglosswasobservedamongfamiliescarryingthesemutations.StudieshaverevealedthatthesemitochondriamutationsaretheprimarymolecularmechanismofgeneticsusceptibilitytoAmAnototoxicity,thoughnuclearmodifiergenesandmitochondrialhaplotypesareknowntomodulatethephenotypicmanifestation.
简介:导出病毒的nucleic酸的细胞的察觉到为对病毒感染的早防卫是必要的。在最近的年里,包括周期的GMP安培synthase(cGAS)和gamma-interferon-inducible蛋白质(IFI16),察觉到蛋白质的DNA的发现导致了房间怎么对带DNA染色体的到来的病原体唤起强壮的天生的有免疫力的回答的理解。发信号由DNA传感器刺激了取决于适配器蛋白质圈套(干扰素基因的激发器),到启用抗病毒的蛋白质的表示,包括类型我干扰素。便于有效感染,病毒发展了大量避免策略,指向的主人DNA传感器,适配器蛋白质和抄写因素。在这评论,STING小径的导致病毒的激活上的当前的文学被介绍,我们讨论在这条抗病毒的小径指向不同的步的最近识别的病毒的避免机制。