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簡(jiǎn)介:THEPOTENTIALROLEOFMICRORNA146INALZHEIMER’SDISEASEBIOMARKERORTHERAPEUTICTARGETLILINGWANGA,YUEHUANGB,GANGWANGA,?,SHENGDICHENA,C,?ADEPARTMENTOFNEUROLOGY2THEMECHANISMSUNDERLYINGTHERELATIONSHIPBETWEENMIR146AALTERATIONSANDTHEPATHOLOGICALPROGRESSIVEPROCESSINADSIMILARQUESTIONSALSOARISEINTHEINVESTIGATIONSOFMIRINSTROKESANDOTHERNEUROLOGICALDISORDERS36,37CONCLUSIONANDPERSPECTIVEINORDERTODETERMINETHEPHYSIOLOGICALFUNCTIONSOFMIR146AANDB,ITISNECESSARYTORECOGNIZETHEIRPOTENTIALTARGETSMIR146INHIBITSAGROUPOFGENESINCLUDINGIRAK1,TRAF6,CFH,ANDTSPAN12WEPROPOSEDTHATBOTHMIR146AANDBAREINVOLVEDINADPATHOGENESISVIASUPPRESSINGTHEABOVEGENESANDALTERINGTHEIRDOWNSTREAMSIGNALINGPATHWAYSINITIALLY,MIR146WASIDENTIFIEDASANEGATIVEFEEDBACKREGULATORINTHECONTROLOFTOLLLIKERECEPTORSANDCYTOKINESIGNALING,YET,THESUPPRESSIONOFIRAK1NFJBSIGNALINGMEDIATEDBYMIR146AEVENTUALLYCAUSEDSTRONGACTIVATIONOFTHEIRAK2NFJBSIGNALINGPATHWAY,RESULTINGINENHANCEDINFLAMMATORYRESPONSETHROUGHANUNKNOWNMECHANISM31INADDITION,THETARGETGENESOFMIR146,SUCHASROCK1,EGFRANDNOTCH1,ALLPLAYCRUCIALROLEINCANCERWHETHERMIR146MEDIATEDINHIBITIONOFTHOSEGENESISINVOLVEDINTHEPATHOGENESISOFADREMAINSTOBEELUCIDATEDINORDERTOEXPANDTHEKNOWLEDGEONTHEFUNCTIONOFMIR146INAD,ITISESSENTIALTOANALYZETHEPHENOTYPEOFMICEWITHTARGETEDDELETIONOFMIR146AORMIR146BINSUMMARY,THEFUNCTIONSOFMIR146INDICATEDTHATITWOULDHAVEAPPLICABLEPOTENTIALSONATLEASTTWOASPECTSTHEFIRSTISASABIOMARKERFORTHEEARLYCLINICALDETECTIONOFAD,ASITSPRESENCEINCIRCULATINGMONOCYTESINADULTBLOODENABLESEASYCOLLECTIONWITHMINIMUMINVASIONINTHISCONTEXT,CLINICALLYCONFIRMEDADCOHORTWITHSUFFICIENTCASENUMBERSHOULDBEUSEDTOEVALUATEITSPOTENTIALTHEOTHERISASAPOTENTIALTHERAPEUTICTARGETDUETOTHEIMPLICATIONSOFMIR146AINADTREATMENTADANDSTRESSEDBRAINCELLSASSOCIATEDWITHASIGNIFICANTDOWNREGULATIONINMIR146ATARGETS,ENCODINGIRAK1,CFHANDTSPAN1214,31THEUSEOFANTIMIR146ATOREPRESSTHEEFFECTSOFUPREGULATEDMIR146AMAYBEAPOTENTIALTHERAPEUTICAPPROACHAPPLYINGANTIMIR146ATOADTRANSGENICMOUSEMODELSISTHEIMMEDIATESTEPTOWARDSANTIMIR146ACLINICALTRIALSFORADCONFLICTOFINTERESTNONEDECLAREDACKNOWLEDGEMENTSTHISSTUDYWASSUPPORTEDBYTHENATIONALBASICRESEARCHDEVELOPMENTPROGRAMOFCHINANO2010CB945200,SHANGHAIKEYDISCIPLINEPROGRAMNOS30202,SHANGHAIKEYPROJECTOFBASICSCIENCERESEARCHNO09DZ1950400ANDTHEPROGRAMFOROUTSTANDINGMEDICALACADEMICLEADERNOLJ06003REFERENCES1DUYCKAERTSC,DELATOURB,POTIERMCLASSIFICATIONANDBASICPATHOLOGYOFALZHEIMERDISEASEACTANEUROPATHOL20091185–362MORALESI,FARIASG,MACCIONIRNEUROIMMUNOMODULATIONINTHEPATHOGENESISOFALZHEIMER’SDISEASENEUROIMMUNOMODULATION201017202–43BOUTAJANGOUTA,QUARTERMAIND,SIGURDSSONEIMMUNOTHERAPYTARGETINGPATHOLOGICALTAUPREVENTSCOGNITIVEDECLINEINANEWTANGLEMOUSEMODELJNEUROSCI20103016559–664JONESL,HOLMANSPA,HAMSHEREML,HAROLDD,MOSKVINAV,IVANOVD,ETALGENETICEVIDENCEIMPLICATESTHEIMMUNESYSTEMANDCHOLESTEROLMETABOLISMINTHEAETIOLOGYOFALZHEIMER’SDISEASEPLOSONE20105E139505VOLLMARP,KULLMANNJS,THILOB,CLAUSSENMC,ROTHHAMMERV,JACOBIH,ETALACTIVEIMMUNIZATIONWITHAMYLOIDBETA142IMPAIRSMEMORYPERFORMANCETHROUGHTLR2/4DEPENDENTACTIVATIONOFTHEINNATEIMMUNESYSTEMJIMMUNOL20101856338–476LULF,LISTONAMICRORNAINTHEIMMUNESYSTEM,MICRORNAASANIMMUNESYSTEMIMMUNOLOGY2009127291–87XIAOC,RAJEWSKYKMICRORNACONTROLINTHEIMMUNESYSTEMBASICPRINCIPLESCELL200913626–368SABAR,GOODMANC,HUZAREWICHRL,ROBERTSONC,BOOTHSAMIRNASIGNATUREOFPRIONINDUCEDNEURODEGENERATIONPLOSONE20083E36529WANGWX,RAJEEVBW,STROMBERGAJ,RENN,TANGG,HUANGQ,ETALTHEEXPRESSIONOFMICRORNAMIR107DECREASESEARLYINALZHEIMER’SDISEASEANDMAYACCELERATEDISEASEPROGRESSIONTHROUGHREGULATIONOFBETASITEAMYLOIDPRECURSORPROTEINCLEAVINGENZYME1JNEUROSCI2008281213–2310PONOMAREVED,VEREMEYKOT,BARTENEVAN,KRICHEVSKYAM,WEINERHLMICRORNA124PROMOTESMICROGLIAQUIESCENCEANDSUPPRESSESEAEBYDEACTIVATINGMACROPHAGESVIATHEC/EBPALPHAPU1PATHWAYNATMED20111764–7011TAGANOVKD,BOLDINMP,CHANGKJ,BALTIMOREDNFKAPPABDEPENDENTINDUCTIONOFMICRORNAMIR146ANINHIBITORTARGETEDTOSIGNALINGPROTEINSOFINNATEIMMUNERESPONSESPROCNATLACADSCIUSA200610312481–612NAKASAT,MIYAKIS,OKUBOA,HASHIMOTOM,NISHIDAK,OCHIM,ETALEXPRESSIONOFMICRORNA146INRHEUMATOIDARTHRITISSYNOVIALTISSUEARTHRITISRHEUM2008581284–9213ARONICAE,FLUITERK,IYERA,ZUROLOE,VREIJLINGJ,VANVLIETEA,ETALEXPRESSIONPATTERNOFMIR146A,ANINFLAMMATIONASSOCIATEDMICRORNA,INEXPERIMENTALANDHUMANTEMPORALLOBEEPILEPSYEURJNEUROSCI2010311100–714LUKIWWJ,ZHAOY,CUIJGANNFKAPPABSENSITIVEMICRORNA146AMEDIATEDINFLAMMATORYCIRCUITINALZHEIMERDISEASEANDINSTRESSEDHUMANBRAINCELLSJBIOLCHEM200828331315–2215PERRYMM,WILLIAMSAE,TSITSIOUE,LARNERSVENSSONHM,LINDSAYMADIVERGENTINTRACELLULARPATHWAYSREGULATEINTERLEUKIN1BETAINDUCEDMIR146AANDMIR146BEXPRESSIONANDCHEMOKINERELEASEINHUMANALVEOLAREPITHELIALCELLSFEBSLETT20095833349–5516CAMERONJE,YINQ,FEWELLC,LACEYM,MCBRIDEJ,WANGX,ETALEPSTEINBARRVIRUSLATENTMEMBRANEPROTEIN1INDUCESCELLULARMICRORNAMIR146A,AMODULATOROFLYMPHOCYTESIGNALINGPATHWAYSJVIROL2008821946–5817CHANGTC,YUD,LEEYS,WENTZELEA,ARKINGDE,WESTKM,ETALWIDESPREADMICRORNAREPRESSIONBYMYCCONTRIBUTESTOTUMORIGENESISNATGENET20084043–5018SONKOLYE,WEIT,JANSONPC,SAAFA,LUNDEBERGL,TENGVALLLINDERM,ETALMICRORNASNOVELREGULATORSINVOLVEDINTHEPATHOGENESISOFPSORIA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    • 簡(jiǎn)介:THEEPIGENETICSOFAUTOIMMUNITYFRANCESCAMEDA1,2,MARCOFOLCI1,ANDREABACCARELLI3,ANDCARLOSELMI1,21DEPARTMENTOFMEDICINEANDHEPATOBILIARYIMMUNOPATHOLOGYUNIT,IRCCSISTITUTOCLINICOHUMANITAS,ROZZANO,MILAN,ITALY2DEPARTMENTOFTRANSLATIONALMEDICINE,UNIVERSITYOFMILAN,ROZZANO,MILAN,ITALY3HARVARDSCHOOLOFPUBLICHEALTH,EXPOSURE,EPIDEMIOLOGYTEL390282245129FAX390282244590CARLOSELMIUNIMIITNIHPUBLICACCESSAUTHORMANUSCRIPTCELLMOLIMMUNOLAUTHORMANUSCRIPTAVAILABLEINPMC2011MAY13PUBLISHEDINFINALEDITEDFORMASCELLMOLIMMUNOL2011MAY83226–236DOI101038/CMI201078NIHPAAUTHORMANUSCRIPTNIHPAAUTHORMANUSCRIPTNIHPAAUTHORMANUSCRIPTEPIGENETICCHANGESKNOWNSOFAR,ANDTHEREFORETHEIRUNDERLYINGPROCESSESWILLBEDISCUSSEDBELOWINFURTHERDETAILSMOREOVER,THENEWESTFIELDOFMICRORNAWILLBEBRIEFLYILLUSTRATEDASANADDITIONALGENEREGULATORYMECHANISMHISTONEMODIFICATIONSASMENTIONEDBEFORE,HISTONESAREHIGHLYCONSERVEDPROTEINSTHATRESIDEWITHINNUCLEIOFEUKARYOTICCELLSTHEYCANBECLASSIFIEDINTOTWOMAINGROUPS1COREHISTONESH2A,H2B,H3,ANDH4THATAREPARTOFTHENUCLEOSOMECORE,THEBASICUNITOFDNAPACKAGINGINEUKARYOTICS,AND2LINKERHISTONESH1,H5TWOOFEACHOFTHECOREHISTONESASSEMBLETOFORMANOCTAMERICNUCLEOSOMECOREPARTICLEBYWRAPPINGABOUT147BASEPAIRSOFDNAAROUNDTHEPROTEINSPOOLINA17LEFTHANDEDSUPERHELICALTURN9FIGURE1,THUSPROVIDINGDNACONDENSATIONANDORGANIZATIONINTHENUCLEUS,ASWELLASMODULATINGDNAACCESSIBILITYTOTHETRANSCRIPTIONMACHINERYTHISLATTERPROCESSCOULDBEREPRESENTEDASADRAWERTHATCANBEOPENEDORCLOSEDFOLLOWINGSPECIFICSTIMULIINFACT,EACHHISTONESUBTYPECANBEMODIFIEDBYDIFFERENTCHEMICALMODIFICATIONATDEFINEDAMINOACIDSLEADINGTOTRANSCRIPTIONMODULATIONAND,THEREFORE,CELLCYCLEREGULATION,DEVELOPMENT,ANDDIFFERENTIATIONEACHOFTHEFOURCOREHISTONESSHARESTHESAMEFOLDINGSTRUCTUREKNOWNASHISTONEFOLDDOMAINHFD,WHICHCONSISTSOFTHREEΑHELICESΑ1,Α2,ANDΑ3SEPARATEDBYTWOLOOPSL1ANDL210THEHFDFOLDTOGETHERINANTIPARALLELPAIRSH3WITHH4ANDH2AWITHH2BTOCONSTITUTETETRAMERSTHESUBSEQUENTASSEMBLYOFTWOTETRAMERSFORMSTHEOCTAMERICCORESTRUCTUREH3/H4H2A/H2B1OFTHENUCLEOSOME11THENTERMINALREGIONSOFHISTONESPROTRUDEOUTSIDETHENUCLEOSOMECOREANDAREPRONETOPOSTTRANSLATIONALMODIFICATIONS,WHICHAREIMPORTANTINCHROMATINCOMPACTIONANDGENEREGULATIONHISTONEPOSTTRANSLATIONALMODIFICATIONSCONCURTODETERMINETHEPATTERNDEFINEDAS“HISTONECODE”ANDWILLBESUMMARIZEDBELOWALLTHESEHISTONEMODIFICATIONSARECAUSEDBYSPECIFICENZYMESWHICHRECOGNIZEHISTONETAILSANDCANWORKTOADDORREMOVEFUNCTIONALGROUPSWHICHAREINTURNRECOGNIZEDBYNUCLEARFACTORSSPECIFICPROTEINSHAVEAFFINITYFORMODIFIEDAMINOACIDRESIDUESFORINSTANCEBROMODOMAINSBINDACETYLATEDLYSINESORCHROMODOMAINSMETHYLATEDLYSINESANDPROMOTESPECIFICCHANGESINCHROMATINDETERMININGRESPECTIVELYTHEACTIVATIONORTHESILENCINGOFGENETRANSCRIPTIONFIGURE2AMONGHISTONEMODIFICATIONS,ACETYLATIONORDEACETYLATIONAREONEOFTHEMOSTIMPORTANTGENEEXPRESSIONREGULATORYMECHANISMSTHESEPROCESSESINVOLVESELECTEDLYSINERESIDUESINTHETAILSOFNUCLEOSOMALHISTONESANDAREINDUCEDBYHISTONEACETYLTRANSFERASEHATANDHISTONEDEACETYLASEHDACENZYMES,RESPECTIVELY12–15HATENZYMESSHARETHEABILITYTOPROMOTEGENEEXPRESSIONBYTRANSFERRINGACETYLGROUPSTOLYSINE16–18WHILEHDACSREMOVEACETYLGROUPSANDGENERALLYASSOCIATEWITHGENEREPRESSION19–21ASECONDMECHANISMINVOLVESHISTONEMETHYLATIONANDITSEFFECTSDEPENDONTHEPOSITIONOFTHEMODIFIEDLYSINERESIDUEWITHINTHEHISTONETAILANDONTHENUMBEROFMETHYLGROUPSADDEDTOSUCHRESIDUESASANEXAMPLE,THEPRESENCEOFTHREEMETHYLGROUPSONLYSINE4RESIDUEONHISTONEH3MEH3K4,HASBEENASSOCIATEDWITHTRANSCRIPTIONALACTIVATIONWHEREASTHETRIPLEMETHYLATIONOFRESIDUES9OR27DETERMINESREPRESSION3,22–26ASATHIRDMECHANISM,ARGININECANALSOBEMETHYLATED/DEMETHYLATEDBYSPECIFICENZYMESANDPLAYACRITICALROLEINTHEDYNAMICREGULATIONOFGENEEXPRESSION27METHYLATIONOFARGININERESIDUE3ONHISTONEH4H4R3ANDARGININE17ONHISTONEH3H3R17HAVEBEENSHOWNTOINDUCEGENEACTIVATION23,28–30FINALLY,UBIQUITINISA76AMINOACIDPROTEINTHATISINVOLVEDINSPECIFICPROTEINLABELINGUBIQUITINATEDPROTEINSARECOMMITTEDTOPROTEOSOMALDEGRADATIONANDUBIQUITINATIONTHUSCONTROLLINGTHESTABILITYANDINTRACELLULARLOCALIZATIONOFNUMEROUSPROTEINSUBIQUITINATIONULTIMATELYINFLUENCESTHESTATUSOFHISTONESMETHYLATIONORMEDAETALPAGE3CELLMOLIMMUNOLAUTHORMANUSCRIPTAVAILABLEINPMC2011MAY13NIHPAAUTHORMANUSCRIPTNIHPAAUTHORMANUSCRIPTNIHPAAUTHORMANUSCRIPT
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    • 簡(jiǎn)介:中文中文7700字出處出處WENTZELJJ,CHATZIZISISYS,GIJSENFJ,ETALENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONSJCARDIOVASCULARRESEARCH,2012,96223443本科外文翻譯內(nèi)皮剪切力在冠狀動(dòng)脈粥樣硬化斑塊和血管重內(nèi)皮剪切力在冠狀動(dòng)脈粥樣硬化斑塊和血管重建進(jìn)展中的作用機(jī)制當(dāng)前的理解和存在的問(wèn)建進(jìn)展中的作用機(jī)制當(dāng)前的理解和存在的問(wèn)題ENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONS學(xué)部(院)電子信息與電氣工程學(xué)部專業(yè)生物醫(yī)學(xué)工程學(xué)生姓名學(xué)號(hào)指導(dǎo)教師完成日期內(nèi)皮剪切力在冠狀動(dòng)脈粥樣硬化斑塊和血管重建進(jìn)展中的作用機(jī)制當(dāng)前的理解和存在的問(wèn)題–2–位的內(nèi)側(cè)緣,這些部位存在紊亂的血流和低ESS。相反,乳溝動(dòng)脈是暴露在生理狀態(tài)下的ESS是抗粥樣硬化的。早期對(duì)ESS和斑塊位置之間聯(lián)系的觀察主要是在尸體解剖材料上,因此,不能觀察到ESS對(duì)動(dòng)脈粥硬化的影響?;谘茉煊昂脱軆?nèi)超聲的在體動(dòng)脈血管三維重建的優(yōu)點(diǎn)開(kāi)辟了新的觀察途徑來(lái)研究ESS在動(dòng)脈粥樣硬化自然進(jìn)程中的作用(圖1)。這些三維重建技術(shù)已經(jīng)得到了在體驗(yàn)證并且在全世界很多的中心得到了應(yīng)用。通過(guò)這些技術(shù),已經(jīng)發(fā)現(xiàn)了低ESS區(qū)域和動(dòng)脈粥樣硬化斑塊,以及低ESS區(qū)域和冠狀動(dòng)脈患者、實(shí)驗(yàn)動(dòng)物的支架內(nèi)再狹窄之間的位置關(guān)聯(lián)。而且,通過(guò)一系列的測(cè)量顯示低ESS環(huán)境在斑塊的進(jìn)展,斑塊向有破裂傾向的斑塊發(fā)展中也起到了作用。另一個(gè)觀察發(fā)現(xiàn)是,開(kāi)始向官腔內(nèi)侵入的成熟(ADVANCED)斑塊回暴露在高水平ESS,這可能參與到急性斑塊的破裂。圖1基于雙平面血管造影和血管內(nèi)超聲融合三維(3D)重建人體冠狀動(dòng)脈。中央面板顯示用相同的方向作為正向和側(cè)向雙平面血管造影描繪左前降支(LAD)三維重建,右冠狀動(dòng)脈(RCA),左回旋(LCX)。左面板和右面板分別顯示正向和側(cè)向雙平面血管造影的冠狀動(dòng)脈。早期損傷發(fā)展到暴露在官腔內(nèi)的成熟(ADVANCED)高危斑塊或是出現(xiàn)管腔狹窄的高危斑塊的病理生理機(jī)制尚不明確。局部ESS環(huán)境,血管重建和血管生物學(xué)之間的動(dòng)態(tài)
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    • 簡(jiǎn)介:ASSESSMENTOFVASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCEANESTEROV,IGAVRILOV,LSELECTOR,IMUDRAYAANDSREVENKO1NATIONALCARDIOLOGYCENTER,RESEARCHINSTITUTEOFUROLOGY,MOSCOW,RUSSIAEMAILS_REVENKOMAILRUABSTRACTFOURIERANALYSISREVEALEDANUMBEROFPERIODICITIESINSMALLVARIATIONSOFBIOIMPEDANCEOFHUMANFINGERINCLUDINGTHEMAJORSPECTRUMPEAKSATTHEFREQUENCIESOFHEARTBEATS,RESPIRATION,ANDMAYERWAVE01HZTHESEPERIODICVARIATIONSOFBIOIMPEDANCEWEREDETECTEDUNDERTHENORMALCONDITIONSANDDURINGBLOODFLOWARRESTINTHEHANDBYAPNEUMATICCUFFPLACEDONTHEARMTHEYAREEXPLAINEDBYPERIODICVARIATIONSINSYSTEMICBLOODPRESSUREANDBYOSCILLATIONSOFREGIONALVASCULARTONERESULTEDFROMNEURALVASOMOTORCONTROLDURINGNORMALBLOODFLOW,THEGREATESTVARIATIONSINBIOIMPEDANCEWEREOBSERVEDATTHEHEARTRATE,ANDTHEIRAMPLITUDESURPASSEDBYANORDEROFMAGNITUDETHEAMPLITUDESOFRESPIRATORYOSCILLATIONSANDMAYERWAVEINCONTRAST,DURINGBLOODARREST,THELARGESTAMPLITUDEOFRHYTHMICALCHANGESOFTHEIMPEDANCECHARACTERIZEDTHEOSCILLATIONSATRESPIRATIONRATE,WHILETHEAMPLITUDEOFOSCILLATIONSATTHEHEARTRATEWASTHESMALLESTDURINGNORMALRESPIRATIONANDCIRCULATION,TWOSIDECARDIACPEAKSWEREREVEALEDINBIOIMPEDANCEAMPLITUDESPECTRUMWHICHDISAPPEAREDDURINGRESPIRATIONARRESTANDTHOUGHTTOREFLECTTHEAMPLITUDERESPIRATORYMODULATIONOFTHECARDIACOUTPUTVIASYMPATHETICINFLUENCESDURINGNORMALBREATHING,THESECONDANDTHETHIRDHARMONICSOFTHECARDIACSPECTRUMPEAKWERESPLITREFLECTINGFREQUENCYRESPIRATORYMODULATIONOFTHEHEARTRATEBYPARASYMPATHETICINFLUENCESTHERESULTSFAVOURAPPLICABILITYOFFOURIERANALYSISOFBIOIMPEDANCEVARIATIONSINASSESSMENTOFREGIONALNEURALINFLUENCESANDNEUROGENICMODULATIONOFCARDIACACTIVITY1INTRODUCTIONASPECTACULARPROGRESSINMICROELECTRONICSRESULTEDINAPPEARANCEOFLOWNOISECHIPSANDPOWERFULCOMPUTERSWHICHMADEITPOSSIBLETOMEASUREANDANALYZESMALLBIOIMPEDANCEVARIATIONSWITHALABORATORYMADEHIGHRESOLUTIONIMPEDANCECONVERTERANDORIGINALSOFTWAREWEANALYZEDBIOIMPEDANCEVARIATIONSINHUMANFINGERWITHFOURIERTRANSFORMINTHEFREQUENCYBANDOF008150HZUNDERTHENORMALCONDITIONSANDDURINGCIRCULATIONARRESTINTHEARMOPTIONALLYCOMBINEDWITHEXPIRATORYDELAYFOR40SECTHEAIMWASTOASSESSTHENEUROGENICCONTRIBUTIONTOBIOIMPEDANCEVARIATIONS,WHICHPROBABLYRESULTFROMVASOMOTORACTIVITYOFSYMPATHETICNERVESYSTEM2METHODSBIOIMPEDANCEWASMEASUREDWITHORIGINALIMPEDANCECONVERTERBASEDONSYNCHRONOUSDETECTIONPRINCIPLERESULTINGINTOTAL“BASIC”REALPARTOFIMPEDANCEINTHEFREQUENCYBANDOF0–15HZRANDTHEVARIABLECOMPONENTOFTHISREALPARTINTHEFREQUENCYBANDOF008–15HZRTHEMEASURING1TOWHOMANYCORRESPONDENCESHOULDBEADDRESSEDINTERNATIONALCONFERENCEONELECTRICALBIOIMPEDANCEIOPPUBLISHINGJOURNALOFPHYSICSCONFERENCESERIES2242010012125DOI101088/17426596/224/1/012125C?2010IOPPUBLISHINGLTD1FIGURE2AMPLITUDESPECTRUMOFBIOIMPEDANCEVARIATIONSINHUMANFINGEROVERBROADFREQUENCYRANGEWITHMAYER’SPEAK1,RESPIRATORYPEAK2,FOURCARDIACHARMONICS3TO3’’’’,ANDTHESIDEPEAKS3L,3R,ETCNOTETHEBREAKINORDINATEANOTHERIMPORTANTOBSERVATIONISSPLITTINGOFHIGHERHARMONICSOFTHECARDIACPEAKOBSERVEDUNDERNORMALCONDITIONSINSOMECASESFIGURE3,ASUCHSPLITTINGWASFARLESSPRONOUNCEDUNDERRESPIRATIONDELAYFIGURE3,BSPLITTINGOFAPEAKCANBEEXPLAINEDBYFREQUENCYMODULATIONOFBASICOSCILLATORYPROCESSWITHANOTHERPROCESSGOINGONATASMALLERRATEINTHISCASE,SPLITTINGCANRESULTFROMVAGALMODULATIONOFTHEHEARTRATEATTHERESPIRATIONFREQUENCYINTHISEXPERIMENT,THEOSCILLATIONSWERECUTOFFBELOW03HZ,SONOMAYERPEAKISSEENINFIGURE3FIGURE3THERESPIRATORY2ANDSIDECARDIACPEAKSLANDRAREOBSERVEDUNDERNORMALCONDITIONSABUTDISAPPEAREDDURINGEXPIRATORYDELAYBINORDERTOASSESSTHECHANGESINBIOIMPEDANCEOFNONPULSATILENONCARDIACORIGIN,WECOMPAREDTHEBIOIMPEDANCESPECTRADURINGNORMALCIRCULATIONFIGURE4,AANDDURINGBLOODARRESTINTHEARMSFIGURE4,BCIRCULATIONARRESTDIDNOTELIMINATEOSCILLATIONSOFBIOIMPEDANCEALTHOUGHDIMINISHEDTHEIRAMPLITUDEFIGURE4,BUNDERTHESECONDITIONS,THEPERIODICBIOIMPEDANCEOSCILLATIONSCOULDBEPRODUCEDEITHERBYNEUROGENICVASOMOTORINFLUENCESORBYSPONTANEOUSVASOMOTIONSTHELATTERARECHARACTERIZEDWITHABROADRANGEATTHELOWFREQUENCIESOF0008–011HZ4THENARROWSHAPEOFALLPEAKSINFIG4DOESNOTFAVOURTHEHYPOTHESISOFSPONTANEOUSNATUREOFTHECORRESPONDINGBIOIMPEDANCEOSCILLATIONSTHUS,ALLTHEPEAKSINFIGURE4,BAREPROBABLYNEUROGENICANDVASOMOTORINNATUREARRESTOFCIRCULATIONDRAMATICALLYREDUCEDTHECARDIACPEAK,WHICHISATRIVIALCONSEQUENCEOFTHEFACTTHATDURINGNORMALCIRCULATIONTHEMAJORVARIATIONSINBIOIMPEDANCEAREPRODUCEDBYPUMPINGACTIONOFTHEHEARTSURPRISINGLY,THERESPIRATORYPEAK2ANDMAYER’SPEAK1DECREASEDBYNOMORETHAN2FOLDITMEANSTHATDURINGNORMALCIRCULATION,THEHEARTANDSYSTEMICBLOODPRESSUREARENOTTHEMAJORPLAYERSWHOCONTROLTHESERHYTHMICVARIATIONSOFBIOIMPEDANCEDURINGCIRCULATIONARREST,THEINTERNATIONALCONFERENCEONELECTRICALBIOIMPEDANCEIOPPUBLISHINGJOURNALOFPHYSICSCONFERENCESERIES2242010012125DOI101088/17426596/224/1/0121253
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    • 簡(jiǎn)介:中文中文2020字,字,1560單詞,單詞,8800英文字符英文字符出處出處NESTEROVA,GAVRILOVI,SELECTORL,ETALASSESSMENTOFVASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCEC//JOURNALOFPHYSICSCONFERENCESERIESIOPPUBLISHING,2010,22410121251使用生物組織阻抗傅里葉分析使用生物組織阻抗傅里葉分析評(píng)估血管舒縮振幅評(píng)估血管舒縮振幅ASSESSMENTOFWASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCETHETITLEOFFOREIGNLANGUAGE學(xué)部(院)電子信息與電氣工程學(xué)部專業(yè)生物醫(yī)學(xué)工程使用生物阻抗諧波分析為診斷工具評(píng)估局部循環(huán)和神經(jīng)活動(dòng)3譜做平均。將阻抗變換器與人的中指(N14)的近端指骨連接,將兩個(gè)輸出電流和兩個(gè)輸出電壓與兩個(gè)AG/AGCL電銀絲(直徑為04MM)電極連接起來(lái),電極表面包裹沾有生理鹽水的窄紗布。電極之間的距離是2CM。為了減弱心臟和肺部引起的機(jī)械振動(dòng),將手臂固定起來(lái)。暫時(shí)用充氣袖帶把手臂血流阻斷,至少是2倍收縮壓來(lái)阻斷手臂的液壓波動(dòng)。3結(jié)果如圖1所示,在正常情況(A)和阻斷左臂血流過(guò)程中(C)測(cè)量基本阻抗R(B)和可變阻抗成分R。心臟的抽吸作用導(dǎo)致了(A,B)的生物阻抗的大振幅,可以在心臟循環(huán)未阻斷時(shí)觀察到更小的一個(gè)(C),這反映了血管舒縮的神經(jīng)活動(dòng)。圖1,人手指的可變分量(A)和基本生物阻抗(B)。(C)手臂循環(huán)阻斷時(shí)的可變分量。另外一個(gè)重要的觀察是心臟波峰的高次諧波的分離,它是在某些正常情況下(圖3,B)觀察到的。波峰的分離可以解釋為另外一個(gè)基礎(chǔ)震蕩過(guò)程的調(diào)頻速率更??;在這種情況下,分離可由心臟迷走神經(jīng)呼吸作用的速率引起。在這個(gè)實(shí)驗(yàn)中,震動(dòng)被切割成低于3HZ的片段,所以圖3中沒(méi)有邁爾波。
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