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簡介：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,ETALMICRORNASNOVELREGULATORSINVOLVEDINTHEPATHOGENESISOFPSORIASISPLO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簡介：中文中文7700字出處出處WENTZELJJ,CHATZIZISISYS,GIJSENFJ,ETALENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONSJCARDIOVASCULARRESEARCH,2012,96223443本科外文翻譯內(nèi)皮剪切力在冠狀動脈粥樣硬化斑塊和血管重內(nèi)皮剪切力在冠狀動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建進(jìn)展中的作用機(jī)制當(dāng)前的理解和存在的問題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)號指導(dǎo)教師完成日期內(nèi)皮剪切力在冠狀動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，乳溝動脈是暴露在生理狀態(tài)下的ESS是抗粥樣硬化的。早期對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對動脈粥硬化的影響?；谘茉煊昂脱軆?nèi)超聲的在體動脈血管三維重建的優(yōu)點(diǎn)開辟了新的觀察途徑來研究ESS在動脈粥樣硬化自然進(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。通過這些技術(shù)，已經(jīng)發(fā)現(xiàn)了低ESS區(qū)域和動脈粥樣硬化斑塊，以及低ESS區(qū)域和冠狀動脈患者、實(shí)驗(yàn)動物的支架內(nèi)再狹窄之間的位置關(guān)聯(lián)。而且，通過一系列的測量顯示低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。另一個觀察發(fā)現(xiàn)是，開始向官腔內(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)之間的動態(tài)

簡介：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估血管舒縮振幅評估血管舒縮振幅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估局部循環(huán)和神經(jīng)活動3譜做平均。將阻抗變換器與人的中指（N14）的近端指骨連接，將兩個輸出電流和兩個輸出電壓與兩個AG/AGCL電銀絲（直徑為04MM）電極連接起來，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，將手臂固定起來。暫時用充氣袖帶把手臂血流阻斷，至少是2倍收縮壓來阻斷手臂的液壓波動。3結(jié)果如圖1所示，在正常情況（A）和阻斷左臂血流過程中（C）測量基本阻抗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)未阻斷時觀察到更小的一個（C），這反映了血管舒縮的神經(jīng)活動。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)阻斷時的可變分量。另外一個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基礎(chǔ)震蕩過程的調(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。在這個實(shí)驗(yàn)中，震動被切割成低于3HZ的片段，所以圖3中沒有邁爾波。

簡介：REVIEWENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONSJOLANDAJWENTZEL1,YIANNISSCHATZIZISIS2,3,FRANKJHGIJSEN1,GEORGEDGIANNOGLOU3,CHARLESLFELDMAN2,ANDPETERHSTONE21BIOMEDICALENGINEERING,DEPARTMENTCARDIOLOGY,ERASMUSMC,ROTTERDAM,THENETHERLANDS2CARDIOVASCULARDIVISION,BRIGHAMANDWOMEN’SHOSPITAL,HARVARDMEDICALSCHOOL,BOSTON,MA,USAAND31STDEPARTMENTOFCARDIOLOGY,AHEPAUNIVERSITYHOSPITAL,ARISTOTLEUNIVERSITYMEDICALSCHOOL,THESSALONIKI,GREECERECEIVED23MARCH2012REVISED12JUNE2012ACCEPTED25JUNE2012ONLINEPUBLISHAHEADOFPRINT29JUNE2012ABSTRACTTHEHETEROGENEITYOFPLAQUEFORMATION,THEVASCULARREMODELLINGRESPONSETOPLAQUEFORMATION,ANDTHECONSEQUENTPHENOTYPEOFPLAQUEINSTABILITYATTESTTOTHEEXTRAORDINARILYCOMPLEXPATHOBIOLOGYOFPLAQUEDEVELOPMENTANDPROGRESSION,CULMINATINGINDIFFERENTCLINICALCORONARYSYNDROMESATHEROSCLEROTICPLAQUESPREDOMINANTLYFORMINREGIONSOFLOWENDOTHELIALSHEARSTRESSESS,WHEREASREGIONSOFMODERATE/PHYSIOLOGICALANDHIGHESSAREGENERALLYPROTECTEDLOWESSINDUCEDCOMPENSATORYEXPANSIVEREMODELLINGPLAYSANIMPORTANTROLEINPRESERVINGLUMENDIMENSIONSDURINGPLAQUEPROGRESSION,BUTWHENTHEEXPANSIVEREMODELLINGBECOMESEXCESSIVEPROMOTESCONTINUEDINFLUXOFLIPIDSINTOTHEVESSELWALL,VULNERABLEPLAQUEFORMATIONANDPOTENTIALPRECIPITATIONOFANACUTECORONARYSYNDROMEADVANCEDPLAQUESWHICHSTARTTOENCROACHINTOTHELUMENEXPERIENCEHIGHESSATTHEIRMOSTSTENOTICREGION,WHICHAPPEARSTOPROMOTEPLAQUEDESTABILIZATIONTHISREVIEWDESCRIBESTHEROLEOFESSFROMEARLYATHEROGENESISTOEARLYPLAQUEFORMATION,PLAQUEPROGRESSIONTOADVANCEDHIGHRISKSTENOTICORNONSTENOTICPLAQUE,ANDPLAQUEDESTABILIZATIONTHECRITICALIMPLICATIONOFTHEVASCULARREMODELLINGRESPONSETOPLAQUEGROWTHISALSODISCUSSEDCURRENTDEVELOPMENTSINTECHNOLOGYTOCHARACTERIZELOCALESSANDVASCULARREMODELLINGINVIVOMAYPROVIDEARATIONALEFORINNOVATIVEDIAGNOSTICANDTHERAPEUTICSTRATEGIESFORCORONARYPATIENTSTHATAIMTOPREVENTCLINICALCORONARYSYNDROMESKEYWORDSSHEARSTRESS?HIGHRISKPLAQUE?INFLAMMATION?VASCULARREMODELLING1INTRODUCTIONATHEROSCLEROTICPLAQUESAREREGIONSINTHEARTERIALSYSTEMCHARACTERIZEDBYINTIMALTHICKENINGWITHEXCESSIVEBUILDUPOFOXIDIZEDLOWDENSITYLIPOPROTEINCHOLESTEROLACCOMPANIEDBYINFLAMMATORYCELLINFILTRATION,SMOOTHMUSCLEPROLIFERATION,ANDEXTRACELLULARMATRIXACCUMULATION1PLAQUESPRONETORUPTURESOCALLEDVULNERABLEPLAQUESAREFURTHERCHARACTERIZEDBYTHEPRESENCEOFALARGENECROTICCORECOVEREDBYANINFLAMEDTHINFIBROUSCAP2RUPTUREOFAVULNERABLECORONARYATHEROSCLEROTICPLAQUEISRESPONSIBLEFORTHEMAJORITYOFACUTECORONARYEVENTS,3WHICHARETHELEADINGCAUSEOFMORBIDITYANDMORTALITYINTHEWESTERNWORLDALTHOUGHTHERISKFACTORSFORATHEROSCLEROTICPLAQUEFORMATION,INCLUDINGHIGHCHOLESTEROL,DIABETES,ANDHIGHBLOODPRESSURE,ARESYSTEMICINNATURE,PLAQUESARELOCATEDATSPECIFICSITESINTHEARTERIALSYSTEMTHESESITESINCLUDESIDEBRANCHES,THEOUTERWAISTOFBIFURCATIONS,ORTHEINNERCURVEOFARTERIES,WHEREDISTURBEDFLOWANDLOWENDOTHELIALSHEARSTRESSESSOCCUR4–7INCONTRAST,ARTERIALREGIONSEXPOSEDTOMODERATE/PHYSIOLOGICALESSAREPROTECTEDFROMATHEROSCLEROSISEARLYOBSERVATIONSONTHERELATIONSHIPBETWEENESSANDPLAQUELOCALIZATIONWEREBASEDMAINLYONAUTOPSYMATERIAL,8,9ANDCONSEQUENTLYDIDNOTALLOWINVESTIGATIONOFTHEINFLUENCEOFESSONATHEROSCLEROSISTHEADVENTOFTHREEDIMENSIONAL3DRECONSTRUCTIONTECHNIQUESFORCORONARYARTERIESINVIVO,10–13BASEDONBIPLANEANGIOGRAPHYANDCORRESPONDINGAUTHORSJJWISATBIOMECHANICSLABORATORY,BIOMEDICALENGINEERING,EE2322,ERASMUSMC,POBOX2040,3000CAROTTERDAM,THENETHERLANDSYSCISATFIRSTDEPARTMENTOFCARDIOLOGY,AHEPAUNIVERSITYHOSPITAL,ARISTOTLEUNIVERSITYMEDICALSCHOOL,1STYLPKURIAKIDISTREET,54636,THESSALONIKI,GREECETEL31107044044JJW,302310994837YSCFAX31107044720,EMAILJWENTZELERASMUSMCNLJJWJOCMEDAUTHGRYSCPUBLISHEDONBEHALFOFTHEEUROPEANSOCIETYOFCARDIOLOGYALLRIGHTSRESERVEDFIGURE3BOFNOTE,THEABSOLUTECUTOFFPOINTFORLOWESSAPPEARSTOBEDEPENDENTONCONCOMITANTCONDITIONSASPRESENTEDBELOWSECTION3LOWESSTYPICALLYOCCURSATTHEINNERAREASOFCURVATURESANDPOTENTIALLYATTHEUPSTREAMSHOULDERSOFASTENOSISLOWOSCILLATORYESSISBIDIRECTIONAL,WITHAFLUCTUATINGMAGNITUDEBETWEENSYSTOLEANDDIASTOLE,RESULTINGINALOWTIMEAVERAGEAPPROXIMATELY,10–15PAFIGURE3BLOWOSCILLATORYESSOCCURSPRIMARILYDOWNSTREAMOFSTENOSES,ATTHELATERALWALLSOFBIFURCATIONSANDATTHEOSTIAOFBRANCHESHIGHESSISCHARACTERIZEDBYASIGNIFICANTLYHIGHTIMEAVERAGEAPPROXIMATELY30PAANDOCCURSATTHEUPSTREAMANDMOSTSTENOTICSITEOFTHEPLAQUE3DYNAMICNATUREOFLOCALESSESSISADYNAMICFACTORTHATCHANGESINDIRECTIONANDMAGNITUDEWITHPLAQUEFORMATIONANDVASCULARREMODELLING35ASACONTINUOUSVARIABLE,ESSCOVERSAWIDESPECTRUMOFVALUES,FROMLOWESSTOMODERATE/PHYSIOLOGICALESSANDTOHIGHESSTHECUTOFFPOINTSDEFININGLOW,MODERATE/PHYSIOLOGICAL,ANDHIGHESSMAYVARYAMONGSPECIES,ANDAMONGVASCULARBEDSEGFEMORAL,CAROTID,ANDCORONARYARTERIESINTHESAMESPECIES36EVENINTHESAMEVASCULARLOCATION,ESSCHANGESOVERTIMEINRESPONSETOSEVERALSYSTEMICANDLOCALFACTORSTHESEVERITYOFSYSTEMICRISKFACTORSEGHYPERCHOLESTEROLAEMIACERTAINLYINFLUENCESTHEEFFECTOFTHELOCALHAEMODYNAMICENVIRONMENTFURTHERMORE,THESTAGEOFATHEROSCLEROSISDEVELOPMENT,THEREMODELLINGRESPONSEOFTHEWALLTOPLAQUEFORMATION,ASWELLASREGIONALSTRUCTURALANDSTIFFNESSCHARACTERISTICSCRITICALLYDETERMINETHELOCALESSENVIRONMENTANDTHESUBSEQUEN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簡介：基于移動手機(jī)平臺的生物醫(yī)學(xué)傳感器技術(shù)1中文中文11800字出處出處LIUL,LIUJBIOMEDICALSENSORTECHNOLOGIESONTHEPLATFORMOFMOBILEPHONESJFRONTIERSOFMECHANICALENGINEERING,2011,62160175基于移動手機(jī)平臺的生物醫(yī)學(xué)傳感器技術(shù)基于移動手機(jī)平臺的生物醫(yī)學(xué)傳感器技術(shù)BIOMEDICALBIOMEDICALSENSORSENSORTECHNOLOGIESTECHNOLOGIESONONTHETHEPLATFORMPLATFORMOFOFMOBILEMOBILEPHONESPHONESLINLIU,JINGLIU清華大學(xué)醫(yī)學(xué)院生物醫(yī)學(xué)工程系,中國北京100084,郵箱JLIUBMETSINGHUAEDUCNJINGLIU中國科學(xué)院化物所中國北京100190摘要摘要生物醫(yī)學(xué)傳感器目前已經(jīng)被廣泛的使用在各種各樣的生物醫(yī)學(xué)實(shí)踐當(dāng)中，并在疾病檢測、診斷、監(jiān)測、治療、健康護(hù)理等方面扮演了重要的角色。但是，大部分生物醫(yī)學(xué)傳感器和他們相關(guān)的平臺通常不是很容易能夠獲取，對于家用而言不是太貴了就是太復(fù)雜了。作為替代，使用移動手機(jī)的新技術(shù)逐漸改變了這樣一個情況。幾乎所有人都擁有的移動手機(jī)通過與各種生物醫(yī)學(xué)傳感器結(jié)合提供一個獨(dú)一無二方式促進(jìn)了醫(yī)療護(hù)理。不僅如此，系統(tǒng)的建立很便捷而且成本低。在這篇論文中，我們描述了生物醫(yī)學(xué)傳感器技術(shù)發(fā)展水平的概況。對基本原理做了一個簡要的介紹，并且介紹了幾個新例子或概念。重點(diǎn)尤其放在基于移動手機(jī)平臺的生物醫(yī)學(xué)傳感器的創(chuàng)新上。一些挑戰(zhàn)問題，包括可行性、易用性、安全性、和效率都提及了。在電子和機(jī)械技術(shù)的幫助下，可以預(yù)見生物醫(yī)學(xué)傳感器和移動手機(jī)平臺的全面結(jié)合將會為即將到來的全民醫(yī)療帶來一個光明的前景。關(guān)鍵詞關(guān)鍵詞生物醫(yī)學(xué)傳感器，普適技術(shù)，移動手機(jī)，復(fù)合系統(tǒng)，健康管理基于移動手機(jī)平臺的生物醫(yī)學(xué)傳感器技術(shù)3明顯。向這樣一個符合系統(tǒng)努力一定會在研究和應(yīng)用方面創(chuàng)造許多機(jī)會。建立這樣一個系統(tǒng)會導(dǎo)致電氣和機(jī)械技術(shù)迅速發(fā)展?？紤]到應(yīng)用，這個平臺將會很容易建立以人類身體行為的基本力學(xué)表征的形式。在這篇論文中，我們首先對生物醫(yī)學(xué)傳感器和基于手機(jī)的傳感系統(tǒng)做一個簡要的介紹。然后，我們回顧一些生物醫(yī)學(xué)傳感器的基本知識并且舉幾個使用新方法和新應(yīng)用的新型生物醫(yī)學(xué)傳感器的例子。基于手機(jī)的傳感系統(tǒng)是一個重要的章節(jié)，通過理論分析和工程實(shí)例我們精心寫作了這一部分。不僅如此，在學(xué)習(xí)復(fù)合系統(tǒng)的過程中一些需要被解決的關(guān)鍵技術(shù)及問題也被提了出來。最后，我們總結(jié)基于手機(jī)的傳感系統(tǒng)的優(yōu)點(diǎn)和發(fā)展前景。2生物醫(yī)學(xué)傳感器的基本概念生物醫(yī)學(xué)傳感器的基本概念眾說周知生物醫(yī)學(xué)傳感器被用來將一種信號的量例如溫度、壓力、速度等等轉(zhuǎn)換成另一種量，通常是電信號。生物醫(yī)學(xué)傳感器獲取表示生理特征的信號并且將它們轉(zhuǎn)換成電信號。因此，生物醫(yī)學(xué)傳感器為生物和電子系統(tǒng)的連接服務(wù)。并且必須對兩方都沒有副作用，因?yàn)閮煞綄鞲衅鞯谋憩F(xiàn)都起了重要作用。根據(jù)被測量來看，生物醫(yī)學(xué)傳感器主要被歸為三個類型，物理，化學(xué)和生物傳感器。例如幾何，熱學(xué)，力學(xué)，液態(tài)變量，使用物理傳感器測量。在這些傳感器的應(yīng)用方面，可能用于測量肌肉位移，血壓，體溫，血流，腦脊液壓，骨生長，磁場和輻射。至于化學(xué)傳感器，被測的化學(xué)量用于識別特定的化學(xué)成分，分析各種化學(xué)成分的濃度，監(jiān)測人體的化學(xué)反應(yīng)。盡管生物傳感器是特殊的化學(xué)傳感器，它們?nèi)匀槐粏为?dú)歸為特別重要的一類，生物傳感器因免疫傳感器，血糖儀，“化學(xué)金絲雀”，“共振的鏡子”，生物芯片和生物計(jì)算機(jī)出名。不僅如此，隨著生物恐怖主義潛在危險的增加，在這方面生物傳感器作為低成本高效的器件被用于日常的應(yīng)用中。人們也能從他們各自的立場看生物醫(yī)學(xué)傳感器。因此，它們可以被大致分類依據(jù)是否被用于臨床診斷和治療和是否被用于生物醫(yī)學(xué)研究的數(shù)據(jù)采集。另一方面，生物醫(yī)學(xué)傳感器可以依據(jù)它們?nèi)绾斡糜诨颊吆脱芯空n題來分類。例如無創(chuàng)型，接觸型，最小傷害，非傷害等等。普通傳感器的基本原理是通過某個特定的傳感單元收集被測數(shù)據(jù)和執(zhí)行被測量和電信號的轉(zhuǎn)換。在被測量和電信號之間有著確定的關(guān)系。一幫來說，一個傳感器由傳感單元，轉(zhuǎn)換單元和信號調(diào)節(jié)單元組成。對于生物醫(yī)學(xué)傳感器來說最基本的，最獨(dú)一

簡介：中文2500字出處ZOUNGASS,KERRPG,LUIM,ETALTHEIMPACTOFGLYCAEMICCONTROLONOUTCOMESINPATIENTSWITHEND‐STAGERENALDISEASEANDTYPE2DIABETESJNEPHROLOGY,2008,132124127血糖控制對血糖控制對2型糖尿病合并型糖尿病合并ESRDESRD患者預(yù)后的影響患者預(yù)后的影響SOPHIAZOUNGAS,PETERGKERR,MICHELLELUIANDHELENAJTEEDE摘要摘要在澳大利亞和新西蘭終末期腎病（ESRD）的發(fā)病率和患病率正迅速增加。預(yù)計(jì)到2007年，僅澳大利亞的經(jīng)濟(jì)負(fù)擔(dān)達(dá)到5億美元（數(shù)據(jù)來自2005年全國慢性腎臟病戰(zhàn)略研討會報告）。在澳大利亞和新西蘭乃至整個發(fā)達(dá)國家，導(dǎo)致終末期腎病的主要原因?yàn)?型糖尿病，在2004年已超過了腎小球腎炎?1?。迄今為止，根據(jù)指南，對糖尿病和ESRD的管理已側(cè)重于ESRD。本評論針對臨床護(hù)理提出了3個緊要問題1、缺乏可靠的工具來測量血糖水平；2、基于目前的數(shù)據(jù)證實(shí)，ESRD患者的血糖控制與預(yù)后有明顯聯(lián)系；3、缺乏對ESRD患者進(jìn)一步護(hù)理和血糖控制的效果評估。關(guān)鍵詞關(guān)鍵詞終末期腎病，血糖控制，預(yù)后，2型糖尿病2型糖尿病和型糖尿病和ESRDESRD的緊要問題的緊要問題在澳大利亞和新西蘭，大約每百萬人口中有740人接受腎臟替代治療，約420人需要透析治療?2?。如圖1所示，隨著時間的推移，上述比例正穩(wěn)步增長?2?。對于那些需要腎臟替代治療的患者，約三分之一的患者即將進(jìn)行透析治療。在澳大利亞和新西蘭，導(dǎo)致ESRD的最常見原因?yàn)樘悄虿　?005年糖尿病腎病患者占新開始透析患者的3241?1?。類似的，在所有需要腎臟替代治療的患者中，糖尿病患者分別占42和46。這些患者的大多數(shù)（約90）為2型糖尿?。▓D2）?1?。其中約有一半接受胰島素治療。透析患者的平均存活率較低。澳大利亞和新西蘭透析患者每年的死亡率分別為145和164每100人年?3?。其中相當(dāng)大的比例，約65的死因歸因于心血管疾?。–VD）和感染（2005ANZDATA注冊報告澳大利亞49CVD，13感染；新西蘭49CVD，15感染）?3?。此外，糖尿病患者中CVD的致死率是同年齡人口的10100倍?3，4?。過去的五十年里，一般人群中CVD所導(dǎo)致的死亡率已經(jīng)下降到50?5?。在患有糖尿病而無ESRD的患者中，心血管事件發(fā)生的概率也在減少?6?。正如ANZDATA的報告?3，7?，ESRD人口中，由心血管事件導(dǎo)致的死亡率保持不變，并未因醫(yī)療的進(jìn)步而有所進(jìn)展（心血管病死亡率1993年和2005年分別為485％和49％）。在為期5年的有關(guān)ESRD患者心血管事件的前瞻性研究中，那些患有糖尿病的患者，其心血管事件發(fā)生的風(fēng)險是其他人群的2倍，這種風(fēng)險不會因?yàn)槟挲g，性別，血壓，CVD既往史，吸煙情況，降脂藥和阿司匹林治療的校正而消失（未經(jīng)校正的危險比為241，P0001，95CI為183–318；校正后的危險比186,P0001,95CI為138–252；未公開數(shù)據(jù)，圖4）。ESRDESRD中加強(qiáng)糖尿病護(hù)理的作用中加強(qiáng)糖尿病護(hù)理的作用迄今為止，盡管糖尿病和ESRD患者已構(gòu)成最高危險組，但強(qiáng)化血糖控制在生存率和心血管事件發(fā)生率方面的影響仍未有前瞻性的研究。這一開創(chuàng)性研究為這一領(lǐng)域作出的貢獻(xiàn)包括糖尿病的干預(yù)和并發(fā)癥實(shí)驗(yàn)（DCCT），糖尿病干預(yù)和并發(fā)癥研究的流行病學(xué)（EDIC），英國糖尿病前瞻性研究（UKPDS）和STENO2研究。在1型和2型糖尿病患者中，所有研究都指出進(jìn)一步的血糖控制對預(yù)防微血管并發(fā)癥和心血管事件的發(fā)生有益。關(guān)于心血管事件，在DCCT/EDIC，強(qiáng)化胰島素治療能降低頸動脈內(nèi)膜中層厚度的進(jìn)展?8?，和改善1型糖尿病心血管疾病的生存率?9?。在UKPDS中嚴(yán)格控制血糖無法使2型糖尿病患者的心血管事件發(fā)生率降低P006?10?，隨后的STENO2研究表明，2型糖尿病患者存在的多種風(fēng)險因素包括高血糖的治療，將降低心血管事件的50?11?。在所有這些干預(yù)研究中未包括ESRD患者。僅有一項(xiàng)研究報告了加強(qiáng)對ESRD患者的糖尿病教育和護(hù)理的作用。在這一研究中，比較標(biāo)準(zhǔn)護(hù)理，有83名透析患者加強(qiáng)了干預(yù)，加強(qiáng)了對血糖的控制，提高了生活質(zhì)量，降低了截止肢和住院治療的概率?12?。這一研究的結(jié)果帶來了希望，同時也突出了對更大項(xiàng)隨機(jī)研究的需要。血糖控制對合并有ESRD的糖尿病患者的生存率影響幾乎沒有研究報道。有些患者表現(xiàn)出血糖控制和預(yù)后間的密切聯(lián)系，而另外一些患者則未表現(xiàn)出上述聯(lián)系?13，15?。一項(xiàng)回顧性研究指出2型糖尿病患者透析前血糖控制（血糖和HBA1C結(jié)合）與透析開始后的結(jié)局相關(guān)?17?。這些研究結(jié)果的不一致，可以用檢測血糖所用工具和研究人群的不同來解釋。最近，KALANTARZADEH等人指出，根據(jù)全國血液透析數(shù)據(jù)庫的數(shù)據(jù)，較高的HBA1C與較高的死亡風(fēng)險相關(guān)。他們的研究結(jié)果表明，嚴(yán)格的控制血糖可提高ESRD患者的存活率?18?。沒有充分控制血糖的糖尿病患者是否需要腎臟替代治療這一問題還未進(jìn)行充分的探討。最近在加拿大，TASCONA等人對100名透析患者進(jìn)行研究發(fā)現(xiàn)，超過一半的透析患者其HBA1C大于7?19?，且HBA1C唯一的獨(dú)立預(yù)測因子是糖尿病病程和血糖監(jiān)測。針對不同腎衰患者，有關(guān)血糖控制的進(jìn)一步數(shù)據(jù)迫切的需要。理想情況下，這些數(shù)據(jù)可以從澳大利亞和新西蘭終末期腎病注冊患者中獲得（ANZDATA注冊表）。血糖控制與終末期腎病預(yù)后的聯(lián)系血糖控制與終末期腎病預(yù)后的聯(lián)系ESRD患者的血糖測量常規(guī)包括自我血糖水平監(jiān)測，并用HBA1C評估長期血糖控制情況。然而，有時這些慢性腎臟病的血糖測定方法遭到質(zhì)疑。之前努力著手于對ESRD患者血糖控制的改進(jìn)，和建立精確評估血糖控制的最適方法。方法問題普遍受使用檢測結(jié)果如何解釋的困擾，包括尿毒癥毒素的干擾（氨甲酰血紅蛋白及脂質(zhì)過氧化物）。血糖控制的測量。這些毒素影響高效液相色譜法（HPLC）的結(jié)果，使糖化血紅蛋白被過高估計(jì)?20?。最近我們單位對上述方法的檢測表明（42名CKD5期患者，其中22名行血液透析，12名行腹膜透析，8名透析前）高效液相色譜法（HPLC）比免疫測定法（IA）測定的平均HBA1C值高（平均HBA1C值為68112％比（IA）的64111％，平均差異為038％，95％CI為046029％，P＜00001配對T試驗(yàn)，未公布的數(shù)據(jù)）。在無糖尿病的ESRD患者中也有相同的發(fā)現(xiàn)?21?。由于非酶蛋白糖基化是一個復(fù)雜的反應(yīng)，通過早期，中期和后期收益，主要取決于葡萄糖濃度和蛋白質(zhì)半衰期，縮短的紅細(xì)胞生存率，貧血，輸血和重組促紅細(xì)胞生成素的使用，這些因素都可能影響測量HBA1C的精度。為此，日本最近的研究報告提出由于貧血和促紅素的使用對HBA1C造成了影響，所以糖化白蛋白可能為透析糖尿病患者評估血糖情況提供了更好的方法?22?。此外，慢性腎臟病的哪一個階段與這些臨床方法問題有關(guān)還不清楚。由于尿毒癥的影響，降低了HBA1C的預(yù)測作用，因此ESRD患者有必要重新定義一個不同的“正常范圍”。最后，需要進(jìn)一步的研究以確定最可行的方法，能夠精確反映合并ESRD的糖尿病患者的平均血糖水平，就像每天血糖的變化一樣。已確立會繼續(xù)探討ESRD患者血糖控制和臨床預(yù)后的關(guān)系以及繼續(xù)研究加強(qiáng)血糖管理的影響。結(jié)論結(jié)論對合并終末期腎病的糖尿病患者進(jìn)行管理是一個緊要的臨床問題。迄今為止，幾乎沒有研究討論了包括臨床護(hù)理中測量工具評估的問題。更多的研究迫切需要，以推動現(xiàn)有證據(jù)基礎(chǔ)，提高臨床指南。