簡介：EFFECTOFTOTALKNEEARTHROPLASTYIMPLANTPOSITIONONFLEXIONANGLEBEFOREIMPLANTBONEIMPINGEMENTHIDEKIMIZUUCHI,MD,PHD,YCLIFFORDWCOLWELLJR,MD,SHUICHIMATSUDA,MD,PHD,YCESARFLORESHERNANDEZ,BS,YUKIHIDEIWAMOTO,MD,PHD,YANDDARRYLDDLIMA,MD,PHDABSTRACTWEGENERATEDPATIENTSPECIFICCOMPUTERMODELSOFTOTALKNEEARTHROPLASTYFROM10PATIENTSTOCOMPUTEMAXIMUMFLEXIONANGLEBEFOREIMPLANTBONEIMPINGEMENTMOTIONWASSIMULATEDFOR5DIFFERENTFEMORALIMPLANTPOSITIONSAND11DIFFERENTTIBIALINSERTPOSITIONSAT4DIFFERENTTIBIALPOSTERIORSLOPESINTHENEUTRALPOSITION,THEMEANMAXIMUMFLEXIONANGLEWAS1363°THERANGEBECAUSEOFANATOMICALVARIATIONAMONGPATIENTSWAS130°ACOMBINATIONOF2MMPOSTERIORTRANSLATIONOFTHEFEMORALCOMPONENTWITHA10MMANTERIORTRANSLATIONOFTHEINSERTANDA7°POSTERIORSLOPEINCREASEDFLEXIONBYAMEANOF14°RELATIVETOTHENEUTRALPOSITIONTHERATEOFCHANGEINFLEXIONANGLEWAS04°/MMTO15°/MMWITHRESPECTTOIMPLANTPOSITIONAND15°/MMINCREASEINTHEPOSTERIORCONDYLAROFFSETKEYWORDSTOTALKNEEARTHROPLASTY,KNEEFLEXIONANGLE,COMPUTERSIMULATION,COMPONENTPOSITION,ANATOMICALVARIATION?2011ELSEVIERINCALLRIGHTSRESERVEDTOTALKNEEARTHROPLASTYTKAHASBECOMEONEOFTHEMOSTSUCCESSFULORTHOPEDICPROCEDURESWITHREPORTEDSURVIVALRATESOFGREATERTHAN90AFTER15YEARS1,2WITHTHEIMPROVEMENTOFLONGTERMOUTCOMES,THEREISRENEWEDINTERESTINMAXIMIZINGRANGEOFMOTIONAFTERTKA310THERANGEOFMOTIONINFLEXIONISEXTREMELYIMPORTANTINASIANCOUNTRIESANDFORPATIENTSWITHLIFESTYLESTHATINVOLVESITTINGONTHEFLOORINDEEPFLEXION3EVENINNORTHAMERICANPATIENTS,UPTO75IDENTIFIEDTHATACTIVITIESREQUIRINGDEEPERKNEEFLEXIONANGLESUCHASSQUATTING,KNEELING,ANDGARDENINGWEREPERFORMEDWITHGREATERDIFFICULTYAFTERTKA4MANYCLINICALSTUDIESHAVEINVESTIGATEDFACTORSAFFECTINGPOSTOPERATIVERANGEOFMOTION5,6,10,11PATIENTRELATEDFACTORSSUCHASPREOPERATIVERANGEOFMOTION,BODYMASSINDEX,DISEASE,AGE,ANDSEXGREATLYINFLUENCETHEPOSTOPERATIVERANGEOFMOTIONSIMILARLY,SURGICALTECHNIQUESCANALSOAFFECTTHEPOSTOPERATIVERANGEOFMOTIONEXAMPLESINCLUDETHEHEIGHTOFJOINTLINE,PATELLARTRACKING,APPROPRIATEGAPBALANCING,RELEASEOFPOSTERIORCAPSULE,ANDREMOVALOFTHEOSTEOPHYTESANOTHERIMPORTANTFACTORISTHEPOSTERIORCONDYLAROFFSETPCO,WHICHHASBEENASSOCIATEDWITHPOSTOPERATIVERANGEOFMOTIONINFLUOROSCOPICANALYSISINVIVO5PREVIOUSSTUDIESHAVEANALYZEDTHEEFFECTOFIMPLANTALIGNMENTANDRELATIVEPOSITIONONPOSTOPERATIVERANGEOFMOTION1215WALKERETAL12REPORTEDTHATPOSTERIORANDPROXIMALFEMORALPLACEMENTANDAGREATERPOSTERIORTIBIALSLOPEINCREASEDMAXIMUMFLEXIONANGLEINPLASTICMODELSOFTHEFEMURANDTIBIAMASSINANDGOURNAY13DEMONSTRATEDTHATGREATERPCOINCREASEDTIBIALPOSTERIORSLOPE,ANDAMOREPOSTERIORFEMOROTIBIALCONTACTPOINTCANINCREASEFLEXIONINASTUDYTHATUSED2DIMENSIONALTEMPLATESOFPROSTHETICCOMPONENTSONLATERALKNEERADIOGRAPHSHOWEVER,THECOMBINEDEFFECTOFTHE3DIMENSIONALANATOMYOFTHEPATIENTANDTHEIMPLANTPOSITIONHASNOTBEENSTUDIEDWEGENERATEDPATIENTSPECIFICANATOMICALMODELSOFIMPLANTBONEIMPINGEMENTTOEVALUATETHEEFFECTOFIMPLANTPOSITIONANDANATOMICALVARIATIONONFLEXIONANGLEOURPRIMARYHYPOTHESISWASTHATIMPLANTPOSITIONWOULDSIGNIFICANTLYAFFECTMAXIMUMKNEEFLEXIONANGLEBEFOREBONEPROSTHESISIMPINGEMENTOURSECONDARYHYPOTHESISWASTHATTHEPCOWOULDCORRELATESIGNIFICANTLYWITHMAXIMUMFLEXIONANGLEFROMTHESHILEYCENTERFORORTHOPAEDICRESEARCHANDEDUCATIONATSCRIPPSCLINIC,LAJOLLA,CAANDYDEPARTMENTOFORTHOPAEDICSURGERY,GRADUATESCHOOLOFMEDICALSCIENCES,KYUSHUUNIVERSITY,FUKUOKA,JAPANSUBMITTEDAPRIL19,2010ACCEPTEDAUGUST1,2010NOBENEFITSORFUNDSWERERECEIVEDINSUPPORTOFTHESTUDYREPRINTREQUESTSDARRYLDDLIMA,MD,PHD,SHILEYCENTERFORORTHOPAEDICRESEARCHANDEDUCATIONATSCRIPPSCLINIC,11025NTORREYPINESROAD,SUITE140,LAJOLLA,CA92037?2011ELSEVIERINCALLRIGHTSRESERVED08835403/260500113600/0DOI101016/JARTH201008002721THEJOURNALOFARTHROPLASTYVOL26NO52011INSERTACONSTANTMASSWASAPPLIEDATAFIXEDDISTANCE300MMFROMTHECLINICALEPICONDYLARAXISOFTHEFEMURTOGENERATEAFLEXIONMOMENTBECAUSEOFGRAVITYTHEFEMURWASTHENALLOWEDTOFLEX,ANDTHEMAXIMUMFLEXIONWASRECORDEDBEFOREIMPINGEMENTBETWEENTHEPOSTERIORCORTEXOFTHEFEMURANDTHETIBIALINSERTFIG2PEAKFLEXIONANGLESWERERECORDEDASTHEINSERTWASMOVEDAT2MMINTERVALSRANGINGFROM10MMANTERIORTO10MMPOSTERIORFOREACHOFTHE5FEMORALIMPLANTPOSITIONSNEUTRAL,2MMANTERIOR/POSTERIOR,AND2MMPROXIMAL/DISTALFROMTHENEUTRALTHISPROCESSWASTHENREPEATEDFOREACHOF4TIBIALPOSTERIORSLOPEANGLES0°,3°,5°,AND7°TOTHEMECHANICALAXISOFTHETIBIAWEALSOMEASUREDTHEPCOFOREACHOFTHEDIFFERENTFEMORALIMPLANTPOSITIONSASDEPICTEDINFIG1BPOSTERIORCONDYLAROFFSETWASMEASUREDASTHEMAXIMUMDISTANCEBETWEENTHEPOSTERIORSURFACEOFTHEDISTALFEMURANDTHEPOSTERIORCONDYLE5VALIDATIONOFTHECOMPUTERMODELFOURFRESHFROZENHUMANCADAVERKNEESWERETESTEDTOVALIDATETHECOMPUTERMODELCOMPUTEDTOMOGRAPHICSCANSWEREOBTAINEDAFTERIMPLANTINGFIDUCIALMARKERSINEACHTIBIAANDFEMUR3TITANIUMSCREWSINEACHBONEKNEEARTHROPLASTYWASPERFORMEDUSINGASURGICALNAVIGATIONSYSTEMSTRYKERNAVIGATION,FREIBURG,GERMANYCOMPONENTALIGNMENTWASSIMILARTOTHATDESCRIBEDFORTHECOMPUTATIONALMODELSCORPIOCRSTRYKERORTHOPAEDICSTIBIALANDFEMORALCOMPONENTSWEREUSEDTHEPATELLAWASNOTRESURFACEDALLSOFTTISSUESAROUNDTHEKNEEJOINTWEREREMOVEDASMUCHASPOSSIBLEEXCEPTTHEPOSTERIORCRUCIATELIGAMENT,THEMEDIALANDLATERALCOLLATERALLIGAMENTS,ANDTHEEXTENSORMECHANISMAFTERARTHROPLASTYTHETIBIAWASMOUNTEDVERTICALLYONACUSTOMRIG,ANDTHEFEMURWASALLOWEDTOFLEXPASSIVELYUNDERGRAVITYSIMILARTOTHESETUPOFTHECOMPUTERMODELTHEFIDUCIALMARKERSWEREUSEDTOREGISTERTHECOMPONENTSANDBONESUSINGTHESURGICALNAVIGATIONSYSTEMKNEEKINEMATICSANDCOMPONENTPOSITIONWEREMEASUREDTHEMAXIMUMPASSIVEFLEXIONPOSSIBLEWITHOUTSUBLUXATIONWASRECORDEDFORCOMPUTATIONALMODELVALIDATION,SUBJECTSPECIFICMODELSWERECONSTRUCTEDUSINGTHEBONEGEOMETRYFROMCTSCANSFROMTHE4CADAVERKNEESANDTHEGEOMETRYOFIMPLANTSUSEDASDESCRIBEDABOVEEXPERIMENTALLYMEASUREDMAXIMUMFLEXIONANGLESWERECOMPAREDWITHTHOSEPREDICTEDBYTHECOMPUTATIONALMODELRESULTSREPEATEDMEASURESANALYSISOFVARIANCEWEREPERFORMEDTOMEASUREDIFFERENCESINMAXIMUMFLEXIONFORTHEVARIOUSIMPLANTPOSITIONSBONFERRONICORRECTEDPOSTHOCTESTSWEREUSEDTODETERMINETHESIGNIFICANCEOFTHEDIFFERENCEINMAXIMUMFLEXIONFOREACHCONDITIONRELATIVETONEUTRALPOSITIONSPEARMANRANKCORRELATIONWASUSEDTODETECTTHESTRENGTHOFTHELINEARCORRELATIONBETWEENPCOANDMAXIMUMKNEEFLEXIONANGLEPOWERANALYSISDETERMINEDTHATASAMPLESIZEOF10WASSUFFICIENTTODETECTADIFFERENCEINMAXIMUMFLEXIONANGLEOF3°ORGREATERWITHAPOWEROF090,ASSUMINGANSDOF25°MAXIMUMFLEXIONANGLESMEASUREDEXPERIMENTALLYINCADAVERKNEESWAS1420°±36°MEAN±SDRANGE,1380°1460°COMPUTERSIMULATEDMAXIMUMFLEXIONUSINGMODELSGENERATEDFROMCADAVERCTSCANSWAS1472°±49°RANGE,1428°1518°,WHICHWASSIMILARTOTHATEXPERIMENTALLYMEASURED,WITHANAVERAGEABSOLUTEERROROF52°±16°RANGE,31°68°IN2OFALL10KNEES,THEFEMURHADTOBETRANSLATEDANTERIORLYBYGREATERTHAN1MM23AND49MMTOAVOIDNOTCHINGOFTHEANTERIORCORTEXTHEDIFFERENCEINFLEXIONANGLEBETWEENTHEMECHANICALAXISANDTHEANATOMICALAXISWAS31°±11°RANGE,12°45°WETHEREFOREALIGNEDTHEFEMORALCOMPONENTTOTHEANATOMICALAXISOFTHEFEMURTOASSESSANYEFFECTONANTEROPOSTERIORPOSITIONTHEMEASUREDANTEROPOSTERIORTRANSLATIONOFANATOMICALLYALIGNEDCOMPONENTSWASLESSTHAN1MMRELATIVETOTHETRANSLATIONOFTHECOMPONENTSALIGNEDTOTHEMECHANICALAXISWITHTHECOMPONENTSINNEUTRALPOSITION,THEMEANMAXIMUMFLEXIONANGLEFOR10KNEESWAS1363°±47°RANGE,13070°1437°THEVARIATIONINFLEXIONINOURCOHORTOF10KNEESWAS130°,WHICHREFLECTSTHEVARIATIONINPATIENTANATOMYOFOURCOHORTWITHTHEPOSTERIORSLOPEOFTHETRAYSETTO0°,AMOREPROXIMALTABLE1DEMOGRAPHICDATAANDIMPLANTSIZEMEANAGEYMEAN±SD,RANGE746±815784FEMOROTIBIALANGLEMEAN±SD,RANGE1806°±41°175°1875°SIZE5MALE/FEMALE0KNEE/2KNEESSIZE7MALE/FEMALE2KNEES/2KNEESSIZE9MALE/FEMALE2KNEES/2KNEESFIG2REPRESENTATIVEIMAGEDEMONSTRATINGTHEPOINTOFIMPINGEMENTATTHEMAXIMUMFLEXIONANGLEIMPLANTPOSITIONONFLEXIONANGLEFORTKA?MIZUUCHIETAL723

簡介：CARDIACTROPONINIRELEASEINACUTEPULMONARYEMBOLISMINRELATIONTOTHEDURATIONOFSYMPTOMSGOPIKRISHNAPUNUKOLLUA,IJAZAKHANB,,RAMESHMGOWDAA,GAURAVLAKHANPALA,BALENDUCVASAVADAA,TERRENCEJSACCHIAADIVISIONOFCARDIOLOGY,LONGISLANDCOLLEGEHOSPITAL,BROOKLYN,NY,USABDIVISIONOFCARDIOLOGY,UNIVERSITYOFMARYLANDSCHOOLOFMEDICINE,22SOUTHGREENESTREETS3B06,BALTIMORE,MD21201,USARECEIVED24JUNE2003RECEIVEDINREVISEDFORM5JANUARY2004ACCEPTED8JANUARY2004AVAILABLEONLINE2APRIL2004ABSTRACTPURPOSETOEVALUATETHERELEASEOFCARDIACTROPONINIINNORMOTENSIVEPATIENTSWITHACUTEPULMONARYEMBOLISMINRELATIONTOTHEDURATIONOFSYMPTOMSMETHODSFIFTYSEVENNORMOTENSIVEPATIENTSWITHACUTEPULMONARYEMBOLISMWEREINCLUDEDINTHESTUDYPATIENTSWEREDIVIDEDINTOTWOGROUPSBASEDONTHEDURATIONOFSYMPTOMSATPRESENTATIONSYMPTOMSOFV72H,GROUPASYMPTOMSOF72H,GROUPBSERUMCARDIACTROPONINILEVELSWEREMEASUREDATPRESENTATIONRESULTSMEANAGEWAS63F18YEARSAND2340PATIENTSWEREMALESTHIRTYTHREE58PATIENTSHADSYMPTOMSOFV72HGROUPAAND2442HADSYMPTOMSOF72HGROUPBBOTHGROUPSHADSIMILARPREVALENCEOFRIGHTVENTRICULARDYSFUNCTIONONECHOCARDIOGRAPHY55N18INGROUPAVS42N10INGROUPB,PNSSIXTEENPATIENTSHADELEVATEDSERUMCARDIACTROPONINIMEANFSD33F23NG/ML,RANGE06–83NG/MLELEVATEDSERUMCARDIACTROPONINIWASSTRONGLYASSOCIATEDWITHRIGHTVENTRICULARDYSFUNCTIONP0015ALLPATIENTSWITHELEVATEDSERUMCARDIACTROPONININ16WEREINGROUPAP72HGROUPBTABLE2THEREWASNODIFFERENCEINTHESEVERITYOFPULMONARYEMBOLISMBETWEENTHETWOGROUPSANDBOTHGROUPSHADSIMILARPREVALENCEOFRIGHTVENTRICULARDYSFUNCTION55N18INGROUPAVS42N10THEPREVALENCEOFCARDIOVASCULARFACTORSWASSIMILARINBOTHGROUPSSIXTEENPATIENTSHADELEVATEDSERUMCARDIACTROPONINIMEANFSD33F23NG/ML,RANGE06–83NG/MLELEVATEDCARDIACTROPONINIWASSTRONGLYASSOCIATEDWITHRIGHTVENTRICULARDYSFUNCTIONP0015ALLPATIENTSWITHELEVATEDSERUMCARDIACTROPONINILEVELSN16WEREINGROUPANONEOFTHEPATIENTSINGROUPBHADELEVATEDSERUMCARDIACTROPONINILEVELSP00001AMONGGROUPA,12OF1867PATIENTSWITHP00005AND4OF1527PATIENTSWITHOUTPNSRIGHTVENTRICULARDYSFUNCTIONHADELEVATEDSERUMCARDIACTROPONINITHIRTEENOF1681PATIENTSWITHELEVATEDSERUMCARDIACTROPONINIHADDURATIONOFSYMPTOMSV24HATPRESENTATIONTABLE3INPATIENTSPRESENTINGWITHIN8HAFTERSYMPTOMONSETN7,THEPEAKSERUMTROPONINILEVELSWEREFOUNDATCLINICALPRESENTATIONIN50N4OFTHEPATIENTS4DISCUSSION41BACKGROUNDCARDIACTROPONINELEVATIONINACUTEPULMONARYEMBOLISMISASSOCIATEDWITHBOTHMASSIVEANDSUBMASSIVEPULMONARYEMBOLISMPACOURETETAL15INITIALLYREPORTEDTHATCARDIACTROPONINILEVELSWEREELEVATEDINSUBMASSIVEPULMONARYEMBOLISMSUBSEQUENTSTUDIESCONFIRMEDTHATSERUMCARDIACTROPONINIANDTLEVELSCOULDBEELEVATEDINBOTHMASSIVEANDSUBMASSIVEPULMONARYEMBOLISMWITHASTRONGCORRELATIONWITHRIGHTVENTRICULARDYSFUNCTION5,6,11,12,16–18THEELEVATEDCARDIACTROPONINSHAVEINDEPENDENTPROGNOSTICVALUEFORINHOSPITALDEATH,HYPOTENSIONANDCARDIOGENICSHOCKINPATIENTSWITHPULMONARYEMBOLISM5,11SIMILARRELATIONWASREPORTEDBYKONSTANTINIDESETAL12WHEREELEVATEDCARDIACTROPONINILEVELSWEREASSOCIATEDWITHINCREASEDOVERALLMORTALITYANDCOMPLICATEDINHOSPITALCOURSETHERISKOFCOMPLICATEDINHOSPITALCOURSEWASREPORTEDTOBEFIVETIMESHIGHERINTHEHIGHCARDIACTROPONINIGROUPCOMPAREDWITHPATIENTSWITHMODERATECTNIELEVATION42CARDIACTROPONINIFORRISKSTRATIFICATIONINPULMONARYEMBOLISMEVENTHOUGHELEVATEDLEVELSOFCARDIACTROPONINIANDTHAVEPROGNOSTICSIGNIFICANCEINACUTEPULMONARYEMBOLISM,THECLINICALUTILITYOFELEVATEDCARDIACTROPONINLEVELSINTHERISKSTRATIFICATIONOFHEMODYNAMICALLYSTABLEPATIENTSISUNKNOWNANDITISAPPEALINGTOSPECULATETHATTROPONINSCOULDFUNCTIONASADISCRIMINATORFORTHROMBOLYTICTHERAPYINPULMONARYEMBOLISMPATIENTSWHOAREHEMODYNAMICALLYSTABLEBUTHAVERIGHTVENTRICULARDYSFUNCTIONLARGEMULTICENTERSTUDIESARENEEDEDTOPROVETHATELEVATEDLEVELSOFCARDIACTROPONINSMAYBEUSEFULINTHERAPEUTICTRIAGEOFNORMOTENSIVEPATIENTSWITHRIGHTVENTRICULARDYSFUNCTIONINACUTEPULMONARYEMBOLISM,WHEREASEQUALLYIMPORTANTWOULDBETOEVALUATETHERELEASEOFTROPONINSINACUTEPULMONARYEMBOLISMESPECIALLYINRELATIONTODURATIONOFSYMPTOMSASTHEWINDOWPERIODFORTHROMBOLYTICTHERAPYINACUTEPULMONARYEMBOLISMCANEXTENDUPTO14DAYS19–2143RELEASEKINETICSOFCARDIACTROPONINITHEMAJORITYOFCARDIACTROPONINSAREBOUNDTOMYOFILAMENTS,ANDTHEREMAINDERISFREEINTHECYTOSOLINACUTEMYOCARDIALINFARCTIONSUFFICIENTMYOCARDIALNECROSISOCCURSTOSUSTAINANABNORMALLYELEVATEDLEVELSOFTROPONINS,WHICHBEGINTORISEIN4–6HANDPEAKATABOUT24HAFTERTHEONSETOFSYMPTOMSTOREACHLEVELSOFABOUT20–50TIMESTHEUPPERREFERENCELIMITTHECONCENTRATIONOFTHESESUBUNITSREMAINELEVATEDINBLOODFORMANYDAYS,ABOUT4–7DAYSFORCARDIACTROPONINIAND10–14DAYSFORCARDIACTROPONINT,DUETOPROTRACTEDRELEASEFROMSTORESBOUNDTODETERIORATINGMYOFILAMENTS22,23ITISESTIMATEDTHAT3–4OFCARDIACTROPONINIAND6–8OFCARDIACTROPONINTISFOUNDASFREECYTOPLASMICCOMPONENTS24,25INMICROINFARCTIONSANDINITIALSTAGESOFMYOCARDIALINJURY,ITHASBEENTHOUGHTTHATRELEASEOFTHECYTOPLASMICTROPONINOCCURSWITHTHEDETECTABLELEVELSOFCARDIACTROPONINSINPERIPHERALBLOOD22INADDITION,OTHERFORMSOFCARDIACTROPONINIANDTHAVEBEENSHOWNTOBERELEASEDINTOTHEBLOODAFTERMYOCARDIALINFARCTION26SOTHERELEASEANDCLEARANCEMECHANISMSOFCARDIACTROPONINIANDTARESTILLINCOMPLETELYUNDERSTOODTHEREARENOSTUDIESWHERECARDIACTROPONINSHAVEBEENEVALUATEDINRELATIONTOTHEONSETOFSYMPTOMSINACUTEPULMONARYEMBOLISM,ALTHOUGHSTUDIESHAVEEVALUATEDTHESEMARKERSINRELATIONTOTHETIMEOFPRESENTATION11,12KONSTANTINIDESETAL12INCLUDED126PATIENTSWITH51OFTHEMPRESENTINGWITHSYMPTOMSOFLESSTHAN24H,BUTDATAONPROPORTIONOFPATIENTSWITHELEVATEDTROPONINLEVELSINRELATIONTOTHEDURATIONOFSYMPTOMSWASNOTEVALUATEDTHEPEAKTROPONINLEVELSWEREOBSERVEDWITHINTHEFIRST4TABLE3ELEVATEDCARDIACMARKERSBASEDONTHEDURATIONOFSYMPTOMSELEVATEDCARDIACMARKERDURATIONOFSYMPTOMSV24HN21DURATIONOFSYMPTOMS24–48HN6DURATIONOFSYMPTOMS48–72HN6CARDIACTROPONINI1362233117CREATINEKINASE210NONENONECREATINEKINASEMB629117NONEALLVALUESARENUMBEROFPATIENTSGPUNUKOLLUETAL/INTERNATIONALJOURNALOFCARDIOLOGY992005207–211209

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,ETALMICRORNASNOVELREGULATORSINVOLVEDINTHEPATHOGENESISOFPSORIASISPLOSONE20072E61019PHILIPPIDOUD,SCHMITTM,MOSERD,MARGUEC,NAZAROVPV,MULLERA,ETALSIGNATURESOFMICRORNASANDSELECTEDMICRORNATARGETGENESINHUMANMELANOMACANCERRES2010704163–7320VOLINIAS,CALINGA,LIUCG,AMBSS,CIMMINOA,PETROCCAF,ETALAMICRORNAEXPRESSIONSIGNATUREOFHUMANSOLIDTUMORSDEFINESCANCERGENETARGETSPROCNATLACADSCIUSA20061032257–6121BHAUMIKD,SCOTTGK,SCHOKRPURS,PATILCK,CAMPISIJ,BENZCCEXPRESSIONOFMICRORNA146SUPPRESSESNFKAPPABACTIVITYWITHREDUCTIONOFMETASTATICPOTENTIALINBREASTCANCERCELLSONCOGENE2008275643–722LIY,VANDENBOOMTG,WANGZ,KONGD,ALIS,PHILIPPA,ETALMIR146ASUPPRESSESINVASIONOFPANCREATICCANCERCELLSCANCERRES2010701486–9523MEIJ,BACHOOR,ZHANGCMICRORNA146AINHIBITSGLIOMADEVELOPMENTBYTARGETINGNOTCH1MOLCELLBIOL2011313584–9224BEHRENSMI,LENDONC,ROECM,ACOMMONBIOLOGICALMECHANISMINCANCER,ALZHEIMER’SDISEASECURRALZHEIMERRES20066196–20425ROECM,BEHRENSMI,XIONGC,MILLERJP,MORRISJC,ALZHEIMERDISEASE,ETALNEUROLOGY200564895–826ROECM,FITZPATRICKAL,XIONGC,SIEHW,KULLERL,MILLERJP,ETALCANCERLINKEDTOALZHEIMERDISEASEBUTNOTVASCULARDEMENTIANEUROLOGY201074106–1227LIYY,CUIJG,HILLJM,BHATTACHARJEES,ZHAOY,LUKIWWJINCREASEDEXPRESSIONOFMIRNA146AINALZHEIMER’SDISEASETRANSGENICMOUSEMODELSNEUROSCILETT201148794–828SETHIP,LUKIWWJMICRORNAABUNDANCEANDSTABILITYINHUMANBRAINSPECIFICALTERATIONSINALZHEIMER’SDISEASETEMPORALLOBENEOCORTEXNEUROSCILETT2009459100–4400LLWANGETAL/MEDICALHYPOTHESES782012398–401

簡介：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

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(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(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)開辟了新的觀察途徑來研究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)

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

簡介：點(diǎn)擊查看更多外文翻譯--國內(nèi)醫(yī)學(xué)儀器工程的現(xiàn)狀和存在的問題精彩內(nèi)容。

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(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，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。暫時(shí)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(dòng)。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(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)震蕩過程的調(diào)頻速率更?。辉谶@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,ASWELLASREGIONALSTRUCTURALANDSTIFFNESSCHARACTERISTICSCRITICALLYDETERMINETHELOCALESSENVIRONMENTANDTHESUBSEQUENTNATURALHISTORYOFINDIVIDUALATHEROSCLEROTICLESIONS33,35,374ROLEOFESSINATHEROGENESISANDEARLYPLAQUEFORMATIONINSTRAIGHTARTERIALREGIONSWITHNONDISTURBEDFLOW,WHEREESSVARIESWITHINAMODERATE/PHYSIOLOGICALRANGE,ENDOTHELIALCELLSEXPRESSVARIOUSATHEROPROTECTIVEGENES,ANDDECREASESEVERALPROATHEROGENICONES,LEADINGTOSTABILITYANDQUIESCENCE34THEROLEOFHIGHESSINEARLYATHEROSCLEROSISISNOTWELLINVESTIGATED,BUTITAPPEARSTOBEATHEROPROTECTIVEINCONTRAST,INREGIONSWITHLOWANDDISTURBEDFLOWWHERELOWESSOCCURS,THEATHEROPROTECTIVEGENESARESUPPRESSED,WHILETHEPROATHEROGENICGENESAREOVEREXPRESSED,THEREBYPROMOTINGATHEROGENESISENDOTHELIALCELLSSENSETHELOCALLOWESSSTIMULITHROUGHSEVERALMECHANORECEPTORSLOCATEDONTHEIRSURFACE32,34,38THESEMECHANORECEPTORSINTURNTRIGGERANETWORKOFINTRACELLULARCASCADES,WHICHCULMINATEINTHEACTIVATIONOFTRANSCRIPTIONFACTORSTHATTRANSMIGRATEINTOTHENUCLEUSANDSHIFTGENEANDSUBSEQUENTLYPHENOTYPICENDOTHELIALCELLEXPRESSIONTOANATHEROSCLEROTICSTATE32,33,39–42THELARGESTBODYOFEVIDENCEREGARDINGTHEROLEOFESSINATHEROSCLEROSISISDERIVEDFROMINVITROANDINVIVOANIMALSTUDIESALTHOUGHTHESESTUDIESUTILIZEDFAIRLYHETEROGENEOUSESSPATTERNSBOTHINDIRECTIONANDMAGNITUDE,WHICHDONOTALWAYSRESEMBLETHEREALHUMANBLOODFLOWCONDITIONS,THEYPROVIDEDTHEFOUNDATIONANDADVANCEDOURUNDERSTANDINGCONCERNINGTHEROLEOFESSINATHEROSCLEROSISFIGURE4SHOWSTHEIMPLICATIONOFLOWESSINTHEPATHOPHYSIOLOGYOFEARLYATHEROSCLEROSIS32,34ESSINDUCESENDOTHELIALDYSFUNCTIONBYREDUCINGNITRICOXIDEANDINCREASINGENDOTHELIN1,43PROVOKESENDOTHELIALCELLAPOPTOSIS44ANDCONFORMATIONALCHANGESOFENDOTHELIALCELLSFROMFUSIFORMTOPOLYGONALSHAPE,45INDUCESSUBENDOTHELIALACCUMULATIONOFLOWDENSITYLIPOPROTEINCHOLESTEROL,46ANDMODULATESTHEOXIDATIVETRANSFORMATIONOFLOWDENSITYLIPOPROTEINCHOLESTEROLBYSTIMULATINGTHEPRODUCTIONOFREACTIVEOXYGENSPECIES47THROUGHFIGURE3ATYPESOFBLOODFLOWBTYPESOFESSADAPTEDFROMCHATZIZISISETAL34JJWENTZELETAL236BYGUESTONNOVEMBER30,2014DOWNLOADEDFROM

簡介：點(diǎn)擊查看更多醫(yī)學(xué)外文翻譯--心肌梗死初級(jí)血管成形術(shù)治療術(shù)后的超聲心動(dòng)圖下舒張功能障礙與磁共振心肌梗死面積的關(guān)系精彩內(nèi)容。

簡介：點(diǎn)擊查看更多醫(yī)學(xué)外文翻譯--股骨柄偏距和股骨頭直徑對(duì)于全髖關(guān)節(jié)置換術(shù)后 髖關(guān)節(jié)安全活動(dòng)范圍的影響精彩內(nèi)容。

簡介：點(diǎn)擊查看更多醫(yī)學(xué)外文翻譯--單中心分析應(yīng)用奧里根一次性套扎治療痔瘡精彩內(nèi)容。

簡介：點(diǎn)擊查看更多醫(yī)學(xué)專業(yè)外文翻譯---基于opta細(xì)化算法的有關(guān)腦動(dòng)脈瘤檢測(cè)的研究精彩內(nèi)容。

簡介：點(diǎn)擊查看更多醫(yī)學(xué)外文翻譯--利用獨(dú)立分量分析對(duì)自然連續(xù)音樂刺激下功能性磁共振（fmri）分解中關(guān)鍵性問題的研究精彩內(nèi)容。

簡介：基于移動(dòng)手機(jī)平臺(tái)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(dòng)手機(jī)平臺(tái)的生物醫(yī)學(xué)傳感器技術(shù)基于移動(dòng)手機(jī)平臺(tái)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(cè)、診斷、監(jiān)測(cè)、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(tái)通常不是很容易能夠獲取，對(duì)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(dòng)手機(jī)的新技術(shù)逐漸改變了這樣一個(gè)情況。幾乎所有人都擁有的移動(dòng)手機(jī)通過與各種生物醫(yī)學(xué)傳感器結(jié)合提供一個(gè)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(duì)基本原理做了一個(gè)簡要的介紹，并且介紹了幾個(gè)新例子或概念。重點(diǎn)尤其放在基于移動(dòng)手機(jī)平臺(tái)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(dòng)手機(jī)平臺(tái)的全面結(jié)合將會(huì)為即將到來的全民醫(yī)療帶來一個(gè)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(dòng)手機(jī)，復(fù)合系統(tǒng)，健康管理基于移動(dòng)手機(jī)平臺(tái)的生物醫(yī)學(xué)傳感器技術(shù)3明顯。向這樣一個(gè)符合系統(tǒng)努力一定會(huì)在研究和應(yīng)用方面創(chuàng)造許多機(jī)會(huì)。建立這樣一個(gè)系統(tǒng)會(huì)導(dǎo)致電氣和機(jī)械技術(shù)迅速發(fā)展?？紤]到應(yīng)用，這個(gè)平臺(tái)將會(huì)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(duì)生物醫(yī)學(xué)傳感器和基于手機(jī)的傳感系統(tǒng)做一個(gè)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(shí)并且舉幾個(gè)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?；谑謾C(jī)的傳感系統(tǒng)是一個(gè)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(hào)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(hào)。生物醫(yī)學(xué)傳感器獲取表示生理特征的信號(hào)并且將它們轉(zhuǎn)換成電信號(hào)。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(duì)兩方都沒有副作用，因?yàn)閮煞綄?duì)傳感器的表現(xiàn)都起了重要作用。根據(jù)被測(cè)量來看，生物醫(yī)學(xué)傳感器主要被歸為三個(gè)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(cè)量。在這些傳感器的應(yīng)用方面，可能用于測(cè)量肌肉位移，血壓，體溫，血流，腦脊液壓，骨生長，磁場(chǎng)和輻射。至于化學(xué)傳感器，被測(cè)的化學(xué)量用于識(shí)別特定的化學(xué)成分，分析各種化學(xué)成分的濃度，監(jiān)測(cè)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(xiǎn)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(chǎng)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(gè)特定的傳感單元收集被測(cè)數(shù)據(jù)和執(zhí)行被測(cè)量和電信號(hào)的轉(zhuǎn)換。在被測(cè)量和電信號(hào)之間有著確定的關(guān)系。一幫來說，一個(gè)傳感器由傳感單元，轉(zhuǎn)換單元和信號(hào)調(diào)節(jié)單元組成。對(duì)于生物醫(yī)學(xué)傳感器來說最基本的，最獨(dú)一