簡介：ULTRASOUNDSCREENINGOFPERIARTICULARSOFTTISSUEABNORMALITYAROUNDMETALONMETALBEARINGSTAKASHINISHII,MD,PHD,TAKASHISAKAI,MD,PHD,YMASAKITAKAO,MD,PHD,YHIDEKIYOSHIKAWA,MD,PHD,YANDNOBUHIKOSUGANO,MD,PHDABSTRACTALTHOUGHMETALHYPERSENSITIVITYORPSEUDOTUMORSARECONCERNSFORMETALONMETALMOMBEARINGS,DETAILEDPATHOLOGIESOFPATTERNS,SEVERITY,ANDINCIDENCEOFPERIPROSTHETICSOFTTISSUELESIONSAREINCOMPLETELYUNDERSTOODWEEXAMINEDTHEPOTENTIALOFULTRASOUNDFORSCREENINGOFPERIARTICULARSOFTTISSUELESIONSAROUNDMOMBEARINGSULTRASOUNDEXAMINATIONSWERECONDUCTEDIN88HIPS79PATIENTSWITHMOMHIPRESURFACINGSORMOMTOTALHIPARTHROPLASTIESWITHALARGEFEMORALHEADFOURQUALITATIVEULTRASOUNDPATTERNSWERESHOWN,INCLUDINGNORMALPATTERNIN69HIPS,JOINTEXPANSIONPATTERNIN11HIPS,CYSTICPATTERNIN5HIPS,ANDMASSPATTERNIN3HIPSHIPSWITHTHELATTER3ABNORMALPATTERNSSHOWEDSIGNIFICANTLYHIGHERFREQUENCYOFCLINICALSYMPTOMS,WITHOUTSIGNIFICANTDIFFERENCESOFSEX,DURATIONOFIMPLANTATION,HEADSIZES,ANDCUPABDUCTION/ANTEVERSIONANGLES,COMPAREDWITHHIPSWITHNORMALPATTERNULTRASOUNDEXAMINATIONPROVIDESSENSITIVESCREENINGOFSOFTTISSUEREACTIONSAROUNDMOMBEARINGSANDMAYBEUSEFULINMONITORINGPROGRESSIONANDDEFININGTREATMENTFORPERIARTICULARSOFTTISSUEABNORMALITIESKEYWORDSMETALONMETAL,ULTRASOUND,MRIMAGING,SOFTTISSUEREACTION,BEARINGS?2012ELSEVIERINCALLRIGHTSRESERVEDINTHE2000S,RENEWEDMETALONMETALMOMHIPRESURFACINGANDTOTALHIPARTHROPLASTYTHAWITHALARGEFEMORALHEADGAINEDGREATPOPULARITYWITHTHEEXPECTATIONOFLOWBEARINGWEAR,HIGHFUNCTIONANDACTIVITYOFPATIENTS,ANDLOWINCIDENCEOFPOSTOPERATIVEDISLOCATION13ASMOMHIPARTHROPLASTIESHAVEBECOMEMOREWIDESPREAD,INCREASINGABNORMALREACTIONSINPERIARTICULARSOFTTISSUEREACTIONSTHATPRESENTASCYSTS,FLUIDCOLLECTION,ENHANCEDBURSAE,SOLIDMASS,ANDINFLAMMATORYMASSESHAVEBEENREPORTED410SOMEOFTHESECASESWERERELATEDTOSEVEREPAININTHEHIPORGROIN,PALPABLEHUGEMASSES,OREXTENSIVEPERIPROSTHETICBONELOSSLEADINGTOREVISIONSURGERYWITHRESECTIONOFSOFTTISSUELESIONS,ANDALTERATIONINBEARINGSWITHOTHERMATERIALS9FROMANALYSESOFRETRIEVEDTISSUEANDCOMPONENTS,ADELAYEDTYPEHYPERSENSITIVEREACTIONSPECIFICALLYTERMEDASEPTICLYMPHOCYTICVASCULITIS–ASSOCIATEDLESIONSORRESPONSETOEXCESSIVEWEARPARTICLESOFMOMBEARINGSWASSUSPECTEDASTHEMAINCAUSEOFTHESOFTTISSUEREACTIONS5,1113HOWEVER,THEDETAILEDPATHOLOGIESOFPATTERNS,SEVERITY,INCIDENCE,ANDNATURALCOURSEOFPERIPROSTHETICSOFTTISSUELESIONSHAVENOTYETBEENELUCIDATEDONEOFTHEDIFFICULTIESENCOUNTEREDININVESTIGATIONOFPERIARTICULARSOFTTISSUEREACTIONSAROUNDARTIFICIALJOINTSISTHEABSENCEOFSENSITIVEIMAGINGMODALITIESPLAINRADIOGRAPHYANDCOMPUTEDTOMOGRAPHYARELESSSENSITIVEFORTHEEVALUATIONOFSOFTTISSUEDISORDERSBECAUSEOFPOORIMAGINGCONTRASTBETWEENNORMALANDABNORMALSTRUCTURESMAGNETICRESONANCEIMAGINGMRIHASTHEADVANTAGESOFSUPERIORIMAGINGCONTRASTFORSOFTTISSUEABNORMALITIESANDTHEREADYAVAILABILITYOF3DIMENSIONALASSESSMENTOFABNORMALLESIONSHOWEVER,THEASSESSMENTOFSOFTTISSUEREACTIONSADJACENTTOTHEIMPLANTWASDIFFICULTBECAUSEOFMETALSUSCEPTIBILITYARTIFACTSEVENWHILEUSINGSOPHISTICATEDMETALARTIFACTREDUCTIONTECHNIQUES9,14,15ULTRASOUNDASSESSMENTAROUNDTHEHIPARTHROPLASTYHASSEVERALADVANTAGESOVEROTHERIMAGINGMODALITIESTHESEINCLUDETHEABSENCEOFIONIZINGRADIATION,ABSENCEOFMETALARTIFACTSINTRODUCEDBYIMPLANTS,ANDRELATIVELYLOWCOST16THEREFORE,ULTRASOUNDASSESSMENTMAYBESUITABLEFORTHESCREENINGOFPERIARTICULARSOFTTISSUEREACTIONSAFTERHIPARTHROPLASTYSOMEREPORTSDEMONSTRATEDTHEUSEOFULTRASOUNDFORTHEEVALUATIONOFPERIARTICULARSOFTTISSUEREACTIONSINMOMBEARINGS6,17,18FROMTHEDEPARTMENTOFORTHOPAEDICMEDICALENGINEERING,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA,JAPANANDYDEPARTMENTOFORTHOPAEDICSURGERY,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA,JAPANSUBMITTEDAPRIL4,2011ACCEPTEDSEPTEMBER16,2011THECONFLICTOFINTERESTSTATEMENTASSOCIATEDWITHTHISARTICLECANBEFOUNDATDOI101016/JARTH201109015REPRINTREQUESTSTAKASHINISHII,MD,DEPARTMENTOFORTHOPAEDICMEDICALENGINEERING,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA5650871,JAPAN?2012ELSEVIERINCALLRIGHTSRESERVED08835403/270600123600/0DOI101016/JARTH201109015895THEJOURNALOFARTHROPLASTYVOL27NO62012COMPONENTAND4“MASSPATTERN”WITHALARGEMASSEXTENDINGANTERIORTOTHEFEMORALCOMPONENTTHEREWERE69HIPSWITHTHENORMALPATTERN,11HIPSWITHTHEJOINTEXPANSIONPATTERN,5HIPSWITHTHECYSTICPATTERN,AND3HIPSWITHTHEMASSPATTERNWHENTHEJOINTEXPANSION,CYSTIC,ANDMASSPATTERNSWERECLASSIFIEDINTOTHEABNORMALPATTERNONULTRASOUND,THEFREQUENCYOFCLINICALSYMPTOMSWASSIGNIFICANTLYHIGHERINHIPSWITHTHEABNORMALPATTERN63THANINHIPSWITHTHENORMALPATTERN25TABLE1THEREWASNOSIGNIFICANTLYDIFFERENCEREGARDINGOTHERPATIENTSPROFILES,DURATIONOFIMPLANTINSITU,TYPESOFOPERATIONANDBEARINGS,CUPANDHEADSIZES,RADIOLOGICPARAMETERSOFTHEIMPLANTPLACEMENT,ANDPRESENCEOFOSTEOLYSIS,BETWEENTHEHIPWITHNORMALANDABNORMALPATTERNSALLOFTHE3PATIENTSSHOWINGMASSPATTERNONULTRASOUNDWEREWOMENWITHMTHAOPERATIONSANDHADONLYSLIGHTPAINORDISCOMFORTINTHEHIPTABLE2FIG1CLASSIFICATIONOFPERIARTICULARSOFTTISSUEREACTIONSONANTERIORLONGITUDINALORTRANSVERSEULTRASOUNDIMAGESNORMALPATTERNA,JOINTEXPANSIONPATTERNB,CYSTICPATTERNC,ANDMASSPATTERNDARROWSINDICATEANTERIORCAPSULEANDARROWHEADSINDICATEMASSLESIONULTRASOUNDSCREENINGOFPERIARTICULARABNORMALITYAROUNDMOMBEARINGS?NISHIIETAL897

簡介：點擊查看更多康復(fù)裝置外文翻譯--關(guān)節(jié)康復(fù)機器人上肢理療和訓(xùn)練精彩內(nèi)容。

簡介：INVITEDCRITICALREVIEWBTYPENATRIURETICPEPTIDEINACUTEPULMONARYEMBOLISMANNAKACZY?SKA,MACIEJKOSTRUBIEC,MICHA?CIURZY?SKI,PIOTRPRUSZCZYK?DEPARTMENTOFINTERNALMEDICINEANDCARDIOLOGY,MEDICALUNIVERSITYOFWARSAW,POLANDABSTRACTARTICLEINFOARTICLEHISTORYRECEIVED14MAY2008RECEIVEDINREVISEDFORM25JUNE2008ACCEPTED19JULY2008AVAILABLEONLINE24JULY2008KEYWORDSACUTEPULMONARYEMBOLISMBNPNTPROBNPRIGHTVENTRICLEDYSFUNCTIONPROGNOSISMYOCARDIALSTRETCHLEADSTOTHENATRIURETICPEPTIDESRELEASEINACUTEORCHRONICLEFTVENTRICULARDYSFUNCTIONHOWEVER,THEREISANACCUMULATINGEVIDENCETHATBTYPENATRIURETICPEPTIDEBNPANDITSNTERMINALFRAGMENTNTPROBNPMAYORIGINATEFROMRIGHTVENTRICLEANDTHEIRCONCENTRATIONSAREELEVATEDINPATIENTSWITHACUTEPULMONARYEMBOLISMAPEESPECIALLYWHENRESULTINGINRIGHTVENTRICULARDYSFUNCTIONRVDRECENTLYITISUNDERLINEDTHATSEVERITYASSESSMENTOFAPEASWELLASTHERISKSTRATIFICATIONANDTHERAPYSELECTIONISBASEDBOTHONPATIENTSHEMODYNAMICSTATUSANDMARKERSOFMYOCARDIALINJURYANDRVDBNPANDNTPROBNPAREHELPFULINIDENTIFYINGPATIENTSWITHRVDINAPE,EMERGINGASANADJUNCTIVETOOLTOECHOCARDIOGRAPHYELEVATEDBNPORNTPROBNPLEVELSAREALSOSIGNIFICANTPREDICTORSOFDEATHAND/ORCOMPLICATEDCLINICALCOURSEINAPE?2008ELSEVIERBVALLRIGHTSRESERVEDCONTENTS1STUDIESSELECTION12BNPANDNTPROBNPASSAYS13BNPANDNTPROBNPINTHEDETECTIONOFRVD24PROGNOSTICVALUEOFBNPANDNTPROBNPINAPE25CONCLUSIONS4REFERENCES4ITISWELLKNOWNTHATMYOCARDIALSTRETCHLEADSTOTHENATRIURETICPEPTIDESRELEASEINACUTEORCHRONICLEFTVENTRICULARDYSFUNCTIONHOWEVER,THEREISANACCUMULATINGEVIDENCETHATCONCENTRATIONSOFBTYPENATRIURETICPEPTIDEBNPANDITSNTERMINALFRAGMENTNTPROBNPAREELEVATEDINPATIENTSWITHACUTEPULMONARYEMBOLISMAPEESPECIALLYWHENRESULTINGINRIGHTVENTRICULARDYSFUNCTIONRECENTLYITISUNDERLINEDTHATSEVERITYASSESSMENTOFACUTEPULMONARYEMBOLISMAPEASWELLASTHERISKSTRATIFICATIONANDTHERAPYSELECTIONISBASEDBOTHONPATIENTSHEMODYNAMICSTATUSANDMARKERSOFMYOCARDIALINJURYANDRIGHTVENTRICULARDYSFUNCTIONRVDRIGHTVENTRICULARFUNCTIONCANBEDIRECTLYASSESSEDATECHOCARDIOGRAPHYAND/ORCONTRASTENHANCEDSPIRALCOMPUTEDTOMOGRAPHYSINCEPLASMACONCENTRATIONOFBRAINNATRIURETICPEPTIDEREFLECTSTHESEVERITYOFRVDITSASSESSMENTWASIMPLOREDINAPERISKSTRATIFICATIONASWELLWEPERFORMEDASYSTEMATICREVIEWAIMEDONBTYPENATRIURETICPEPTIDESINAPEESPECIALLYFORTHERVDDETECTIONANDCLINICALCOURSEPREDICTION1STUDIESSELECTIONOVERALL49ARTICLESWEREFOUNDSEARCHINGPUBMEDBYTERMS‘PULMONARYEMBOLISM’,‘BNP’AND‘NTPROBNP’FROM1997TOMARCH2008THIRTYTWOPAPERSWEREEXCLUDEDFROMCURRENTREVIEWBECAUSETHEYWERECASEREPORTS,REVIEWPAPERS,EDITORIALSORLETTERSTHEYDIDNOTREPORTONENDPOINTSORDIDNOTPROVIDEVALUESOFBIOMARKERSCONCENTRATIONEVENTUALLY,17STUDIESCONCERNINGTHEINFLUENCEOFELEVATEDBNPANDNTPROBNPONSHORTTERMMORTALITY,ADVERSEOUTCOMEEVENTSDEATH,CARDIOGENICSHOCK,NEEDFORTHROMBOLYSIS,CATHETERORSURGICALEMBOLECTOMY,USEOFVASOPRESSORS,NEEDFORENDOTRACHEALINTUBATIONANDMECHANICALVENTILATION,CARDIOPULMONARYRESUSCITATIONANDRVDWERESELECTEDTABLE12BNPANDNTPROBNPASSAYSPROPEPTIDEFORBTYPENATRIURETICPEPTIDEPROBNPISCLEAVEDTOEQUIMOLARAMOUNTSOFBTYPENATRIURETICPEPTIDEBNPANDNTERMINALFRAGMENTNTPROBNPBNPISPHYSIOLOGICALLYACTIVEBNPCONCENTRATIONISASSESSEDUSINGSEVERALRADIOIMMUNOLOGICASSAYSORIMMUNOFLUOROMETRICASSAYS,WHILEFORNTPROBNPONETESTISCLINICACHIMICAACTA39820081–4?CORRESPONDINGAUTHORDEPARTMENTOFINTERNALMEDICINEANDCARDIOLOGY,MEDICALUNIVERSITYOFWARSAW,ULLINDLEYA402005WARSAW,POLANDTEL48225021144FAX48225022142EMAILADDRESSPIOTRPRUSZCZYKAMWAWEDUPLPPRUSZCZYK00098981/–SEEFRONTMATTER?2008ELSEVIERBVALLRIGHTSRESERVEDDOI101016/JCCA200807020CONTENTSLISTSAVAILABLEATSCIENCEDIRECTCLINICACHIMICAACTAJOURNALHOMEPAGEWWWELSEVIERCOM/LOCATE/CLINCHIMCOMPLICATEDCLINICALCOURSEWITHOR8095CI13–501,P0026INTERESTINGLYAUTHORSALSOATTEMPTEDTOIDENTIFYTHEMOSTSENSITIVEBNPCUTOFFLEVELFORIDENTIFYINGLOWRISKAPEPATIENTSITTURNEDTOBEB50PG/MLWITHITSNEGATIVEPREDICTIVEVALUEOF972ELEVATEDBNPWASALSOFOUNDTOBEAPREDICTOROFALLCAUSEASWELLASAPERELATEDMORTALITYINGROUPOF110PATIENTS12THREEMONTHMORTALITYWAS10INTERESTINGLYALLDEATHSOCCURREDINPATIENTSWITHBNPCONCENTRATIONINSECONDANDTHIRDTERTILEIEEXCEEDING25PMOL/LAND217PMOL/L,RESPECTIVELYINTHESTUDYBYKRüGERETAL3,HOWEVER,BNPCUTOFFVALUEOFN90PG/ML,ASCALCULATEDFROMROCANALYSIS,WASNOTDIRECTLYASSOCIATEDNEITHERWITHINHOSPITALCOMPLICATEDCOURSENORWITHSHORTTERMMORTALITYHOWEVER,ASMENTIONEDEARLIERITWASREPORTEDTOBEUSEFULINRVDPREDICTIONIMPORTANTLY,ASEXPECTED,HIGHERINCIDENCEOFCOMPLICATIONSASWELLASTRENDTOWARDHIGHERMORTALITYWASOBSERVEDINPATIENTSWITHRVDCONVERSELY,ASMALLSTUDYONUNSELECTEDGROUPOF17PATIENTSWITHAPE,INCLUDINGPATIENTSBOTHWITHANDWITHOUTRVDREPORTEDSIGNIFICANTLYHIGHERCONCENTRATIONOFBNPINPATIENTSWHODIEDOFPETHANINTHOSEWHOSURVIVED916775–3362VS144119–274PMOL/L,P00213THEFOLLOWINGSTUDYCOMPRISING61INITIALLYHEMODYNAMICALLYSTABLEPATIENTSREPORTEDHIGHERBNPCONCENTRATIONONADMISSIONINPATIENTSWITHSUBSEQUENTCOMPLICATEDCLINICALCOURSETHANWITHFAVORABLEOUTCOME950±314VS296±353PG/ML,PB0000114IMPORTANTLYALL4INHOSPITALDEATHSAND11COMPLICATIONSOBSERVEDINTHISSTUDYOCCURREDINPATIENTSWITHBNPINTHEHIGHESTTERTILE,NAMELY527–1300PG/MLROCANALYSISCONFIRMEDCUTOFFPOINTOF487PG/MLASINDICATINGPATIENTSWITHHIGHERRISKOFCOMPLICATIONSAUC09895CI096–099,SENSITIVITY86,SPECIFICITY100INTHEANALYSISOFCLINICALTRIALMATISSESTUDYASSESSINGEFFICACYANDSAFETYOFFONDAPARINUXINAPE,S?HNEETALPERFORMEDROCANALYSISFORBNPASSESSEDONADMISSIONINPREDICTINGFATALOUTCOMEAND/ORVENOUSTHROMBOEMBOLISMRECURRENCEWITHINFOLLOWING3MONTHS15THECALCULATEDCUTOFFPOINTOF125PMOL/LSHOWEDSENSITIVITYOF60ANDSPECIFICITYOF60WITHPOSITIVEPREDICTIVEVALUEFORCOMBINEDENDPOINTOF57AUC06395CI056–070THEFOLLOWINGOBSERVATIONONELDERLYPATIENTSN65YEARSALSOREPORTEDSIGNIFICANTLYHIGHERBNPCONCENTRATIONINPATIENTSWITHCOMPLICATEDTHANWITHUNCOMPLICATEDCLINICALCOURSE274142–581VS7833–230PG/ML,PB00516INTHISSTUDY,HOWEVER,THEBESTTHRESHOLDINROCANALYSISFORSERIOUSADVERSEEVENTPREDICTIONWAS200PG/MLWITHNEGATIVEPREDICTIVEVALUEOF86FORUNFAVORABLEOUTCOMEAUC07295CI058–083SIMILARLY,INTHESTUDYON67PATIENTS,ALL9PATIENTSWITHCOMPLICATEDCLINICALCOURSEHADBNPN100PG/MLAPPLIEDCUTOFFVALUEUSEDINPREDICTINGRVD4INTHESTUDYOFTULEVSKIETALHALFOFPATIENTSHADELEVATEDBNPCONCENTRATIONONADMISSIONARBITRARYCHOSENLEVELN10PMOL/LTWOREPORTEDDEATHSOCCURREDINPATIENTSWITHBNPN10PMOL/L17INTHEFIRSTREPORTONNTPROBNPINAPEFROMKUCHERETAL6INGROUPOF73PATIENTS,NTPROBNPWASSIGNIFICANTLYHIGHERINPATIENTSWITHADVERSEOUTCOMETHANINPATIENTSWITHFAVORABLEOUTCOME425080–49,607VS12116–34,802PG/ML,PB00001AUTHORSIDENTIFIEDINROCANALYSISCUTOFFPOINTOF500PG/MLNEGATIVEPREDICTIVEVALUEOFNTPROBNPB500PG/MLFORADVERSEOUTCOMEWAS97ALSOINMULTIVARIABLEANALYSISNTPROBNPHASPROVEDTOBEPREDICTORFORCOMPLICATEDCLINICALCOURSEOR14695CI15–1390,P002THEFOLLOWINGTHREESINGLECENTEROBSERVATIONS7,8,18CONFIRMEDTHEROLEOFNTPROBNPINAPERISKSTRATIFICATIONNTPROBNPCONCENTRATIONWASASIGNIFICANTPREDICTOROFBOTHINHOSPITALMORTALITYOR21595CI13–356ANDCOMPLICATEDCLINICALCOURSEOR18895CI129–2747INOBSERVATIONBYGERMANGROUPON124PATIENTSWITHLVEJECTIONFRACTION≥30ROCANALYSISIDENTIFIEDACONCENTRATIONOF1000PG/MLASACUTOFFLEVELFORPREDICTINGDEATHORCOMPLICATEDCLINICALCOURSE19AMONGPATIENTSWITHNTPROBNPB1000PG/MLNOINHOSPITALDEATHOCCURREDNTPROBNPB1000PG/MLHADNEGATIVEPREDICTIVEVALUEOF95FORCOMPLICATEDCLINICALCOURSEAND100FORMORTALITYTHESAMEVALUEOF1000PG/MLWASPOSITIVELYVERIFIEDINANOTHERSTUDYAUC080920NTPROBNPN1000PG/MLALLOWEDTOPREDICTANADVERSEOUTCOMEOR117995CI16–527,P0007THEREWASALSOANOBSERVEDTRENDTOWARD4FOLDHIGHERMORTALITYINPATIENTSWITHNTPROBNPN1000PG/MLTHANWITHB1000PG/ML164VS41,P0056INPATIENTSWITHAPEEFFECTIVEEARLYTREATMENTSHOULDSIGNIFICANTLYDECREASETHELOADOFPULMONARYARTERYTHROMBOEMBOLIANDRESULTINPROGRESSIVEIMPROVEMENTOFRIGHTVENTRICULARFUNCTIONTHEREFORE,SERIALMEASUREMENTOFNTPROBNPPERFORMEDWITHINTHEFIRST24HOFTREATMENTISOFPOTENTIALVALUEINRISKASSESSMENTINDEED,NTPROBNPCONCENTRATIONSASSESSEDONADMISSIONANDAFTER12AND24HIN113PATIENTSWITHAPEDECREASEDSIGNIFICANTLYINSURVIVORSINNONSURVIVORS,MEDIANNTPROBNPCONCENTRATIONSATBASELINE11,491618–60,958PG/MLREMAINEDELEVATEDAFTER24H813935–70,018PG/ML,PNSTHE30DAYMORTALITYRATEINTHEGROUPOF18PATIENTSWITHNTPROBNPN7500PG/MLONADMISSIONANDALESSTHAN50?CREASEOFNTPROBNPWITHIN24HWASASSOCIATEDWITH30DAYMORTALITYOF6195CI39–8418ASWASMENTIONEDBEFORE,UNLIKELYINCASEOFLVCONGESTIVEHEARTFAILURE,THEREISNOESTABLISHEDSINGLECUTOFFPOINTFORDETECTINGRVDFORBNPCONCENTRATIONITRANGESFROM90TO200PG/MLASCALCULATEDFROMROCANALYSIS5,14,3,4FORNTPROBNPONEANALYSISREPORTSCUTOFFVALUEOF500PG/ML6TABLE2LOWERTHRESHOLDVALUESOF90–100PG/MLHAVEHIGHERSENSITIVITYWITHMODERATESPECIFICITY,WHILETAKINGHIGHERTHRESHOLDVALUESIMPROVESSPECIFICITYINDETECTINGRVDALSOTHEREARESEVERALCUTOFFPOINTSCOUNTEDFORPREDICTINGUNFAVORABLEOUTCOMEINAPEASFORBNPASSESSMENTWITHRIAMETHOD3VALUESWEREPROPOSED125PMOL/L,25PMOL/LAND10PMOL/L15,17,12TWOLATTERHAVESIMILARSENSITIVITY,BUTHIGHERSPECIFICITYFAVORSVALUEOF10PMOL/LTABLE3FORBNPASSESSEDWITHIMMUNOASSAYTHRESHOLDVALUESBETWEEN50PG/MLAND487PG/MLWEREEVALUATED14,3,16,4,2PROPOSEDCUTOFFTABLE2BNPANDNTPROBNPINPREDICTINGRVDAUTHORPEPTIDECUTOFFVALUESENSITIVITYSPECIFICITYKRüGERETAL3BNP90PG/ML6494PIERELLIETAL14BNP189PG/ML86100LOGEARTETAL4BNP200PG/ML8387100PG/ML10064YARDANETAL5BNP90PG/ML9391KUCHERETAL6NTPROBNP500PG/ML9775TABLE3BNPANDNTPROBNPINPREDICTINGCOMPLICATEDCLINICALCOURSEAUTHORPEPTIDEENDPOINTCUTOFFVALUESENSITIVITYSPECIFICITYS?HNEETAL15BNPCCC125PMOL/L6062TULEVSKIETAL17BNPDEATH10PMOL/L10054TENWOLDEETAL12BNPDEATH25PMOL/L10037PIERELLIETAL14BNPCCC487PG/ML10083KRüGERETAL3BNPDEATH90PG/ML5060CCC2639RAYETAL16BNPCCC200PG/ML6966LOGEARTETAL4BNPCCC100PG/ML10034KUCHERETAL2BNPCCC50PG/ML9560BINDERETAL19NTPROBNPDEATH1000PG/ML8552CCC10049KUCHERETAL6NTPROBNPCCC500PG/ML9557KOSTRUBIECETAL8NTPROBNPDEATH7600PG/ML6086PRUSZCZYKETAL7NTPROBNPDEATH600PG/ML10033CCC9635PULSETAL20NTPROBNPDEATH1000PG/ML8054CCC92563AKACZY?SKAETAL/CLINICACHIMICAACTA39820081–4

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展中的作用機制當(dāng)前的理解和存在的問建進展中的作用機制當(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展中的作用機制當(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)點開辟了新的觀察途徑來研究ESS在動脈粥樣硬化自然進程中的作用（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、實驗動物的支架內(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

簡介：點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)頻速率更小；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。在這個實驗中，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,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：點擊查看更多醫(yī)學(xué)外文翻譯--心肌梗死初級血管成形術(shù)治療術(shù)后的超聲心動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于全髖關(guān)節(jié)置換術(shù)后 髖關(guān)節(jié)安全活動范圍的影響精彩內(nèi)容。

簡介：點擊查看更多醫(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。