简介：大腿骨的髁的孤立的花冠破裂在成年人是稀罕的并且Hoffa骨折不属于工会被报导仅仅在文学的一些时间。我们分析了六个案例在三年的一个时期上的Hoffa破裂不属于工会。三个病人保存地被对待，三个病人有固定失败。表示的延期是到一年的2个月。治疗协议与膝arthrolysis一起由开的减小，pseudoarthrosis的切除，骨头grafting和内部固定组成了。联合在平均数16星期在所有病人被完成。治疗Hoffa破裂不属于工会要求小心的外科手术前的计划和过细的外科的技术。关于在破裂管理和外科的技术的争吵的文学被考察。

简介：Plantcelllinesdifferredgreatlyintheabilitytowithstandshearstresses.Usingto-baccocellsandlicoricecellsasmodelplantcells,westudiedtheeffectsofshearstressesonthevi-abilityofplantcells.OurexperimentswerecarriedoutonahighshearrateCouetterheometerprovidinghomogeneousandconstantshearstressesoflaminarflow.TheviabilitywasdeterminedbyTTC（2,3,5-Triphenyltetrazoliumchloride）.Theresultswereasfollows.（1）Theviability（V）droppedexponentiallywithtime（t）,namelyV=Exp（-kt）,（k>oisaconstant）.Thismeantthetenabilityofstatisticalhomogeneity.（2）Thevalueofkwasafunctionofplantcells’mechanicalpropertiesandtheshearstressactingontheplantcells.Theshearratecorrespondingtok=owasthecriticalshearratethattheplantcellscouldwithstand.Itcanbeeasilydetermindedbyextrapo-lation.For7-day-oldtobaccocells,itwas1090s-1andfor9-day-oldlicoricecells,itwas6566s-1.（3）Theplantcellsuspensionswerepseudoplasticfluidsfittingτ=Kγn.Forthetobaccocellsus-pensiontested,n=O.73,andforthelicoricecellsuspensiontestedn=0.7.Thusthecriticalshearstressforthetobaccocellswas25dynes/cm2andforthelicoricecellsitwas80dynes/cm2.（4）Oneoftheirreasonsforlicoricecellstohavegreatertolerancetoshearstressesthantobacaccocellsmaybethegeometricfeaturesofthecellsandthesizesofthecells.Thelicoricecellswererod-shaped,butthetobaccocellsweresphericalandlargerthanthelicoricecells.

简介：AIM:Toinvestigateenoughvalidmeasurements(VMs)toassessliverfibrosisinchronichepatitisBpatients(CHB).METHODS:OnehundredandtwelveCHBpatients(25women,87men)withameanageof38.43yearsreceivedliverstiffnessevaluationsusingreal-timeshearwaveelastographyfor10VMs.Allpatientsunderwentliverbiopsy.Basedonthebiopsypathology,theliverstiffnessdataobtainedfromdifferentVMs(1,2,3,5and10times)werecomparedfortheevaluationofliverfibrosis.ThecorrelationbetweentheelasticmodulusmeansoftheliverobtainedfromdifferentVMsofdetectionateachpathologicalstagewasanalysed.Thereceiveroperatingcharacteristic(ROC)curvewasemployedtodeterminethediagnosticperformanceofdifferentVMsofdetection,andtheareasundertheROCcurveofdifferentgroupswerecompared.RESULTS:Theliverstiffnessvaluesobtainedfrom1VM,2VMs,3VMs,5VMsandall10VMsforstageF0were6.95±2.01kPa,6.87±1.83kPa,6.90±1.88kPa,6.95±1.93kPaand7.15±1.89kPa,respectively(F=0.043,P=0.996).ForstageF1,thesevalueswere7.12±1.72kPa,7.24±1.72kPa,7.21±1.74kPa,7.10±1.78kPaand7.04±1.70kPa,respectively(F=0.075,P=0.990).ForstageF2,theywere9.37±3.87kPa,9.18±3.68kPa,9.19±3.81kPa,9.18±3.81kPaand9.19±3.53kPa,respectively(F=0.012,P=1.000).ForstageF3,thesewere11.91±3.88kPa,11.78±4.04kPa,11.83±4.07kPa,11.94±4.17kPaand12.00±4.02kPa,respectively(F=0.010,P=1.000).ForstageF4,thereadingswere19.30±7.63kPa,19.40±7.36kPa,19.54±7.43kPa,19.73±7.21kPaand20.25±7.22kPa,respectively(F=0.054,P=0.995).Therewerenosignificantdifferencesbetweenthesegroups.Intraclasscorrelationcoefficientsamongdifferentpathologicalstages(F0-F4)withdifferentdetectionVMswere0.995,0.993,0.996,0.994and0.996,respectively.Themeanelasticityvaluesfrom1VM,2VMs,3VMs,5VMsand10VMscanaccuratelydistinguishfibrosisstages(F0vsF1234,F01vsF234,F012vsF34andF0123vsF4)withnosignificantdifferencesinthefivegroups(P>0.05forall).CONCLUSION:One

简介：LargeconductanceCa~(2+)-activatedK~+(BK_(Ca))channelexhibitsaphenotype-dependentexpressiononvascularsmoothmusclecells(VSMCs),whichpreferstocontractilephenotype.Meanwhile,shearstressdefinitelyinfluencesVSMCsproliferationandcontraction.Thereby,ahypothesiswasraised,wouldshearstresschangetheBK_(Ca)expressionandcorrelatewithVSMCphenotype?Inordertoinvestigateit,VSMCswereexposedtoshearstressinaparallel-plateflowchamberwith12dynes/cm~2for12h.Subsequently,theeffectofshearstressonVSMCproliferation,BK_(Ca)channelexpressionandcontractilephenotypemarker,α-smoothmusclecellactin(α-SMA)andsmoothmusclemyosinheavychain(SMMHC),wasdeterminedbyimmunofluorescencemicroscopy,flowcytometeryaswellasreversetranscriptionpolymerasechainreaction(RT-PCR),respectively.DatashowthatshearstressenhancedtheexpressionofBK_(Ca)channelwhileinhibitingVSMCproliferation.Paralleledtothosephenomena,theexpressionofbothα-SMAandSM-MHCweredecreasedsignificantly.TheseresultsdemonstratedthatupregulationofBK_(Ca)channelwasirrelevanttothemaintenanceVSMCofcontractilephenotypeundershearstress.ThisfindingprovidesanewinsightintounderstandingthecorrelationofBK_(Ca)channelandVSMCphenotype.

简介：ＥＦＦＥＣＴＯＦＳＵＣＰＥＮＤＩＮＧＭＥＤＩＵＭＶＩＳＣＯＳＩＴＹＯＮＯＲＩＥＮＴＡＴＩＯＮＡＮＤＤＥＦＯＲＭＡＴＩＯＮＯＦＲＢＣＳＩＮＡＳＨＥＡＲＦｌＯＷＦＩＥＬＤＷｅｎＺｏｎｇ－ｙａｏ，ＭａＷｅｉｙｕａｎ，ＧａｏＴｉｅ，ＳｕｎＤａｇｏｎｇＤｅｐａ...

简介：AIM:Toevaluatethecorrelationofshearwaveelastography(SWE)resultswithliverfibrosishistologyandquantitativefunctionreserve.METHODS:Weeklysubcutaneousinjectionof60%carbontetrachloride(1.5mL/kg)wasgivento12caninesfor24wktoinduceexperimentalliverfibrosis,witholiveoilgivento2controlcanines.At24wk,liverconditionwasevaluatedusingclinicalbiochemistryassays,SWEimaging,lidocainemetabolitemonoethylglycine-xylidide(MEGX)test,andhistologicfibrosisgrading.Clinicalbiochemistryassayswereperformedattheinstitutionalcentrallaboratoryforroutineliverfunctionevaluation.Liverstiffnesswasmeasuredintriplicatefromthreedifferentintercostalspacesandexpressedasmeanliverstiffnessmodulus(LSM).PlasmaconcentrationsoflidocaineanditsmetaboliteMEGXweredeterminedusinghigh-performanceliquidchromatographyrepeatedinduplicate.Liverbiopsysampleswerefixedin10%formaldehyde,andliverfibrosiswasgradedusingthemodifiedhistologicalactivityindexKnodellscore(F0-F4).Correlationsamonghistologicgrading,LSM,andMEGXmeasureswereanalyzedwiththePearsonlinearcorrelationcoefficient.RESULTS:At24wkliverfibrosishistologicgradingwasasfollows:F0,n=2(control);F1,n=0;F2,n=3;F3,n=7;andF4,n=2.SWELSMwaspositivelycorrelatedwithhistologicgrading(r=0.835,P<0.001).Specifically,theF4grouphadasignificantlyhigherelasticmodulusthantheF3,F2,andF0groups(P=0.002,P=0.003,andP=0.006,respectively),andtheF3groupalsohadasignificantlyhighermodulusthanthecontrolF0group(P=0.039).LSMwasnegativelyassociatedwithplasmaMEGXconcentrationsat30min(r=-0.642;P=0.013)and60min(r=-0.651;P=0.012),timeto?ofthemaximumconcentration(r=-0.538;P=0.047),andtheareaunderthecurve(r=-0.636;P=0.014).Multiplecomparisonsshowedidenticaldifferencesinthesethreemeasures:significantlylowerwithF4(P=0.037)andF3(P=0.032)ascomparedtoF0a

简介：Invitrocellloadingexperimentsareusedtoinvestigatestimulationofstraintocellularproliferation.Astheflowingconditionsofculturefluidinloadingsystemshasbeenlittleknown,strictlypeoplecannotdetecttheinfluenceofstraintocellularproliferationexactlybecauseshearflowcanenhancecellproliferationeither.Basedontheworkingprincipleandcyclicloadingparameters,wesimplifyNavier-Stokesequationtodescribetheflowofculturefluidonsubstratesofuniaxialandequi-biaxialfiattensileloadingsystemsandfourpointbendingsystem.Withapproximatesolutions,thedistributionsofvelocityfieldandwallshearflowtocellsaregained.Resultsshow:shearflowsarezerointhemiddle(orfixedpointorline)ofsubstrateforallsystems,andtheygetlargerproportionallytodistancefrommiddleandsubstrateelongate;theshearflowonthesubstrateoffourpointbendingsystemismuchgreaterthanthoseofothers.Thisshearflowinfourpointbendingsystem,confirmedbyOwan,I.,etalwithOPNmRNAincreaseintheirexperiment,couldcausemoreinfluencetoosteoblast-likecellsthanthatcausedbystrain.WeestimatetheaveragemagnitudeofshearstressinOwan'sdevice,theresultsareconsistentwithotherexperimentaldataaboutshearflow.Inconclusionourstudymakesitpossibletodifferentiatetheinfluenceofstrainoncellularproliferationtothatofshearflowinloadingexperimentswiththedevicesmentionedabovequantitatively.

简介：Thispaperaimstotheresearchoftheimpactoffluidshearstressontheadhesionbetweenvascularendothelialcellsandleukocyteinducedbytumornecrosisfactor-α(TNF-α)bymicrofliudicchiptechnology.Microfluidicchipwasfabricatedbysoftlithograph;Endothelialmicrofluidicchipwasconstructedbyoptimizingtypesoftheextracellularmatrixproteinsmodifiedinthemicrochannelandcellincubationtime;humanumbilicalveinendothelialcellsEA.Hy926linedinthemicrochannelwereexposedtofluidshearstressof1.68dynes/cm~2and8.4dynes/cm~2respectively.Meanwhile,adhesionbetweenEA.Hy926cellsandleukocytewasinducedbyTNF-αunderaflowcondition.EA.Hy926cellculturedinthestaticconditionwasusedascontrolgroup.Thenumbersoffluorescently-labeledleukocyteinmicrochannelwerecountedtoquantizetheadhesionlevelbetweenEA.Hy926cellsandleukocyte;cellimmunofluorescencetechniquewasusedtodetecttheintercellularadhesionmolecule(ICAM-1)expression.TheconstructedendothelialmicrofluidicchipcanaffordtothefluidshearstressandrespondtoexogenousstimulusofTNF-α;comparedwiththeadhesionnumbersofleukocyteincontrolgroup,adhesionbetweenEA.Hy926cellsexposedtolowfluidshearstressandleukocytewasreducedunderthestimulusofTNF-αataconcentrationof10ng/ml(P<0.05);leukocyteadhesionwithEA.Hy926cellsexposedtohighfluidshearstresswasreducedsignificantlythanEA.Hy926cellsincontrolgroupandEA.1Hy926cellsexposedtolowfluidshearstress(P<0.01);theregulationmechanismoffluidshearstresstotheadhesionbetweenEA.Hy926cellsandleukocyteinducedbyTNF-αwasthroughthewayofICAM-1.Theendothelialmicrofluidicchipfabricatedinthispapercouldbeusedtostudythefunctionsofendothelialcellinvitroandprovideanewtechnicalplatformforexploringthepathophysiologyoftherelatedcardiovascularsystemdiseasesunderaflowenvironment.