简介：AIM:Toevaluatethelong-termresultsandcomplicationsofahmedglaucomavalve(AGV)implantationinrefractoryglaucoma.·METHODS:Aretrospectivereviewof13patients(13eyes)withrefractoryglaucomawhounderwentAGVimplantationandhadaminimumfollow-upof18monthswasperformed.Allpatientsunderwentacompleteophthalmologicexaminationandintraocularpressure(IOP)measurementbeforesurgeryandat1month,3months,6months,1yearaftersurgeryandyearlyafterwards.Complicationsandthenumberofantiglaucomamedicationsneededwererecorded.·RESULTS:Meanagewas27.3±16.0years.Alleyes(100%)hadatleastonepriorincisionalsurgery.Meanfollow-upwas61.3±30.8months.IOPwasreducedfromameanof35.0±7.0mmHgto18.2±7.9mmHgat12monthsandto17.0±4.1mmHgat96months(P<0.05)withalowernumberofmedicationsfrombaseline,76.9%patientsrequiredadditionalprocedurestoachievethesuccesscriteriasetbypreviouslypublishedseries.Themostcommoncomplicationswereencapculatedcystformationineighteyes(61.5%)andtubeexposureinfoureyes(30.8%).·CONCLUSION:EncapsulatedcystformationwasthemostcommoncomplicationwhichhinderedsuccesfulIOPcontrolafterAGVimplantinsertionforrefractoryglaucoma.Despitecystexcisionwithanti-fibroticagents,successfulIOPreductionwasnotachievedin76.9%ofthepatientswithoutantiglaucomamedication.

简介：·Glaucomaisoneoftheleadingcausesofvisualimpairmentandblindnessworldwide.Ofknownriskfactorsforglaucoma,anincreasedinintraocularpressureismosthighlycorrelatedwithglaucomatousdamage.Irrespectiveofthecause,apoptosisoftheretinalganglioncellsistheeventualoutcome.Itiswidelyacceptedthatglaucomaisaneurodegenerativediseasethatisstronglycorrelatedwithcentralnervoussystemdisorders,suchasAlzheimer’sdisease.Thesetwodisordersalsosharesomesimilaritiesinpathogenicmechanisms.Recentstudiessuggestthatthetransientreceptorpotentialcanonical6channelcouldworktogetherwithbrain-derivedneurotrophicfactortopromoteneuronsurvivalinbrainandretina.Inthisstudy,weproposethattransientreceptorpotentialcanonical6maycontributetothepathogenesisofhumanglaucomaandbecomeapotentialtherapeutictarget.

简介：资料患者女性，21岁。因左鼻腔反复鼻塞、流脓涕、涕中带血2周余于2011年12月5日入院。体格检查：一般情况良好，血压正常，浅表淋巴结均未触及。专科检查：外鼻无畸形，左侧中鼻甲明显肿大，表面黏膜呈暗红色、光滑，触之不易出血，对麻黄碱无收缩反应；中鼻道无法显露；下鼻道见少量脓性分泌物；鼻咽部未见新生物。

简介：AIM:Toevaluatetheefficacyofintralesionalradiofrequencyablationinthetreatmentofperiorbitalsyringomas.·METHODS:Wetriedtheintralesionalradiofrequencyablationfor64patientswithperiorbitalsyringomasfrom2007to2011.Theoperationwasperformedunder2.5loupemagnifications.Thehandpiecewasassembledwithaneedleelectrodeandconnectedtotheradiofrequencyablationapparatus.Theelectrodewastheninsertedintothetargetlesionsindermisanddeliveringinjurytothebaseofthesetumors.Resultswereassessedclinicallybycomparingpre-andpost-treatmentphotographsandpatientsatisfactionrates.·RESULTS:Clinicalimprovementincreasedwitheachsubsequenttreatmentsession.Thepercentofpatientswhoseclinicimprovementgradewere≥3aftereachsessionwasrespectively71.9%(Session1),83.3%(Session2),and100%(Session3).Thestatisticalresultsindicatedtheconcordanceoftheclinicalassessmentandthesatisfactionlevelofpatients(kappa=0.78ofthesession1;kappa=0.82ofthesession2).Themajorityofpatientshadgoodorexcellentcosmeticresults.Postoperatively,therewerenopermanentsideeffectsorrecurrences.·CONCLUSION:Asanewtechniqueofminimallyinvasion,theintralesionalradiofrequencyablationwasfoundtobeaneffective,inexpensive,highlypreciseandsafewayoftreatingperiorbitalsyringomas.

简介：AIM:Toinvestigatewhether15-Lipoxygenase-1(15-LOX-1)playsanimportantroleintheregulationofangiogenesis,inhibitinghypoxia-inducedproliferationofretinalmicrovascularendothelialcells(RMVECs)andtheunderlyingmechanism.METHODS:PrimaryRMVECswereisolatedfromtheretinasofC57/BL6JmiceandidentifiedbyanevaluationforFITC-markedCD31.ThehypoxiamodelswereestablishedwiththeBio-bagandevaluatedwithablood-gasanalyzer.ExperimentswereperformedusingRMVECstreatedwithandwithouttransferAd-15-LOX-1orAd-vectorbothunderhypoxiaandnormoxiaconditionat12,24,48,72hours.Theefficacyofthegenetransferwasassessedbyimmunofluorescencestaining.CellsproliferationwasevaluatedbytheCCK-8method.RNAandproteinexpressionsof15-LOX-1,VEGF-A,VEGFR-2,eNOsandPPAR-rwereanalyzedbyreal-timereversetranscriptionpolymerasechainreaction(RT-PCR)andWesternblot.RESULTS:RoutineevaluationforFITC-markedCD31showedthatcellswerepure.Theresultsofblood-gasanalysisshowedthatwhenthecultureswereexposedtohypoxiaformorethan2hours,thePo2was4.5to5.4Kpa.WeverifiedRMVECscouldbeinfectedwithAd-15-LOX-1orAd-vectorviaFluorescencemicroscopy.CCK-8analysisrevealedthattheproliferativecapacitiesofRMVECsinhypoxicgroupweresignificantlyhigherateachtimepointthantheywereinnormoxicgroup(P<0.05).Inahypoxiccondition,theproliferativecapacitiesofRMVECsin15-LOX-1groupweresignificantlyinhibited(P<0.05).Real-timeRT-PCRanalysisrevealedthattheexpressionsofVEGF-A,VEGF-R2andeNOsmRNAincreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).However,theexpressionsof15-LOX-1,PPAR-rmRNAdecreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).Italsoshowedthatinahypoxiccondition,theexpressionsofVEGF-A,VEGF-R2andeNOsmRNAdecreasedsignificantlyin15-LOX-1groupcomparedwithhypoxiagroup(P<0.01).However,15-LOX-1andPPAR-rmRNAincreasedsigni

简介：AIM:ToinvestigatetheinterferingeffectofY-27632,aROCK-Iselectiveinhibitor,onthesignaltransductionpathwayoftransforminggrowthfactor-β1(TGF-β1)inocularTenoncapsulefibroblasts(OTFS)invitro.METHODS:AfterOTFSfrompassages4to6invitrowereinducedbyTGF-β1andthentreatedbyY-27632,thechangesoftheOTFScellcycleswereanalyzedviaflowcytometry,andtheproteinsexpressionoftheα-smoothmuscularactin(α-SMA),connectivetissuegrowthfactor(CTGF),collagenIwerecalculatedbyWesternblot.AfterOTFStreatedbythedifferentconcentrationsofY-27632,theexpressionlevelsoftheα-SMA,CTGFandcollagenImRNAwereassayedbyRT-PCR.RESULTS:Y-27632hadnomarkedlyeffectontheOTFScellcycles.AftertreatedbyTGF-β1,OTFSinG1periodsignificantlyincreased.ThecellcyclesdistributionbybothTGF-β1andY-27632hadnoremarkabledifferencefromthatincontrolgroup.Y-27632significantlyinhibitedtheproteinsexpressionsofbothα-SMAandCTGF,whiletosomeextentinhibitedthatofcollagenI.TGF-β1significantlypromotedtheproteinsexpressionsofα-SMA,CTGFandcollagenI.AfterOTFStreatedbybothTGF-β1andY-27632,ofα-SMA,theproteinexpressionwassimilarwiththatincontrolgroup(P=0.066>0.05),buttheproteinexpressionofCTGForcollagenI,respectively,wassignificantlydifferentfromthatincontrolgroup(P=0.000<0.01).Thedifferencesofexpressionsoftheα-SMA,CTGFandcollagenImRNAin30,150,750μmol/LY-27632groupwerestatisticallysignificant,comparedwiththoseincontrolgroup,respectively(α-SMA,P=0.002,0.000,0.000;CTGF,P=0.014,0.002,0.001;collagenI,P=0.003,0.002,0.000).CONCLUSION:BlockingtheRho/ROCKsignalingpathwaybyusingofY-27632couldinhibitthecellularproliferationandtheexpressionofbothCTGFandα-SMAwhateverOTFSinducedbyTGF-β1ornot.Y-27632suppressedtheexpressionofcollagenImRNAwithoutinduction.

简介：AIM:Toinvestigatethelevelsofserumsolubleintercellularadhesionmolecules-1(sICAM-1)andneutrophilicexpressionofCD18inpatientswithvariousstagesofdiabeticretinopathyandtodeterminetheirdifferentexpressionpatterninthedevelopmentofdiabeticretinopathy(DR).·METHODS:LevelsofserumsICAM-1andCD18onthesurfaceofneutrophileweremeasuredin41DRpatients,theywereclassifiedinthreesubgroupsaccordingtothestageofretinopathyasdeterminedbyfund’sophthalmoscopy;10controlsubjectswerealsostudied.sICAM-1weremeasuredbyenzyme-linkedimmunosorbentassayandCD18byflowcytometry.·RESULTS:TheneutrophilicCD18expressionandserumsICAM-1levelwereallsignificantlyelevatedinalldiabeticsubgroupscomparedtocontrolsubjects(P<0.01).ThedifferencesofCD18andsICAM-1amongthediabeticsubgroupsweresignificantinCD18butnotinsICAM-1.TheprogressionofretinopathywasassociatedwithanincreasebothinCD18andinsICAM-1levelsbysimplecorrelationanalysis(β=0.74,P<0.001;β=0.38,P<0.01,respectively).ButstepwisemultipleregressionanalysisrevealedthatonlyCD18wasindependentdeterminantofretinopathy(β=1.04,P<0.01).·CONCLUSION:OurresultsconfirmthecontributionofendothelialandneutrophilicactivationinthedevelopmentofDRasindicatedbyincreasedlevelsofCD18andsICAM-1.However,adirectimplicationofCD18andICAM-1intheprogressionofDRcanbesupportedonlyintheCD18butnotICAM-1.CD18andICAM-1mayplaydifferentroleinthedevelopmentofdiabeticretinopathy.