简介:例1,男52岁.因咽部不适、头痛睡眠不好2年,在内地医疗单位诊断为阻塞性睡眠呼吸暂停低通气综合征(obstructvesleepapneahypopneasyndrome,OSAHS).在全身麻醉下行悬壅垂腭咽成形术(uvulopalatopharyngoplasty,UPPP),术后20d返回高原.1wk后出现咽痛、咽干、吞咽困难,夜间症状加重.检查:咽部充血,咽腔宽大,黏膜干燥无光泽,咽后壁较多黄白色干痂贴附.
简介:AIM:ToinvestigatetheregulationofEaf2proteininmouselenscellsapoptosisinducedbyultraviolet(UV)radiation.METHODS:AneyeofEaf2geneknockoutmiceornormalcontrolmicewasexposedtoUVradiation,andtheotheronewasnon-exposed.AlloflenseswereanalyzedbyTUNELandcaspase3activityassaystodeterminethedifferenceoftheapoptosisinducedbyUVradiation.Inaddition,exposedandnon-exposedlenseswereanalyzedbyquantifiedp53expressionandreal-timereversetranscription-polymerasechainreaction(RT-PCR)ofBax,Bid,Apaf-1,PumaandNoxa,tocompareEaf2geneknockoutmiceandnormalcontrolmice.RESULTS:UVradiationcausedapoptosisoflenscellsinnormalcontrolmiceandEaf2knockoutmice.Activityofcaspase3wassignificantlyhigherinnormalcontrolmicethanEaf2knockoutmice.Expressionofp53proteinwassignificantlyhigherinlensesexposedtoUVradiationthannonexposedlenses,butwassimilarbetweenEaf2geneknockoutmiceandnormalcontrolmiceinthesameUVcondition.AfterexposingtoUVradiation,theanalysisofreal-timeRT-PCRdemonstratedthatmRNAlevelsofPumaandNoxaweresignificantlyhigherinlensesofnormalcontrolmicethanEaf2geneknockoutmice,andthatmRNAlevelsofBax,BidandApaf-1werenotsignificantlydifferentbetweengeneknockoutmiceandnormalcontrolmice.CONCLUSION:Eaf2increaseslenscellsapoptosisinducedbyultravioletradiation.AndEaf2up-regulatesexpressionofthePumaandtheNoxatoactonlenscellsapoptosisafterUVradiation.
简介:AIM:Toinvestigatewhethertheresponseofacentralhexagonalelementcorrespondingtothemacularareainconventionalmultifocalelectroretinography(mfERG)testswasthesameasthatofexperimentalmfERGusingsinglecentralhexagonalelementstimulation.METHODS:Prospective,observationalstudy.Thirtyhealthysubjectswereincludedinthisstudy.mfERGrecordingswereperformedaccordingtotwoprotocols:stimuluswith37hexagonalelements(protocol1),andstimuluswithasinglecentralelementcreatedbydeactivatingtheother36hexagonalelements(protocol2).Wecompareddifferencesbetweenring1parametersineachprotocol.RESULTS:Inprotocol1,thefirstpositivecomponent(P1)implicittimeandP1amplitudewere37.8±1.8msand6.3±2.7μV.Aftersingleelementstimulation(protocol2),doublepositivewavesappeared.TheimplicittimeandamplitudeofP1were40.7±2.4ms(P<0.001)and9.1±3.3μV(P=0.001),respectively.Theimplicittimeandamplitudeofthesecondpositivecomponent(P2)were68.0±4.5ms(P<0.001,comparedwithP1inprotocol1)and12.3±4.7μV(P<0.001,comparedwithP1inprotocol1),respectively.TheamplitudeofP2inprotocol2wasabouttwotimeshigherthanthatofP1inprotocol1.CONCLUSION:mfERGresponsesofacentralhexagonalelementinasingleelementstimulationprotocolaredifferentfromthoseofmultipleelementstimulation.Thepositivewaveismoreenhancedcomparedtothatoftheconventionalprotocolanditelongatedintotwowavelets.
简介:目的:探讨白内障合并晶状体脱位范围〉2个象限的患者,Ⅰ期行白内障囊内摘除术+前部玻璃体切割术,术后3mo矫正视力〉0.3者,Ⅱ期行小切口两点固定人工晶状体悬吊术的临床疗效。方法:对2014-07/2016-12我院白内障科就诊的34例34眼白内障合并晶状体脱位范围〉2个象限的患者,Ⅰ期行白内障囊内摘除术+前部玻璃体切割术,3mo后矫正视力〉0.3者,Ⅱ期行小切口两点固定人工晶状体悬吊术,分别观察患者术后1wk,1、3mo裸眼视力、最佳矫正视力、眼压、角膜散光度、术后并发症情况。结果:随着术后恢复时间的延长,患者各期的裸眼视力和最佳矫正视力均较术前有明显提高。术后3mo最佳矫正视力0.1~〈0.3者1眼,0.3~〈0.5者8眼,0.5~〈0.7者16眼,〉0.7者9眼,达到或接近术前的最佳矫正视力。术后1wk,1、3mo眼压处于正常范围内。手术并没有明显增加角膜的散光度。结论:对于白内障合并晶状体脱位范围〉2个象限的患者,Ⅰ期行白内障囊内摘除术+前部玻璃体切割术,3mo后矫正视力〉0.3者,Ⅱ期行小切口两点固定人工晶状体悬吊术能有效确切地提高视力,稳定眼压,术后并发症少,是较为安全可靠的治疗方式。
简介:AIM:ToidentifythefunctionofST2andexploretheroleofIL-33/ST2signalinginregulatingthepro-allergiccytokineproductioninhumancornealepithelialcells(HCECs).METHODS:HumancornealtissuesandculturedprimaryHCECsweretreatedwithIL-33indifferentconcentrationswithoutorwithdifferentinhibitorstoevaluatetheexpression,locationandsignalingpathwaysofST2inregulatingproductionofpro-allergiccytokineandchemokine.TheexpressionofmRNAwasdeterminedbyreversetranscriptionandrealtimePCR,andproteinproductionwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA),immunohistochemicalandimmunofluorescentstaining.ST2proteinwasdetectedindonorcornealepithelium,andST2signalwasenhancedbyexposuretoIL-33.·RESULTS:IL-33significantlystimulatedproductionofpro-allergiccytokinesthymicstromallymphopoietin(TSLP)andchemokine(CCL2,CCL20,CCL22)inHCECsatbothmRNAandproteinlevels.Thesestimulatedproductionsofpro-allergicmediatorsbyIL-33wereblockedbyST2antibodyorsolubleST2protein(P<0.05).Interestingly,theIκB-αinhibitorBAY11-7082orNF-κBactivationinhibitorquinazolineblockedNF-κBp65proteinnucleartranslocation,andalsosuppressedtheproductionsofthesepro-allergiccytokinesandchemokineinducedbyIL-33.CONCLUSION:ThesefindingsdemonstratethatIL-33/ST2signalingplaysanimportantroleinregulatingIL-33inducedpro-allergicresponses.IL-33andST2couldbecomenovelmoleculartargetsfortheinterventionofallergicdiseasesinocularsurface.
简介:目的:观察MoriaM2型90与110μm角膜刀制作角膜瓣在准分子激光角膜原位磨镶术(laserinsitukeratomileusis,LASIK)的疗效和并发症,探讨MoriaM2型90刀头在LASIK中应用的有效性、安全性和优点。方法:选取通过术前检查并自愿行LASIK手术的患者105例202眼,按随机数字表分成两组,使用MoriaM2型90刀头LASIK患者51例98眼,110刀头LASIK患者54例104眼做对照,术后即使用光学相干断层扫描仪(OCT)检测两组角膜瓣厚度,观察两组术后1d;1wk;1,3mo裸眼视力、矫正视力和角膜瓣形态、对合情况、并发症。结果:90刀头组术后角膜瓣厚度为118.3±15.2μm,110刀头组术后角膜瓣厚度为130.5±17.1μm,有显著性差异。90刀头组均未发现层间点状金属碎屑,110刀头组有层间点状金属碎屑个例(12例),有显著性差异。两组角膜瓣形态、对合情况、术后反应、术后裸眼视力相当。结论:应用90刀头LASIK的疗效及并发症和110刀头LASIK相当,但90刀头保留角膜基质床相对较厚,可矫治的屈光度更大,术后层间点状金属碎屑并发症更少,具有更好的安全性和更宽的适应范围。
简介:研究内源性大麻素N-花生四氢酸氨基乙醇(anan-damide,AEA)对体外培养的牛眼小梁细胞细胞骨架及PGE2表达的影响。方法:对牛眼小梁细胞进行原代及传代培养,并行鉴定。对传3代的牛眼小梁细胞分别施加AEA浓度分别为0,0.1,1.0,10/μmol/L的无血清培养液,作用24h后提取细胞上清液,并将细胞置于倒置显微镜下摄像,计算机图像分析系统计算细胞面积。用ELISA法检测PGE2浓度的变化。结果:AEA可以产生明显的细胞舒张效应,呈浓度依赖性。而且在一定范围内可以成剂量依赖性的促进PGE2的表达。与对照组均有显著性差异(P〈0.05)。结论:AEA可引起小梁细胞的舒张和促进PGE2的释放。
简介:目的:探讨眼附属器B细胞非霍杰金淋巴瘤(B—cellnon-Hodgkinlymphoma,NHL)中Skp2,p27和PTEN的表达。方法:收集1995年到2011年青岛大学附属医院眼科石蜡包埋标本,用免疫组化法分别检测眼附属器B细胞NHL(n=30)标本中Skp2,p27和PTEN的表达,以眼部反应性淋巴组织增生(n=10)作为对照组。以患者的年龄、性别、发病部位,病理类型作为眼附属器B细胞NHL的的分类标准。结果:Skp2,p27和PTEN的表达与患者的年龄、性别、发病部位无关,而与病例类型有关。眼附属器B细胞NHLSkp2表达率与眼部反应性淋巴组织增生相比显著增高。p27,PTEN表达率与反应性淋巴组织增生相比显著降低。随眼附属器B细胞NHL病理分级的提高,Skp2的表达显著增高,p27和PTEN的表达显著降低。在黏膜相关淋巴组织结(mucosa—associatedlymphoidtissue,MALT)外边缘区B细胞淋巴瘤(diffuselargeB—celllymphoma,DLBCL)中,Skp2分别与p27,VFEN成负相关,p27和PTEN成正相关。结论:Skp2的表达升高,p27,PTEN蛋白的缺失以及可能与眼附属器B细胞NHL的发生有关;其中在MALT外边缘区DLBCL中,三种蛋白存在相关性。联合三种蛋白的检测眼附属器B细胞NHL的不同病理类型有重要意义。
简介:AIM:Toassesstheawarenessofeyecomplicationsandtheprevalenceofretinopathy,inthefirstvisittoeyeclinic,amongtype2diabeticpatientsattendingatertiarymedicalcentreinKualaLumpur,Malaysia.METHODS:Aninvestigator-administeredquestionnairewasgivento137patientswithdiabetesundergoingfirsttimeeyescreeningintheeyeclinic.Thiswasfollowedbyadetailedfundusexaminationbyaseniorophthalmologisttoassessforpresenceofretinopathy.RESULTS:Almost86%ofrespondentswereawareofdiabeticeyecomplications,especiallyinpatientswhohadachievedtertiaryeducationallevel(96.3%).Themajorityofthepatients(78.8%)werereferredbytheirphysiciansandonly20.4%cameontheirowninitiative.Manyofthepatients(43.8%)didnotknowhowfrequenttheyshouldgoforaneyecheck-upand72.3%didnotknowwhattreatmentswereavailable.Lackofunderstandingondiabeticeyediseases(68.6%)wasthemainbarrierformostpatientsfornotcomingforeyescreeningearlier.Despiteahighlevelofawareness,only21.9%hadrecordedHbA1clevelof<6.5%while31.4%wereundertheerroneousassumptionofhavingagoodbloodsugarcontrol.Atotalof29.2%haddiabeticretinopathyintheirfirstvisiteyetesting.CONCLUSION:Inthepresentstudy,29.2%oftype2diabeticpatientshadretinopathyintheirfirsttimeeyetesting.Althoughtheawarenessofdiabeticeyecomplicationswashighamongfirsttimeeyescreeningpatients,theappropriateeyecare-seekingbehaviorwascomparativelylessandshouldberectifiedtopreventtheriseofthissightthreateningeyedisease.
简介:目的观察1,25(OH)2D3对高糖诱导牛视网膜血管内皮细胞(BRECs)中血管内皮生长因子(VEGF)的表达水平变化及对细胞凋亡水平的影响。方法将分离培养的BRECs分为三组,分别为正常糖组、高糖组和高糖处理组。正常对照组细胞培养液含5mmol/L葡萄糖,高糖组细胞培养液含30mmol/L葡萄糖,高糖处理组细胞培养液含30mmol/L葡萄糖和50nM,1,25(OH)2D3。培养48h后收集细胞蛋白。蛋白免疫印迹法检测细胞VEGF及细胞凋亡相关蛋白Bax和Bcl-2表达水平;PI/Hoechst双染色法检测细胞凋亡。结果相比于正常糖组,高糖组中VEFG水平和Bax/Bcl-2比值显著增加;而在高糖处理组中表达水平远远低于高糖组,差异均有统计学意义(P〈0.05)。高糖的细胞凋亡水平高于正常糖组,而经过1,25(OH)2D3处理后,其细胞凋亡水平则有所下降,差异均有统计学意义(P〈0.05)。结论1,25(OH)2D3可以抑制高糖诱导BRECs中VEGF表达增加及细胞凋亡。
简介:AIM:ToinvestigatetheexpressionsoftypeIcollagen,α2integrinandβ1integrinintheposteriorscleraofguineapigswithdefocusmyopiaandwhetherbasicfibroblastgrowthfactor(bFGF)injectioninhibitstheformationanddevelopmentofmyopiabyupregulatingtheexpressionoftypeIcollagen,α2integrinandβ1integrin.METHODS:After14daysoftreatment,therefractivestateandaxiallengthweremeasuredandthelevelsoftypeIcollagen,α2integrinandβ1integrinwereassayedintheposteriorscleraeofgroupsofguineapigsthatworeamonocular-7Dpolymethylmethacrylate(PMMA)lensorhad-7DlenswearfollowedbytheperibulbarinjectionofPhosphateBufferSolution(PBS)orbFGF.Theuntreatedfelloweyeservedasacontrol.Guineapigswithnotreatmentservedasnormalgroup.·RESULTS:Theresultsshowedthat14daysofmonoculardefocusincreasedaxialeyelengthandrefraction,whilebFGFdeliveryinhibitedthemmarkedly.Further,itwasalsofoundthatthemonocular-7DlenscoulddecreasethelevelsoftypeIcollagen,α2integrinandβ1integrinexpressions,while,unlikePBS,bFGFincreasedthemsignificantlyincomparisontocontralateralcontroleyesandnormaleyes.CONCLUSION:bFGFcanpreventtheformationanddevelopmentofdefocusmyopiabyupregulatingtheexpressionsoftypeIcollagen,α2integrinandβ1integrin.Takentogether,ourresultsdemonstratethatbFGFpromotesscleraremodelingtopreventmyopiainguineapigs.
简介:AIM:ToidentifythegeneticdefectinaChinesefamilywithbilateralprogressivechildhoodposteriorcataract.METHODS:Atwo-generationfamilywasrecruitedinthisstudy.Familyhistoryandclinicaldatawererecorded.AllreportedcandidategenesassociatedwithcongenitalposteriorcataractwerescreenedbydirectDNAsequencing.·RESULTS:Allaffectedindividualspresentedposterioropacitiesinthelens.Directsequencingofthecandidategenesshowedaheterozygousc.2668C>TvariationinEPHA2gene,whichresultedinthereplacementofargininebycysteineatcodon890(p.R890C).Thismutationwasfoundintwoaffectedindividuals,butwasnotobservedin200normalcontrols.·CONCLUSION:Wereportanovelmutation(p.R890C)intheEPHA2receptortyrosinekinasegene.ThefindingexpandsthemutationspectrumofEPHA2inassociationwithposteriorcataract.
简介:AIM:ToInvestigatetheeffectsoftransforminggrowthfactorβ2(TGF-β2)andconnectivetissuegrowthfactor(CTGF)ontransdifferentiationofhumanlensepithelialcells(HLECs)culturedinvitroandsynthesisofextracellularmatrix(ECM).METHODS:HLECsweretreatedwithTGF-β2(0,0.5,1.0,5,10μg/L)andCTGF(0,15,30,60,100μg/L)fordifferenttimes(0,24,48,72h)invitroandtheexpressionofα-smoothmuscleactin(α-SMA),themaincomponentoftheextracellularmatrixtypeⅠcollagen(Col-1)andfibronectin(Fn)weremeasuredbyusingreal-timepolymerasechainreaction(PCR)andwestern-blot.RESULTS:TGF-β2andCTGFsignificantlyincreasedexpressionofα-SMAmRNAandprotein(P<0.05,P<0.001),FnmRNAandprotein(P<0.001),Col-1mRNAandprotein(P<0.001).TGF-β2couldinduceHLECsexpressionofCTGFmRNAandproteinindosedependentmanner(P<0.05,P<0.001).TGF-β2andCTGFcouldinduceHLECstoexpressα-SMA,FnandCol-1intime-dependentmanner.EachtimeofTGF-β2andCTGFinducedHELCsexpressionofα-SMA,Fn,Col-1mRNAandproteinwassignificantincreasecomparedwithcontrol(P<0.05,P<0.001).CONCLUSION:TGF-β2andCTGFcouldinduceHLECsepithelialmesenchymaltransitionandECMsynthesis.