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: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：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：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：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: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.