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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: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:目的比较24h眼压监测中夜间即刻坐位眼压值和坐起休息10min后测得的眼压值,探讨夜间眼压的不同测量方法对青光眼24h眼压昼夜波动的影响。方法对已确诊且未用药、未做过手术的48例正常眼压性青光眼及17例原发性开角型青光眼患者进行24h眼压监测,每2h1次,其中测量夜间0:00、2:00、4.00眼压时,逐个唤起患者后立即测,后嘱患者坐起休息10min再测,采用SPSS软件以配对t检验分析比较测量结果。结果夜间即刻坐位眼压值和坐起休息10rain后测得的眼压值差异有统计学意义(P〈0.001),正常眼压性青光眼与原发性开角型青光眼间眼压差值差异有统计学意义(P〈0.05)。结论即刻坐位眼压值能更准确反映夜间眼压,对24h眼压测量及青光眼诊断及治疗更有价值,值得临床应用。
简介:目的:研究高氧诱导的视网膜新生血管模型鼠中转录因子Islet-1的表达差异。方法:采用高氧诱导的方法制作鼠视网膜新生血管模型,运用荧光造影视网膜铺片及视网膜切片苏木精-伊红染色观察视网膜新生血管的形态。于小鼠出生后第7,12,14,17,26d取视网膜组织,采用Real-timePCR及Westernblot技术测定视网膜组织中Islet-1的表达水平。结果:模型组视网膜铺片及组织切片可见大量视网膜新生血管形成。小鼠出生后第7d,模型组与正常组视网膜组织中Islet-1表达水平无明显差异;小鼠出生后第12~14d,模型组视网膜组织中Islet-1表达水平明显上调;出生后17d,模型组视网膜组织中Islet-1表达水平仍高于正常组;出生后26d,随着视网膜新生血管消退,视网膜组织中Islet-1表达水平降至正常水平。结论:模型鼠视网膜新生血管发生过程中,持续缺氧的视网膜组织通过增加转录因子Islet-1的表达,从而诱导视网膜新生血管的发生。
简介:目的:观察翼状胬肉切除联合自体球结膜瓣移植术后,局部应用1g/L环孢霉素A对胬肉复发的抑制效果。方法:对原发性翼状胬肉患者58例58眼进行前瞻性研究。所有入选眼均采用翼状胬肉切除联合自体球结膜瓣移植术,根据术后是否应用1g/L环孢霉素A滴眼液分为试验组和对照组。术后追踪随访1a,观察患者的胬肉复发率。结果:术后试验组基础泪液分泌试验(SchirmerⅠtest,SⅠt)结果明显优于对照组(9.93±1.59vs8.47±1.53mm/5min);SⅠt结果也显示1g/L环孢霉素A使患眼术后的泪液分泌量较术前有所增加。术后1a试验组与对照组的胬肉复发率分别为10%和39%。对照组并发症的出现率要高于试验组,差异具有统计学意义(P=0.029)。结论:翼状胬肉切除术后局部应用1g/L环孢霉素A滴眼液能够安全有效地降低胬肉的复发率。
简介:目的:研究富含半胱氨酸蛋白61(CCN1/Cyr61)在氧诱导小鼠视网膜新生血管(retinalneovascularization,RNV)中的表达及意义,探讨特异性抑制CCN1对RNV形成的抑制作用。方法:取C57BL/6J小鼠200只,随机分为对照组、高氧组、高氧对照组和CCN1治疗组,每组各50只。高氧对照组和CCN1治疗组分别玻璃体腔内注射空载体质粒和CCN1siRNA表达质粒。ADP酶视网膜铺片观察视网膜血管形态,HE染色计数突破视网膜内界膜的新生血管内皮细胞核数,免疫组织化学、Westernblot和RT-PCR法检测CCN1蛋白及mRNA的表达情况。结果:高氧组和高氧对照组视网膜可见大片无灌注区和大量突破内界膜的新生血管内皮细胞核(25.25±1.26个;23.12±1.16个),CCN1治疗组较高氧组和高氧对照组的无灌注区及新生血管内皮细胞核数(8.47±1.15个)明显减少。高氧组和高氧对照组较对照组相比,CCN1蛋白及mRNA表达显著增高,CCN1治疗组较高氧组和高氧对照组显著减弱,均有统计学意义(均为P〈0.05)。结论:CCN1的异常表达可能与RNV形成密切相关,特异性抑制CCN1能有效抑制RNV的形成,为预防和治疗ROP提供新的思路及对策。