简介：近视眼的发病与多种因素相关,其中最主要的是遗传和环境因素.大量的近视相关研究提示近视的发生是在异常视觉信息的作用下,视网膜、脉络膜内多种神经递质和生长因子的表达发生改变,通过一系列信号传导过程引起巩膜重塑、眼轴延长而成.多种细胞因子通过NMDAR-1/NO-cGMP、TGF-β1/Smad3、JAK-Stat3等信号通路调控近视的形成与发展.本文就影响近视形成的几个主要信号传导通路的研究进展做一综述.

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：研究近视患者LASIK术后视疲劳的发生与融合范围的关系，及同视机融合功能训练改善LASIK术后视疲劳的疗效观察。方法：对60例120眼近视患者（．1．50--8．00D）施行LASIK手术，于术前戴全矫眼镜用同视机法测定融合范围，并进行视疲劳的问卷调查。术后将其随机平分为两组：A组进行同视机融合功能训练30d，B组不进行同视机融合功能训练，分别对其术后1wk；1mo行同视机法测定融合范围，并进行视疲劳的问卷调查及统计学分析。结果：A、B组术后融合范围均较术前减小。术后1wk时融合范围两组分别为18．58±8．91和13．45±8．87，二者差异有统计学意义（P〈0．05）。术后1mo时，两组融合范围分别为20．55±7．23和18．12±6．10，二者差异无统计学意义。术后1wk时A组视疲劳评分3．92±1．65，B组评分5．16±2．34，二者差异有统计学意义（P〈0．05）。术后1mo时两组评分分别是1．28±0．96和1．45±0．99分，二者差异无统计学意义。结论：近视眼LASIK术后双眼的融合功能下降是出现视疲劳的一个重要因素。术后早期进行同视机融合功能训练可以有效的改善视疲劳症状。

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.