简介：目的：观察脉冲射频联合神经阻滞治疗眼睑带状疱疹神经痛的疗效分析。方法：2011-01/2014-08张家港市第一人民医院诊治的81例81眼眼睑带状疱疹患者,随机分为A、B、C三组。A组27例,全身静滴阿昔洛韦、地塞米松药物治疗。B组27例,在阿昔洛韦抗病毒药物治疗基础上,复方倍他米松等眶上神经阻滞。C组27例,在阿昔洛韦抗病毒药物治疗基础上,予脉冲射频联合神经阻滞治疗。比较三组治疗前,治疗后1、7、30、90d的疼痛视觉模拟评分（visualanaloguescale,VAS）、临床治疗效果、并发症等情况。结果：A组患者治疗前,治疗后1、7、30、90dVAS分别为8.2±1.5、7.3±1.6、6.5±1.4、6.1±1.1、5.9±0.7;B组患者治疗前,治疗后1、7、30、90dVAS分别为8.2±1.3、6.3±1.1、5.7±0.9、5.1±1.1、4.1±0.7;C组患者治疗前,治疗后1、7、30、90dVAS分别为8.1±1.5、2.1±0.7、2.2±0.8、2.9±0.7、2.7±0.8。C组患者在脉冲射频联合神经阻滞治疗后疼痛明显缓解,在1、3mo后疼痛评分虽略有恢复,但仍明显低于对照组。三组治疗后第1、7、30、90dVAS评分差异有统计学意义（F=10.320、5.207、2.364、2.805,均P〈0.05）。C组患者除减轻疼痛外,无严重并发症,例如角膜知觉减退等,并且角膜炎及角膜溃疡发生的可能减少。结论：脉冲射频联合神经阻滞治疗能迅速减轻疼痛,并减少该疾病引起的并发症,是眼睑带状疱疹神经痛的一种安全、有效的治疗方法。

简介：我科采用鼻内镜下射频凝固伴明胶海绵填塞治疗鼻出血139例，报告如下。

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：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.