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简介：AIM:Toestablishtheratmodelofstreptozotocin(STZ)induceddiabeticretinopathy(DR),whichisthemostcommoncauseofvisuallossandblindnessinpatientswithdiabetes,andobservethegeneexpressionofvascularendothelialgrowthfactor(VEGF)anditsreceptorsduringthedevelopmentofDR.METHODS:AratmodelofdiabeteswasestablishedbyintraperitonealinjectionofSTZ.Thediabeticratswerehousedfor2,3and4monthsafterthedevelopmentofdiabetes.Retinalhistopathologicalobservationwasperformed.TheretinalvesselswereobservedbyimmunofluorescencestainingbyCD31.ThemRNAexpressionofVEGF,VEGFreceptor1and2(VEGFR1/2)inratretinawasdetectedbyreversetranscriptionpolymerasechainreaction(RT-PCR)analysis.RESULTS:Retinalhistopathologicalobservationshowedthemorphologicalchangesofinnernuclearlayer(INL)andouternuclearlayer(ONL)atanytime-point,andalsodemonstratedtheincreasednewvesselsatboth3,4monthsafterthedevelopmentofdiabetes.TheCD31stainingresultsshowedthatthenumberofvesselswasincreasedintheretinasofdiabeticratsatboth3and4monthsafterthedevelopmentofdiabetes.Ascomparedtothenormalrats,themRNAexpressionofVEGFwasincreasedinretinasofdiabeticratsat3monthsafterthedevelopmentofdiabetes,whileVEGFR1andVEGFR2mRNAexpressionwasincreasedat2,3and4monthsafterthedevelopmentofdiabetes.CONCLUSION:Takentogether,ourresultsdemonstratedthatDRwasoccurredat3monthsafterthedevelopmentofdiabetes,andthemRNAexpressionofVEGF,VEGFR1andVEGFR2wereincreasedintheprocessofDR.ThepresentstudyfurtherevidencedtheinvolvementofVEGFanditsreceptorsintheprocessofDR.

简介：AIM:Toinvestigatethemorphologicalalteringeffectoftransforminggrowthfactor-β2(TGF-β2)onuntransfectedhumancornealendothelialcells(HCECs)invitro.METHODS:AfteruntransfectedHCECsweretreatedwithTGF-β2atdifferentconcentrations,themorphology,cytoskeletondistribution,andtypeIVcollagenexpressionofthecellswereexaminedwithinvertedcontrastlightmicroscopy,fluorescencemicroscopy,immunofluorescenceorWesternBlot.RESULTS:TGF-β2attheconcentrationof3-15μg/LhadobviouslyalterativeeffectsonHCECsmorphologyindoseandtime-dependentmanner,and9μg/Lwasthepeakconcentration.TGF-β2(9μg/L)alteredHCEcellmorphologyaftertreatmentfor36h,increasedthemeanopticaldensity(P<0.01)andthelengthofF-actin,reducedthemeanopticaldensity(P<0.01)ofthecollagentypeIVinextracellularmatrix(ECM)andinducedtherearrangementofF-actin,microtubuleincytoplasmandcollagentypeIVinECMaftertreatmentfor72h.·CONCLUTION:TGF-β2hasobviouslyalterativeeffectonthemorphologyofHCECsfrompolygonalphenotypetoenlargedspindle-shapedphenotype,indoseandtime-dependencemannerbyinducingmore,elongationandalignmentofF-actin,rearrangementofmicrotubuleandlargerspreadareaofcollagentypeIV.

简介：AIMTo报告角膜的营养障碍(液晶显示器)与二个变化，R124C和A546D联系了的格子的一个phenotypic变体家谱，在导致贝它的基因(TGFBI).METHODSA详细说明了的转变生长因素，眼睛的检查为一个液晶显示器家庭的所有参加者被参加。从每个参加者的外部血白血球被提取获得DNA。TGFBI基因的所有十七exons的聚合酶链反应(PCR)被执行。产品被定序并且分析。在从proband.RESULTSGenetic分析的右眼睛的渗透的keratoplasty证明proband和所有6个影响个人两个都在codon怀有异质接合的CGC到TGC变化以后，组织学的检查被执行124并且异质接合的GCC到在codon的GAC变化546TGFBI。任何一个100个控制题目和未受影响的家庭成员都不为这二个变化是积极的。眼睛的检查显示了多重refractile在在外部角膜的中央角膜和小小粒的存款的前面的基质的像格子的暗。存款与红显示是的刚果断然被染色在自然淀粉、位于主要观察的前面、中间的stroma.CONCLUSIONWe在TGFBI基因带了二个病原的变化(R124C和A546D)的一个新奇液晶显示器家庭。phenotypic特征与与相应单个变化联系的那些显然不同。结果表明尽管明确的变化是疾病的最重要的基因原因，一些不同修饰词等位基因可以影响显型。

简介：在反脉管的endothelial生长的一个年以后与有斑点的浮肿的分辨率和foveal消沉的恢复在眼睛报导foveal厚度减小为包含中心的糖尿病的有斑点的浮肿(DME)的因素(anti-VEGF)治疗.METHODSFoveal厚度与光连贯断层摄影术被估计决定中央子字段foveal厚度(CSFT)并且在有DME的42只眼睛的有斑点的体积(CSFT>275湥獴愠?潣灭牡摥琠?敨污桴?潣瑮潲?牧畯？

简介：AIM:Toevaluatetheefficacyandsafetyofanti-vascularendothelialgrowthfactor(VEGF)combinedwithphotodynamictherapy(PDT)versusanti-VEGFmonotherapyforpolypoidalchoroidalvasculopathy(PCV).METHODS:WeconductedaMeta-analysisof9studiestocomparetheefficacyandsafetybetweencombinedtherapyandanti-VEGFmonotherapyforPCV.TheprogramsofRevMan5.3andStata12.0wereusedtoanalyzedata.RESULTS:Thebestcorrectedvisualacuity(BCVA)incombinedtherapygroupweresignificantlybetterthanthoseofanti-VEGFmonotherapygroupat6,24and36mo,withpooledweightedmeansdifferences(WMDs)of0.12(0.06,0.18),0.25(0.12,0.38)and0.28(0.13,0.43),respectively.Thecentralretinalthickness(CRT)reductionsincombinedtherapygroupwerehigherthanthatinantiVEGFmonotherapygroupat1,3,6and9mo,withpooledWMDsof63.90(20.41,107.38),33.47(4.69,62.24),30.57(0.12,60.01)and28.00(2.51,53.49),respectively.Theregressionrateofpolypsincombinedtherapygroupwasmuchhigherthanthatinanti-VEGFmonotherapygroup[RD:0.47(0.26,0.68);P<0.0001].Theadverseeventretinalhemorrhagedidnotdiffersignificantlybetweenthetwogroups.CONCLUSION:OurfindingsclearlydocumentthatantiVEGFcombinedwithPDTisamoreeffectivetherapyforPCVcomparedwithanti-VEGFmonotherapy.Furthermore,combinedtherapydoesnotincreasetheincidenceofretinalhemorrhage.

简介：AIMTo学习discoidin象我一样domaincontaining蛋白质3的效果(EDIL3)在人的透镜的增长和上皮间充质的转变(EMT)上的弄空上皮的房间(LEC).METHODSRNA干扰被用来在vitro在人的LEC禁止EDIL3的表示。房间的形态学用一台转换显微镜被观察。房间增长用EdU工具包被估计。房间移植用Transwell房间被调查，LEC的EMT用共焦的显微镜并且西方的弄污被估计。转变生长因素(TGF)小径用数据显示出的西方的blotting.RESULTSThe被调查那个silencingEDIL3表达式改变了LEC形态学并且压制了LEC增长(P<0.05)并且移植(P<0.01)。而且，西方的弄污的结果证明那EDIL3弄空减少了光滑的肌肉肌动朊的表示(-SMA)(P<0.001)并且vimentin(P<0.01)，当增加时E-cadherin的表示(P<0.001)。EDIL3弄空能压制Smad2的phosphorylation(P<0.01)并且Smad3(P<0.01)并且exracellular信号的激活调整了kinase(英皇家空军之阶级最低之兵)(P<0.05).CONCLUSIONThe调查结果显示EDIL3可能经由TGF小径在LEC参予增长和EMT并且可以是为以后的囊opacification的处理的一个潜在的治疗学的目标。

简介：AIMTo在cells.METHODSARPE-19细胞是的网膜的颜料上皮(RPE)上调查高葡萄糖层次和反脉管的endothelial生长因素(VEGF)代理人(bevacizumab，ranibizumab和aflibercept)的效果在不同葡萄糖层次(5.5mmol/L，25mmol/L，和75mmol/L)有教养。房间生存能力被MTT试金与D葡萄糖在处理以后在3d评估。房间迁居能力被创伤愈合试金在3d测量。一个房间死亡察觉工具包被用来在3点估计apoptosis并且14d。房间增长被EdU试金在3d估计。文化媒介在临床上相关的集中与anti-VEGF代理人被对待。实验然后在一个不同葡萄糖level.RESULTSThe生存能力被重复，ARPE-19房间的移植显著地作为与5.5mmol/L葡萄糖相比面对75mmol/L被减少。TUNEL积极的房间的百分比显著地被增加，proliferative潜力与5.5mmol/L葡萄糖相比与75mmol/L被减少。在在25mmol/L和5.5mmol/L葡萄糖之间的结果没有重要差别。面对75mmol/L葡萄糖，与anti-VEGF对待的组显示出减少的房间生存能力和增长并且增加了apoptosis。然而，anti-VEGFgroups.CONCLUSIONHigh葡萄糖水平减少之间没有重要差别RPE房间的生存能力，创伤愈合能力，和增长，当增加apoptosis时。而且，anti-VEGF代理人在高葡萄糖的条件下面防碍RPE房间的生理的功能，在房间生存能力和增长由减少伴随了。