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。

简介：

简介：在细胞的增长和内长的脉管的endothelial生长因素(VEGF)上调查melatonin的效果的目的在胰腺的癌房间(PANC-1)的表示。方法PANC-1房间为这研究是有教养的。在文化媒介的分泌VEGF集中用ELISA方法被决定，在肿瘤房间的VEGF生产被immunocytochemistry，和VEGFmRNA表示检测被RT-PCR决定。更高结果melatonin集中显著地禁止了细胞的增长，与展出最高禁止的效果的1mmol/L集中(P<0.01)。在房间文化上层清液和intra小房的VEGF集中都显著地在melatonin(1mmol/L)以后被减少孵化(P<0.05)。VEGFmRNA表示在观察时期期间以一种时间依赖者方式显著地减少了(P<0.05)。结论高melatonin集中显著地禁止了胰腺的癌房间的增长。内长的VEGF表示被melatonin孵化也压制。

简介：AIM:Tumorangiogenesishasbeenshowntobepromotedbyvascularendothelialgrowthfactor(VEGF)viastimulatingendothelialcellproliferation,migration,andsurvival.BlockadeofVEGFsignalingbydifferentmeanshasbeendemonstratedtoresultinreducedtumorgrowthandsuppressionoftumorangiogenesisindistincttumorentities.Here,wetestedarecombinantadenovirus,AdsFIt1-3,thatencodesanantagonisticallyactingfragmentoftheVEGFreceptor1(Flt-1),forsystemicantitumoreffectsinpre-establishedsubcutaneousCRCtumorsinmice.METHODS:Murinecolorectalcarcinomacells(CT26)wereinoculatedsubcutaneouslyintoBalb/cmiceforinvivostudies.Tumorsizeandsurvivalweredetermined.293celllinewasusedforpropagationoftheadenoviralvectors.HumanlungcancerlineA549andhumanumbilicalveinendothelialcellsweretransfectedforinvitroexperiments.RESULTS:InfectionoftumorcellswithAdsFlt1-3resultedinproteinsecretionintocellsupernatant,demonstratingcorrectvectorfunction.Asexpected,thesecretedsFlt1-3proteinhadnodirecteffectonCT26tumorcellproliferationinvitro,butendothelialcellfunctionwasinhibitedbyabout46%ascomparedtotheAdLacZcontrolinatubeformationassay.WhenAdsFlt1-3(5×109PFU/animal)wasappliedtotumorbearingmice,wefoundatumorinhibitionby72%atd12aftertreatmentinitiation.Inspiteoftheseantitumoraleffects,thesurvivaltimewasnotimproved.AccordingtoreducedintratumoralmicrovesseldensityinAdsFIt1-3-treatedmice,theantitumormechanismcanbeattributedtoangiostaticvectoreffects.WedidnotdetectincreasedsystemicVEGFlevelsafterAdsFlt1-3treatmentandlivertoxicitywaslowasjudgedbyserumalanineaminotransferasedetermination.CONCLUSION:InthisstudyweconfirmedthevalueofasystemicadministrationofAdsFIt1-3toblockVEGFsignalingasantitumortherapyinanexperimentalmetastaticcolorectalcarcinomamodelinmice.

简介：客观：在牛的心包的非细胞组成的新鲜标本在endothelial细胞(Ecs)的粘附和增长上调查脉管的endothelial生长因素(VEGF)和它的效果的绑定和版本，它被heparinization.Methods修改:牛的心包的Cross-linked非细胞组成的新鲜标本是由三个方法的heparinized:(1)heparinizedN-(3-dimethylaminopropyl)-N'-ethylcarbodiimidehydrochloride(EDC)对待非细胞组成的织物样品；(2)(ethyleneimine)(PEI)heparinizedpoly对待

简介：

简介：Objective:Toexploretheprobabilityofvascularendothelialgrowthfactor(VEGF)antisenseoligodeoxynucleotidesasadevelopingnewtherapeuticstrategyforglioma.Methods:VEGFproteinexpressionwasdetectedbyS-Pimmunohistochemicaltechnique.TumorcellapoptosiswasobservedbyTUNELmethod.Results:Comparedwithcontrol,VEGFproteinexpressionwasinhibitedbyantisenseoligodeoxynucleotidesinvitro.Andtheinhibitoryeffectsincreasedwiththeincreasingconcentration.VEGFpositiveratewas82.10%incontrolgroup,whilein2.5,5,10(mol/LAODNgroups,theywere70.00%,57.85%,53.20%respectively.Noinhibitioneffectwasfoundinthecelllinestreatedwithmissenseandsenseoligodeoxynucleotides.Invivo,antisenseoligodeoxy-nucleotidestherapyalsoinhibitedVEGFproteinexpressionandinducedtheincreaseofapoptotictumorcells.However,ithasnoeffectontumorcellproliferation.Conclusion:ItishopefulthatVEGFantisenseoligodeoxynucleotidesmaybeanewgenetherapymethodtogliomathroughitsantiangiogenesiseffectbyinhibitionofVEGF.

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：Objective:Toanalyzetheexpressionofinduciblenitricoxidesynthase(iNOS),endothelialnitricoxidesynthase(eNOS)andvascularendothelialgrowthfactor(VEGF)inhepatocellularcarcinoma(HCC)anditsrelationtoangiogenesis.Methods:Tissuesectionsfrom71HCCpatientswereexaminedimmunohistochemicallyforproteinexpressionofiNOS,eNOS,andVEGF.Microvessaldensity(MVD)wascountedbyendothelialcellsimmunostainedbyanti-CD34antibody.Results:PositiveimmunostainingforiNOS,eNOSwasdetectedin83.1%and85.9%ofHCCrespectively.INOSandeNOSwerenotdetectedinnormalhepatictissue.MVDwas34.3±1.5/HPand38.6±1.6/HPinHCCwithpositivestainingforiNOSandVEGFwhileitwas31.2±2.8/HP,and22.4±2.0/HPinHCCwithnegativestainingforiNOSandVEGF(P<0.01).AcorrelationbetweenNOSexpressionandVEGFinHCCwasnotobserved.Conclusion:iNOSandeNOSmayplayaroleinmalignanttransformationfpost-hepaticcirrhosis.TheexpressionofiNOSandVEGFfavorsangiogenesisofHCC.

简介：Neuroprotectionbyischemicpreconditioninghasbeenconfirmedbymanystudies,buttheprecisemechanismremainsunclear.Inthepresentstudy,weperformedcerebralischemicpreconditioninginratsbysimulatingatransientischemicattacktwice(eacha20-minuteocclusionofthemiddlecerebralartery)beforeinducingfocalcerebralinfarction(2hourocclusion-reperfusioninthesameartery).Wealsoexploredthemechanismunderlyingtheneuroprotectiveeffectofischemicpreconditioning.Sevendaysafterocclusion-reperfusion,tetrazoliumchloridestainingandimmunohistochemistryrevealedthattheinfarctvolumewassignificantlysmallerinthegroupthatunderwentpreconditioningthaninthemodelgroup.Furthermore,vascularendothelialgrowthfactorimmunoreactivitywasconsiderablygreaterinthehippocampalCA3regionofpreconditionedratsthanmodelrats.Ourresultssuggestthattheprotectiveeffectsofischemicpreconditioningonfocalcerebralinfarctionareassociatedwithupregulationofvascularendothelialgrowthfactor.

简介：BACKGROUND:Brainischemiainvolvessecondaryinflammation,whichsignificantlycontributestotheoutcomeofischemicinsults.Vascularendothelialgrowthfactor(VEGF)mayplayanimportantroleinthevascularresponsetocerebralischemia,becauseischemiastimulatesVEGFexpressioninthebrain,andVEGFpromotesformationofnewcerebralbloodvessels.Minocycline,atetracyclinederivative,protectsagainstcerebralischemiaandreducesinflammation,oxidativestress,andapoptosis.OBJECTIVE:ToobservetheinfluenceofminocyclineonVEGF,interleukin-1beta(IL-1β),andtumornecrosisfactoralpha(TNF-α)expressioninWistarratswithfocalcerebralischemia/reperfusioninjury,andtostudytheneuroprotectionmechanismofminocyclineagainstfocalcerebralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:Randomized,controlledexperiment,whichwasperformedintheChongqingKeyLaboratoryofNeurologybetweenMarch2007andMarch2008.MATERIALS:Atotalof36female,Wistarratsunderwentsurgerytoinsertathreadintotheleftmiddlecerebralartery.Animalswererandomlydividedintosham-operation,minocyclinetreatment,andischemia/reperfusiongroups,with12ratsineachgroup.Minocycline(HuishiPharmaceuticalLimitedCompany,China)wasdissolvedto0.5g/Linnormalsaline.METHODS:A0.5-1.0cmthreadwasinsertedintoratsfromthesham-operationgroup.Ratsintheischemia/reperfusiongroupunderwentischemiaandreperfusion.Theminocyclinegroupreceivedminocycline(50mg/kg)12and24hoursfollowingischemiaandreperfusion,whereastheothergroupsreceivedsalineatthecorrespondingtimepoints.MAINOUTCOMEMEASURES:mRNAandproteinexpressionofIL-1βandTNF-αwasmeasuredbyreversetranscriptase-polymerasechainreaction(RT-PCR)andenzymelinkedimmunosorbentassay(ELISA),respectively.VEGFmRNAandproteinexpressionwasexaminedbyRT-PCR,Westernblot,andELISA.RESULTS:Minocyclinedecreasedthefocalinfarctvolume.VEGF,IL-1β,andTNF-αexpressionw

简介：组织缺氧和转变生长factor-β；1(TGF-β；1)在很多恶意增加脉管的endothelial生长因素A(VEGFA)表示。组织缺氧和TGF-β的这效果；1可能为肿瘤前进和先进前列腺癌症的转移负责。在现在的学习，TGF-β；1被显示从两根正常房间线(HPV7和RWPE1)和前列腺癌症房间线(DU145和PC3)导致VEGFA165分泌物。相反地，刺激组织缺氧的VEGFA165分泌物仅仅在前列腺癌症房间线被观察。组织缺氧导致了TGF-β；在PC3前列腺癌症房间的1表情，和TGF-β；打字我部分堵住的受体(ALK5)kinase禁止者调停组织缺氧的VEGFA165分泌物。组织缺氧的这效果提供新奇机制在前列腺癌症房间增加VEGFA表示。尽管VEGFA发信号的autocrine在前列腺癌症前进和转移被含有，联系机制糟糕被描绘。VEGFA活动经由VEGF受体(VEGFR)被调停1(Flt-1)并且2(Flk-1/KDR)。而VEGFR-1mRNA在正常前列腺被检测，上皮的房间，VEGFR-2mRNA和VEGFR蛋白质仅仅在PC3房间被表示。VEGFA165治疗在PC3房间然而并非在HPV7房间导致了细胞外的调整信号的kinase1/2(ERK1/2)的phosphorylation，建议VEGFA的autocrine功能可以特别地与前列腺癌症被联系。由VEGFA165的VEGFR-2的激活被显示提高PC3房间的移植。类似的效果也被观察，内长的VEGFA由TGF-β导致了；1并且组织缺氧。这些调查结果说明那经由VEGFR-2的VEGFA的一个autocrine环为TGF-β的tumorigenic效果是批评的；1并且变形前列腺癌症上的组织缺氧。

简介：AbstractBackground:Uveal melanoma (UM) is the most common primary intraocular malignancy in adults. It has been demonstrated that microRNA-145 (miR-145) is correlated with the progression of various cancers by regulating the expression of multiple target genes, especially a number of genes that regulate angiogenesis and proliferation. However, the underlying mechanisms of miR-145 in tumor angiogenesis of UM are still not well illustrated. Thus, we aimed to explore the potential target genes or pathways regulated by miR-145 in UM and the effect of miR-145 on invasion and angiogenesis.Methods:Totally, 24 choroid samples were collected in our study, including 12 UM samples and 12 normal uveal tissues. The expression of neuroblastoma RAS viral oncogene homolog (N-RAS), phosphorylated protein kinase B (p-AKT), and vascular endothelial growth factor (VEGF) in UM tissues and normal uveal tissues was analyzed using Western blotting analysis. Lentivirus expression system was used to construct MUM-2B and OCM-1 cell lines with stable overexpression of miR-145. Transwell and endothelial cell tube formation assay were used to measure the effects of miR-145 on the invasion and angiogenesis of UM in vitro. The downstream target genes of miR-145 were predicted by bioinformatics and confirmed using a luciferase assay. BALB/c nude mice models were established to investigate the mechanisms of miR-145 on tumor growth and angiogenesis in vivo. Group data comparisons were performed using analysis of Student’s t test. A two-tailed P < 0.05 was considered as statistically significant.Results:The results of Western blotting analysis indicated that the expressions of N-RAS (1.10 ± 0.35 vs. 0.41 ± 0.36, t = 3.997, P = 0.012), p-AKT (1.16 ± 0.22 vs. 0.57 ± 0.03, t = 7.05, P = 0.001), and VEGF (0.97 ± 0.32 vs. 0.45 ± 0.21, t = 3.314, P = 0.008) in UM tumor tissues were significantly higher than those in normal uveal tissue. Luciferase assay demonstrated N-RAS and VEGF as downstream targets of miR-145. Moreover, tube formation assay revealed that miR-145-transfected human microvascular endothelial cell line formed shorter tube length (36.10 ± 1.51 mm vs. 42.91 ± 0.94 mm, t = 6.603, P = 0.003) and less branch points (350.00 ± 19.97 vs. 406.67 ± 17.62, t = 3.685, P = 0.021) as compared with controls. In addition, the numbers of invaded MUM-2B and OCM-1 cells with miR-145 overexpression were significantly lower than the controls (35.7 ± 3.3 vs. 279.1 ± 4.9, t = 273.75, P < 0.001 and 69.5 ± 4.4 vs. 95.6 ± 4.7, t = 21.27, P < 0.001, respectively). In vivo, xenografts expressing miR-145 had smaller sizes (miR-145 vs. miR-scr, 717.41 ± 502.62 mm3vs. 1694.80 ± 904.33 mm3, t = 2.314, P = 0.045) and lower weights (miR-145 vs. miR-scr, 0.74 ± 0.46 g vs. 1.65 ± 0.85 g, t = 2.295, P = 0.045).Conclusion:Our results indicated that miR-145 is an important tumor suppressor and the inhibitory strategies against N-RAS/VEGF signaling pathway might be potential therapeutic applications for UM in the future.

简介：AbstractObjective:The role of Vitamin D-binding protein (DBP) in preeclampsia (PE) pathogenesis is unknown. In this study, we compared the expression of DBP in the placentas of PE patients with the placentas of normotensive pregnant women with placenta previa controls, and aimed to explore the effect of DBP on endothelial cells (ECs) and the underlying mechanism.Methods:DBP expression in placental tissues collected from PE patients and controls was evaluated by immunohistochemistry. The downregulation and upregulation of DBP expression in HTR-8/SVneo cells were examined using DBP-targeting small interfering RNA (siRNA) and DBP-expression vector, respectively. The conditioned media of these DBP-overexpressing and DBP-siRNA HTR-8/SVneo cells were collected and added to human umbilical vein EC (HUVEC) cultures. Angiogenic effects on HUVECs were assessed by tube formation assays, and the proliferation and migration of HUVECs were examined using the Real-Time Cell Analyzer. The expression of vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR)-2, as well as the phosphorylation of different residues of VEGFR-2 in HUVECs, were determined by western blotting.Results:DBP expression was significantly increased in the placental tissues collected from PE patients. The conditioned medium of DBP-overexpressing HTR-8/SVneo cells potently inhibited tube formation by HUVECs, in addition to their proliferation and migration. Furthermore, treatment of HUVECs with the conditioned medium of DBP-overexpressing HTR-8/SVneo cells decreased the phosphorylation of VEGFR-2 at tyrosine 996, whereas the treatment of these cells with the conditioned medium of DBP-siRNA HTR-8/SVneo cells increased the phosphorylation of VEGFR-2 at tyrosine 951, 996, and 1,175.Conclusions:The expression of DBP is increased in the placentas of PE patients. DBP plays potential roles in endothelial dysfunction, which contributes to PE development, by inhibiting tyrosine phosphorylation of VEGFR-2 in ECs.

简介：Angiogenesisintheinfarctperipherycanimprovebloodflow.Vascularendothelialgrowthfactor(VEGF)hasbeenconsideredapotentialtherapeutictargetforstroke.BuyangHuanwudecoction(BYHWD)isaclassictraditionalformulaintraditionalChinesemedicineandisusedtotreatstroke;inaddition,thepromotioneffectsonVEGFproteinexpressionhavebeenconfirmed.However,littleisknownabouthowBYHWDregulatesangiogenesis,orabouttheeffectsofBYHWDonVEGFmRNAexpression.Forthisreason,thepresentstudymeasuredmicrovesseldensityinratswithcerebralischemiausingimmunohistochemistry.Inaddition,VEGFexpressionwasmeasuredbyreverse-transcriptionpolymerasechainreactionandenzyme-linkedimmunosorbentassaytode-terminetheeffectsofBYHWDonangiogenesisandVEGFexpressioninratswithcerebralischemia.Resultsdemonstratedthatmicrovesseldensity,aswellasVEGFmRNAandproteinexpression,increasedafter7and14daysofBYHWDtreatment,whichsuggeststhatBYHWDpromotedan-giogenesisfollowingcerebralischemiaandupregulatedVEGFmRNAandproteinexpressioninischemiccerebralregions.

简介：AIM:Toexploretheeffectsandmechanismofvascularendothelialcadherin(VE-cadherin)onexperimentalcornealneovascularization(CRNV).·METHODS:MousecorneaswereburnedwithsodiumhydroxidetobuildaCRNVmodel.Theburnedcorneaswerelocallyadministratedwithanti-mouseVE-cadherinneutralizingantibody.AnnexinVandclusterofdifferentiation31(CD31)doublestainingwasusedtomeasurevascularendothelialcellapoptosiswiththeuseofflowcytometry(FCM).TheproteinexpressionofNADPHoxidase2(Nox2),caspase-3,andproteinkinaseC(PKC)intheburnedcorneaswereexaminedbyWesternblot.Humanretinalendothelialcell(HREC)proliferationwasdetectedusingaCellCountingKit8(CCK-8)assayinvitro.·RESULTS:TheamountofCRNVpeakedtwoweeksafterthealkaliburn.FCMconfirmedthatVE-cadherinneutralizingantibodytreatmentincreasedCD31positivecellapoptosis.WesternblotrevealedthattheintracornealproteinexpressionofNox2andcaspase-3wereup-regulated,whilePKCwasdown-regulatedintheVE-cadherinneutralizingantibodyadministratedgroup.CCK-8assayshowedthatVE-cadherinneutralizingantibodymarkedlyinhibitedHRECproliferation.·CONCLUSION:VE-cadherinexhibitedananti-apoptosiseffectthroughenhancedPKCsignalingandanenhancedcellproliferationpathway.

简介：AbstractBackground:Proliferative diabetic retinopathy (PDR) is a progressive stage of diabetic retinopathy featured by the formation of neovascular and proliferative membrane. Vascular endothelial growth factor (VEGF) acts as a pivot factor in the development of neovascularization. This study was to investigate the changes of intravitreal VEGF concentrations of severe PDR after intravitreal injection of conbercept (IVC) and its potential advantages to the following vitrectomy.Methods:This was a prospective, interventional, randomized controlled study. Sixty eyes (60 patients) with severe PDR and 20 eyes from 20 patients with rhegmatogenous retinal detachment complicated with proliferative vitreoretinopathy were enrolled in this study. PDR eyes were randomly assigned to three groups by sortation randomization method with 20 eyes in each based on the interval of preoperative IVC (group A: 7 days, group B: 14 days, group C: non-IVC). Another 20 eyes without diabetes were enrolled as the non-diabetic control group (group D), receiving PPV directly. Vitreous specimens of all 80 patients were collected and evaluated afterwards. The intravitreal VEGF concentration of the four groups, and the total surgical time and the intraoperative bleeding rate of the PDR groups were recorded.Results:The mean intravitreal VEGF concentrations of groups A-D were 66.6 ± 43.3, 93.1 ± 52.3, 161.4 ± 106.1 and 1.8 ± 1.2 pg/mL, respectively. It increased significantly in PDR patients (groups A, B and C) (P = 0.002, <0.001, and <0.001, respectively). PDR patients with preoperative IVC (groups A and B) presented significantly lower VEGF concentrations (P < 0.001 and 0.001), intraoperative bleeding rates (P= 0.004) and total surgical time (P < 0.001, P= 0.003) compared with group C. No statistical differences were presented between groups A and B on the three parameters.Conclusion:Seven days and 14 days of preoperative IVC are equally efficient and safe for the vitrectomy of severe PDR patients through decreasing vitreous VEGF concentrations, intraoperative bleeding rate and total surgical times.

简介：瞄准：在微容器密度(MVD)和脉管的内皮生长的表情调查差别，并且在MVD之中探索关联在前列腺癌症(PCa)之间的因素(VEGF)，VEGF-C和VEGFreceptor-3(VEGFR-3)纸巾和邻近的良性的纸巾，Jewett-Whitmore阶段，格利森分数和在PCa的前进的VEGF，VEGF-C和VEGFR-3的表情。方法：免疫组织化学的途径被采用在癌症区域和71个主要职业人员静电干扰腺癌标本的外部良性的区域检测CD34，VEGF，VEGF-C和VEGFR-3的表情。统计分析然后被执行根据试验性并且诊所数据。结果：都显著地与邻近的良性的上皮(P<0.01)相比在恶意的上皮/癌症房间在VEGF，VEGF-C和VEGFR-3的调整表情上面被发现。当在肿瘤区域(P<0.01)比较VEGF-C或VEGFR-3的表示时，在阶段D的病人在阶段A，B或C比病人有一个显著地更高的分数。另外，重要关联在Jewett-Whitmore阶段和VEGF-C之间被观察(r=0.738，P<0.01)，临床的阶段和VEGFR-3(r=0.410，P<0.01)，VEGF-C和格利森分数(r=0.401，P<0.01)，VEGFR-3和格利森分数(r=0.581，P<0.001)并且MVD和VEGF(r=0.492，P<0.001)。结论：VEGF和VEGF-C的增加的表情仔细与PCa的前进被联系。为PCa前进的增加的VEGF表示的主要贡献到过起来调整MVD，它维持了肿瘤织物的生长优点。然而，VEGF-C和VEGFR-3的增加的表情的主要角色是提高lymphangiogenesis并且提供一条主要小径让癌症房间传播。