简介：

简介：

简介：无

简介：Age-relatedhearingloss(AHL),orpresbycusis,isthemostcommonneurodegenerativedisorderandtopcommunicationdeficitoftheagedpopulation.GeneticpredispositionisoneofthemajorfactorsinthedevelopmentofAHL.Generally,AHLisassociatedwithanage-dependentlossofsensoryhaircells,spiralganglionneuronsandstriavasculariscellsintheinnerear.Althoughthemechanismsleadingtogenetichearinglossarenotcompletelyunderstood,caspase-familyproteasesfunctionasimportantsignalsintheinnerearpathology.ItisnowacceptedthatmousemodelsarethebesttoolstostudythemechanismofgenetichearinglossorAHL.Here,weprovideabriefreviewofrecentstudiesonhearingimprovementinmousemodelsofAHLbyanti-apoptotictreatment.

简介：AIM:ToevaluatethehighsensitivityC-reactiveprotein(hsCRP),Fetuin-Aandmatrixγ-carboxyglutamateprotein(MGP)asthemainfactorsforvascularcalcificationandinflammationinserumofpatientswithadvancedage-relatedmaculardegeneration(ARMD)incomparisontohealthycontrols.METHODS:Thesubjectswere40patientswithchoroidalneovascularization(CNV)havingameanageof70.9±9.1yandamatchedgroupof49apparentlyhealthycontrolsubjects.TheARMDwasdiagnosedusingaslitlampwithsuperfieldlens,fundusphotographyandfluoresceinangiography.MeasurementofhsCRPwasdonebynephelometrymethod.LevelsofFetuin-AandMGPweremeasuredbyenzyme-linkedimmunosorbentassay(ELISA)technique.RESULTS:hsCRP[0.45(0.07-2.63)mg/Lvs0.25(0.03-1.2)mg/L,P=0.02)]andFetuin-Alevels(50.27±5.04vs44.99±10.28ng/mL,P=0.009)werehigherinthepatientsthaninthecontrolgroups.WecouldnotfindsignificantdifferenceinMGPlevelbetweentwogroups(P=0.08).TherewasnotasignificantcorrelationbetweenMGPwithFetuin-AandhsCRPamongthepatients(P=0.7,P=0.9respectively).AsignificantnegativecorrelationofhsCRPwithFetuin-Awasobservedinbothcaseandcontrolgroups(P=0.004,r=-0.33andP=0.001,r=-0.54,respectively).CONCLUSION:AlthoughourstudyshowsthatserumhsCRPandFetuin-AisincreasedinCNVpatientsaswellasnegativelycorrelatedwithbothstudygroups,theirdirectroleonpathogenesisofARMDrequiredfuturestudies.

简介：无

简介：AIM:Tocomparetheeffectivenessandsafetybetweenbevacizumabandranibizumabinthetreatmentofagerelatedmaculardegeneration(AMD)throughasystematicreviewandmeta-analysis.METHODS:Weperformedacomprehensivesearchofrandomizedcontrolledtrials(RCTs),non-RCTs,casecontrolandcohortstudiesthatcomparedbevacizumabandranibizumabusingPubMedandtheCochraneLibrary.Aftertherelateddatawereextractedbytwoinvestigatorsindependently,pooledweightedmeandifferences(WMDs)andriskratios(RRs)with95%confidenceintervals(CIs)wereestimatedusingarandom-effectsorafixed-effectsmodel.RESULTS:AtotaloffourRCTsinvolving1927patientsandelevenretrospectivecaseseriesinvolving2296patientswereincluded.Fortheprimaryoutcomes,nosignificantdifferenceswerefoundbetweenranibizumabgroupandbevacizumabgroupinvisualacuity(WMD:-0.04;95%CI:-0.08to0.00;P=0.06),bestcorrectedvisualacuity(WMD:-0.05;95%CI:-0.10to0.00;P=0.05),retinathickness(WMD:-4.69;95%CI:-13.15to3.76;P=0.86)andfovealthickness(WMD:10.91;95%CI:-14.73to36.56;P=0.40).Thepooledanalysesintheevaluationofsafetyshowedthatcomparedtobevacizumab,ranibizumabwasassociatedwithdecreasedrisksofocularinflammation(RR:0.45;95%CI:0.23to0.89;P=0.02)andvenousthromboticevents(RR:0.27;95%CI:0.08to0.89;P=0.03).However,therewerenosignificantdifferencesobservedindeaths(P=0.69)andarterialthromboembolicevents(P=0.71)betweenthetwogroups.CONCLUSION:Withequalclinicalefficacy,ranibizumabwasfoundtobeassociatedwithlessadverseeventscomparedtobevacizumab,indicatingthatranibizumabmightbeasafermanagement.

简介：Age-relatedmaculardegeneration(AMD)causesirreversiblelossofcentralvisionforwhichthereisnoeffectivetreatment.IncipientpathologyisthoughttooccurintheretinaformanyyearsbeforeAMDmanifestsfrommidlifeonwardstoaffectalargeproportionoftheelderly.Althoughgeneticaswellasnon-genetic/environmentalrisksarerecognized,itscomplexaetiologymakesitdifficulttoidentifysusceptibility,orindeedwhattypeofAMDdevelopsorhowquicklyitprogressesindifferentindividuals.HerewesummarizetheliteraturedescribinghowtheAlzheimer's-linkedamyloidbeta(Aβ)groupofmisfoldingproteinsaccumulateintheretina.ThediscoveryofthiskeydriverofAlzheimer'sdiseaseinthesenescentretinawasunexpectedandsurprising,enablinganaltogetherdifferentperspectiveofAMD.WearguethatAβfundamentallydiffersfromothersubstanceswhichaccumulateintheageingretina,anddiscussourlatestfindingsfromamousemodelinwhichphysiologicalamountsofAβweresubretinally-injectedtorecapitulatesalientfeaturesofearlyAMDwithinashortperiod.OurdiscoveriesaswellasthoseofotherssuggestthepatternofAβaccumulationandpathologyindonoraged/AMDtissuesarecloselyreproducedinmice,includinglate-stageAMDphenotypes,whichmakesthemhighlyattractivetostudydynamicaspectsofAβ-mediatedretinopathy.Furthermore,wediscussourfindingsrevealinghowAβbehavesatsingle-cellresolution,andconsiderthelong-termimplicationsforneuroretinalfunction.WeproposeAβasakeyelementinswitchingtoadiseasedretinalphenotype,whichisnowbeingusedasabiomarkerforlatestageAMD.

简介：为neovascular在诊断和预后调查neutrophil-to-lymphocyte比率(NLR)和platelet-to-lymphocyte比率(PLR)的地方年龄相关的有斑点的退化(AMD).METHODSOne百个AMD病人和100健康控制在学习被包括。血样品从静脉的血被获得，它被用于平淡的分析，并且这些样品被使遭到完成血计数。NLR被定义为淋巴细胞的数字划分的嗜中性的计数，并且PLR被定义为lymphocytes.RESULTSNo的数字划分的血小板计数统计上重要的差别以人口统计的特征在考虑下面在二个组之间被观察(P>0.05)。在耐心的组的平均NLR被发现在健康控制组比那显著地高(P<0.05)。平均PLR作为与控制组相比在耐心的组是显著地更高的(P<0.05)。当最好改正的视觉尖酸(BCVA)增加了，NLR和PLR减少了(在49.8%和63.0%点的重要否定关联，分别地)而当中央有斑点的厚度(CMT)增加了，NLR和PLR增加了(在59.3%和70.0%点的重要积极关联，分别地).CONCLUSIONNLR和PLR层次作为与健康控制相比在neovascularAMD病人之中是更高的组。NLR和PLR层次被发现与BCVA并且直接相反地成正比与CMT成正比。

简介：AIMTo调查经历了intravitrealranibizumabmonotherapy对待neovascular的病人的长期的视觉、解剖的结果年龄相关的有斑点的退化(AMD)并且为经历了ranibizumabmonotherapy因为neovascularAMD在这回顾的study.RESULTSThe一般水准病人年龄被包括的74个病人的74只眼睛的至少2y.METHODSA总数跟随起来是72.1

简介：AIM:Todeterminereallifeclinicaloutcomesinpoorlyresponsiveandtreatment-naveneovascularage-relatedmaculardegeneration(nvAMD)patientsusingbimonthlyfixeddosingafliberceptregimen.METHODS:Thiswasaretrospectivestudyof165eyeswithnvAMDstartedonafliberceptatSouthamptonEyeUnitbetweenJune2013andJune2014.Patientswereeitherswitchedfromprorenata(PRN)ranibizumab/bevacizumabduetopoorresponse(107eyes),ortreatment-nave(58eyes).Patientsinitiallyreceived3-monthlyintravitrealafliberceptinjectionsfollowedby2-monthlyfixeddoses.Clinicvisitswerescheduledatmonth0,4,10and12.Meanchangeinbest-correctedvisualacuity(BCVA)andcentralretinalthickness(CRT)frombaselinewereassessedusingtheWilcoxonsignedranktest.TheproportionofpatientsmaintainingBCVA(<15lettersloss)at12mowasalsoevaluated.RESULTS:MeanBCVAchangeatmonth12was+3.29and+4.67lettersintheswitchedandnaveafliberceptgroupsrespectively(P<0.01).BCVAwasmaintainedin95.3%ofswitchedand96.6%ofnavepatients.CRTatmonth12showedadecreaseof-6.16μmintheswitchedgroupand-35.36μminthenavegroup(P<0.01).Patientspreviouslytreatedwithranibizumab/bevacizumabhadonaveragereceived7.4ranibizumab/bevacizumabinjectionsover12.6mo,attending10clinicvisits.Thefixeddosingafliberceptregimenrequiredanaverageof7.1injections(navegroup),7.5injections(switchedgroup)and4clinicvisitsperyear.CONCLUSION:Fixedbimonthlyafliberceptiseffectiveinbothtreatment-naveandpoorlyresponsivenvAMDpatients.Adoptingafixeddosingregimencanreducepatientburdenwithoutcompromisingonoutcomes.

简介：

简介：AbstractBackground:Age-related macular degeneration (AMD) is the leading cause of vision loss worldwide. However, the mechanisms involved in the development and progression of AMD are poorly delineated. We aimed to explore the critical genes involved in the progression of AMD.Methods:The differentially expressed genes (DEGs) in AMD retinal pigment epithelial (RPE)/choroid tissues were identified using the microarray datasets GSE99248 and GSE125564, which were downloaded from the gene expression omnibus database. The overlapping DEGs from the two datasets were screened to identify DEG-related biological pathways using gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. The hub genes were identified from these DEGs through protein-protein interaction network analyses. The expression levels of hub genes were evaluated by quantitative real-time polymerase chain reaction following the induction of senescence in ARPE-19 with FK866. Following the identification of AMD-related key genes, the potential small molecule compounds targeting the key genes were predicted by PharmacoDB. Finally, a microRNA-gene interaction network was constructed.Results:Microarray analyses identified 174 DEGs in the AMD RPE compared to the healthy RPE samples. These DEGs were primarily enriched in the pathways involved in the regulation of DNA replication, cell cycle, and proteasome-mediated protein polyubiquitination. Among the top ten hub genes, HSP90AA1, CHEK1, PSMA4, PSMD4, and PSMD8 were upregulated in the senescent ARPE-19 cells. Additionally, the drugs targeting HSP90AA1, CHEK1, and PSMA4 were identified. We hypothesize that Hsa-miR-16-5p might target four out of the five key DEGs in the AMD RPE.Conclusions:Based on our findings, HSP90AA1 is likely to be a central gene controlling the DNA replication and proteasome-mediated polyubiquitination during the RPE senescence observed in the progression of AMD. Targeting HSP90AA1, CHEK1, PSMA4, PSMD4, and/or PSMD8 genes through specific miRNAs or small molecules might potentially alleviate the progression of AMD through attenuating RPE senescence.

简介：AIM:Tocomparetheefficacyandsafetyofcombinationofranibizumabwithphotodynamictherapy(PDT)vsranibizumabmonotherapyinthetreatmentofage-relatedmaculardegeneration(AMD).METHODS:TheCochraneCentralRegisterofControlledTrials(CENTRAL)intheCochraneLibrary,Pubmed,andEmbaseweresearched.Therewerenolanguageordatarestrictionsinthesearchfortrials.Onlyrandomizedcontrolledtrials(RCTs)wereincluded.MethodologicalqualityoftheliteratureswasevaluatedaccordingtotheJadadScore.RevMan5.2.6softwarewasusedtodothemeta-analysis.RESULTS:Sevenstudieswereincludedinoursystematicreview,amongwhichfourofthemwereincludedinquantitativeanalysis.Theresultshowsthattheranibizumabmonotherapygrouphadabettermeanbestcorrectedvisualacuity(BCVA)changevsbaselineatmonth12comparedwiththatofthecombinationtreatmentgroup,andthestatisticaldifferencewassignificant(WMD,-2.61;95%CI,-5.08to-0.13;P=0.04).However,aftertheremovalofonestudy,thedifferencebetweenthetwogroupsshowednosignificantdifference(WMD,-2.29;95%CI,-4.81to0.23;P=0.07).Meanwhile,nosignificantcentralretinalthickness(CRT)reductionwasfoundinthecombinationtreatmentgroupandtheranibizumabmonotherapygroupat12monthsfollow-up.Nevertheless,thecombinationgrouptendedtohaveagreaterreductioninCRT(WMD,-4.13μm;95%CI,-25.88to17.63,P=0.71).Theproportionofpatientsgainingmorethan3linesatmonth12intheranibizumabgroupwashigherthaninthecombinationgroupandtherewasasignificantdifference(RR,0.72;95%CI,0.54to0.95;P=0.02).Whereastherewasnosignificantdifferencefortheproportionofpatientsgainingmorethan0lineatmonth12betweenthetwogroups(RR,0.93;95%CI,0.76to1.15;P=0.52).Thegeneraltendencyshowsareductioninranibizumabretreatmentnumberinthecombinationtreatmentgroupcomparedwiththeranibizumabmonotherapygroup.Asmajoradverseevents,thedifferencesinthenumberofeyepain,endophthalmitis,hypertensionandarterialt

简介：研究是否特定的等位基因HLA一级(HLA--A和HLA-B)并且班II(HLA医生)是风险因素因为年龄的exudative类型的发展联系了有斑点的退化(ARMD)，HLA抗原与ARMD在正常、影响的眼睛两个都被表示。我们设计了未来的控制盒子的研究。我们与主要经典或秘密的choroidalneovascularization招募了75个病人，对ARMD第二等，并且与光力学的治疗对待。超过55岁的250个病人，没有ophthalmologic病理，为分析平淡的检查去了医院的人，被用作控制。数据的分析显示出二个组之间的重要差别。等位基因HLA-B27与ARMD断然相关(p<0.0113)。然而，我们没发现等位基因否定地联系了。因此HLA-B27是等位基因预先安排承受ARMD。

简介：TheAMDcausesadeteriorationofthecentralfieldofvisionofthehumaneyecausedbylossoffunctionofthemacula.Themaculaisthecentralpartoftheretina,thepartthatreceivesthemostfinelydetailedinformationsinceitcontainsaconsiderablenumberofdaylightsensitiveandcoloursensitivephotoreceptorcells.PeoplewithlittleskinpigmentslikeEuropeanpeoplearemorefrequentlyaffectedthanpeoplefromtheAsiancontinentforexample.ThreequartersofthepeoplewhoareaffectedbyAMDsufferfromthedry

简介：影片讲述了在冰河世纪这个充满惊喜与危险的蛮荒时代,因为一名突如其来的人类婴儿，让三只性格迥异的动物凑在一起的故事。其中，曼菲德和席德一心想护送婴儿返回亲人身边，而迭哥则试图将他们带入自己族类设下的埋伏圈。

简介：认一认高音狗和小伙伴们一起来到博物馆，参观有趣的恐龙展览。下面的恐龙，你认识哪些？

简介：

简介：信息产业时代的到来，中国载人飞船的成功发射，数码风暴的“狂风巨浪”，都为我们生活的祥和空间平添一份精彩！