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：在最近的十年，从动物和临床的研究积累证据建议了一个足够地激活的免疫系统可以强烈扩充癌症治疗的各种各样的类型，包括光力学的治疗(太平洋夏季时间)。通过反应的氧种类的产生，太平洋夏季时间根除由触发局部性的肿瘤损坏并且导致反肿瘤免疫的肿瘤。作为反肿瘤免疫的主要部件，在太平洋夏季时间的调停房间的有免疫力的回答的参与很好在过去的十年被调查了，而体液的免疫的角色仍然保持相对未经勘探。在现在的调查，使用photosensitizerBAM-SiPc和CT26忍受肿瘤的BALB/c老鼠模型，调停房间、体液的适应有免疫力的部件能涉及太平洋夏季时间，这被表明。与脉管的太平洋夏季时间(VPDT)政体，BAM-SiPc能根除~的肿瘤70%；忍受肿瘤的老鼠和扳机能持续超过1年的反肿瘤免疫者回答。Th2cytokines的举起是在VPDT以后的检测前vivo，显示体液的回答的潜在的参与。从治好VPDT的老鼠的浆液的分析也揭示了肿瘤特定的抗体的提高的层次。而且，这浆液能有效地妨碍肿瘤生长并且保护老鼠免于进一步以一种T-cell-dependent方式重新质问。一起拿，体液的部件在BAM-SiPc-VPDT以后导致了的这些结果表演能帮助反肿瘤免疫的发展。

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：BackgroundIntensive锻练为葡萄糖和为它的新陈代谢反应负责的几条生物化学的小径改变生理的需要。在他们之中是包含胰岛素，像胰岛素的生长因素(IGF-1)，和IGF有约束力的蛋白质(IGFBP)的那些。锻练的不同类型和度，以及运动员健康，可以关于为改变需要的集中和时间导致回答的一个范围。工作的想法是发现是否并且insulin/IGF轴怎么在已经训练的题目对另外的物理活动作出回应并且如果那么，是从在校园里的4星期的集中的训练的新陈代谢的control.MethodsThe效果的方面潜在地有益的改编(准备训练)胰岛素的onthelevels，在最大的进步锻练期间，一辆踏车上的测试(MPET)与在MPET期间获得的结果相比的IGF-1，和IGFBP在一个常规训练季节以后进行了17戠慩s

简介：Intracerebralhemorrhage(ICH)isthemostseverecerebrovasculardisease,whichrepresentsaleadingcauseofdeathanddisabilityindevelopedcountries.However,therapeuticoptionsarelimited,soismandatorytoinvestigaterepairingprocessesafterstrokeinordertodevelopnewtherapeuticstrategiesabletopromotebrainrepairprocesses.TherapeuticangiogenesisandvasculogenesisholdpromisetoimproveoutcomeofICHpatients.Inthisregard,circulatingendothelialprogenitorcells(EPCs)haverecentlybeensuggestedtobeamarkerofvascularriskandendothelialfunction.Moreover,EPClevelshavebeenassociatedwithgoodneurologicalandfunctionaloutcomeaswellasreducedresidualhematomavolumeinICHpatients.Finally,experimentalandclinicalstudiesindicatethatEPCmightmediateendothelialcellregenerationandneovascularization.Therefore,EPC-basedtherapycouldbeanexcellenttherapeuticoptioninICH.Inthismini-review,wediscussthepresentstatusofknowledgeaboutthepossibletherapeuticroleofEPCsinICH,molecularmechanisms,andthefutureperspectivesandstrategiesfortheiruseinclinicalpractice.

简介：DearEditor,IamSatoruKase,fromtheDepartmentofOphthalmology,FacultyofMedicineandGraduateSchoolofMedicine,HokkaidoUniversity,SapporoCity,Japan.Iwritetopresentacaseofneurofibromatosistype1(NF1)showingmassivehemorrhageduringinvolutionalblepharoptosissurgery.

简介：Thepresentstudywasdesignedtoexaminetheanti-hyperuricemicandanti-inflammatoryeffectsandpossiblemechanismsofvaticaffinol,aresveratroltetramerisolatedfromethanolextractsofDipterocarpusalatus,inoxonate-inducedhyperuricemicmice.At1hafter250mg·kg~(-1)potassiumoxonatewasgiven,vaticaffinolat20,40,and60mg·kg~(-1)wasintragastricallyadministeredtohyperuricemicmiceoncedailyforsevenconsecutivedays.Vaticaffinolsignificantlydecreasedserumuricacidlevelsandimprovedkidneyfunctioninhyperuricemicmice.Itinhibitedhepaticactivityofxanthinedehydrogenase(XDH)andxanthineoxidase(XOD),regulatedrenalmRNAandproteinlevelsofuratetransporter1(URAT1),glucosetransporter9(GLUT9),organicaniontransporter1(OAT1),organiccationtransporter1(OCT1),OCT2,organiccation/carnitinetransporter1(OCTN1),andOCTN2inhyperuricemicmice.Moreover,vaticaffinolmarkedlydown-regulatedrenalproteinlevelsofNOD-likereceptor3(NLRP3),apoptosis-associatedspeck-like(ASC),andCaspase-1,resultinginthereductionofinterleukin(IL)-1β,IL-18,IL-6andtumornecrosisfactor-α(TNF-α)levelsinthisanimalmodel.Additionally,HPLCandLC-MSanalysesclearlytestifiedthepresenceofvaticaffinolinthecrudeextract.Theseresultssuggestthatvaticaffinolmaybeusefulforthepreventionandtreatmentofhyperuricemiawithkidneyinflammation.

简介：AIMTo调查在patients.METHODSNon-DSEK在接枝拒绝率，和它的全面程序的有效性上剥去endothelialkeratoplasty(non-DSEK)的non-Descemet的影响在64个病人，和程序的结果的65只眼睛上被执行包括接枝的拒绝事件，失败和脱臼，最好改正的视觉尖酸(BCVA)，endothelial房间密度(ECD)，和另外的复杂并发症，是65看的分析retrospectively.RESULTSOf，63从bullouskeratopathywi恢复了吝啬的后续时间是26.4mo(范围，6-84mo)。吝啬的BCVA在外科以后在1y在3mo，在6mo的0.46logMAR，和0.37logMAR外科手术前地从1.70logMAR改善了到0.54logMAR。成功地经历了镜子的显微镜的检查的25个病人的手术后的施主ECD是1918<

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简介：Anti-globalizationtrendsareinplayintheUSandWesternEuropewhereelectoratesarerecalcitranttoallowimmigrantsintotheirsocieties,nationalsovereigntyissoughtincertaingeographicareas,andthenationalmoodseekstosuppressnewlyrisingcountries'tradeanddevelopment.ThecontinuationofeconomicdownturninWesterncountriesisreinforcedbytheirinternalwealthgapandexternalcompetition.Ascapitalism'sdemandforprofitisnowbeingcritiquedalongwiththeemergentprofitprospectstobedeliveredbypendingtechnologicalprogress,thetemperofthetimescouldtemporarilyslowdownbutnotreverseglobalization.Timelydiscussionsaboutreformofinternationaleconomicorderandaboutaneffectivenationaldevelopmentmodelshouldseeksustainablesolutionsforhealthy,stableglobalizationanddevelopmentoftheworldeconomy.

简介：IntroductionAsIreflectbackonmytimeasaneditor,Irecallafewissuesthatbotheredmerelatingtopublicationsinmedicaljournals,e.g.Impactfactorandtherelationshipofeditorialsandself-citationontheimpactfactorandacceptanceratesfororiginalpublications.Whatfollowsaresomethoughtsonthesubject.

简介：ShouwuisatraditionalChinesemedicine(TCM)withneuroprotectiveeffect.ShouwuYizhidecoction(SYD)wasdesignedbasedonTCMtheory.However,littleisknownabouttherolesofSYDinVasculardementia(VaD).ThepresentstudyaimedtoevaluatethepotentialeffectsofSYDonthevascularcognitiveimpairmentandexploretheunderlyingmechanismbyestablishingfocalcerebralischemia/reperfusion(I/R)ratmodeltoinduceVaD.SYDadministration(54mg·kg~(-1))for40daysobviouslyimprovedthevascularcognitiveimpairmentinthemiddlecerebralarteryocclusion(MCAO)ratsasevidencedbythedeclinedneurologicaldeficitscoreandshortenedescapelatencyvianeurologicaldeficitassessmentandMorriswatermazetest.Moreover,SYDdecreasedneurondamage-inducedcelldeathandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,therebyalleviatingVaD.Mechanistically,SYDcausedincreasesintheexpressionofvascularendothelialgrowthfactor(VEGF),CD34andCD31,comparedwiththeMCAOratsincoronalhippocampus.Simultaneously,theexpressionlevelofmiR-210waselevatedsignificantlyafterSYDadministration,comparedwiththevehiclerats(P<0.01).TheexpressionofNotch4atbothmRNAandproteinlevelswasupregulatedremarkablyalongwiththenotablydownregulatedDLL4expressionunderSYDadministrationcomparedwiththevehiclerats(P<0.05).Overall,theaboveresultsindicatedthatSYDpromotedangiogenesisbyupregulatingVEGF-inducedmiR210expressiontoactivateNotchpathway,andfurtheralleviatedneurondamageandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,ultimatelyenhancingthecognitionandmemoryofMCAOrats.Therefore,ourfindingspreliminarilyidentifiedtheeffectandthemechanismofactionforSYDonVaDinrats.SYDcouldbeapotentialcandidateintreatmentofVaD.

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简介：Theresearchgroupwassuccessfulingeneratingavasculargraftwithbiomimeticcircumferentialtensilestrengthandexpressionofsmoothmusclecellspecificgenesoverstaticculture.

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简介：Hydrationcracksofmagnesia-spinelbricksincementindustryhavebeenseriousproblemsforbothrefractoryproducersandrefractoryusersforalongtime.Whenmagnesia-spinelbricksarekeptformorethan6months,thebrickstendtohavereactionwithwaterormoistureandresultincracksandlossontheirstructuralstrength.Thosebrickscannotbeusedanymoreandcausesubstantiallossfortherelatedparties.In2013,theSiamRefractoryIndustryCo.,Ltd.,Thailand,successfullydevelopedandappliedaspecialnano-technologytocreate'Anti-HydrationMagnesia-SpinelBricks'forcementindustrywhichcanhavethestoragetimemorethantwoyearseveninhighhumidityareas.Thecementproducerscanensurethatallbricksstillhavegoodpropertiesasthenewones.

简介：Pyrimidinederivativeshavebeenreportedasneuroprotectiveagentsusefulforthetreatmentofvariousneurodegenerativedisorders.Inthepresentstudy,severalpyrimidineanalogueshavebeenevaluatedasneuroprotectiveagentsinMorriswatermazemodel.Itwasobservedthatpyrimidinederivatives8–17considerablyimprovelearning,memory,andmovementdeficitsinanimalmodels.Biochemicalestimationsofbrainserumoftreatedanimalsrevealedsuppressionofoxidativeandnitrosativestress,acetylcholinesteraseactivity,andotherparameterswhichleadstoneurodegenerationofbrain.Ofallthepyrimidinederivatives,thiomorpholinederivative8andpiperazineethanolderivative17werefoundtobethemostactiveneuroprotectiveagentsandproducedeffectscomparabletostandarddrugrivastigmineintermsofbehavioral,biochemical,andmolecularaspects.

简介：Theunpredictableruptureofsaccularaneurysmsespeciallyoftheintracerebralaneurysmisaknottyproblemthatalwaysresultsinhighmortality.Traditionaldiagnosisofmedicalimages,whichgivestheaneurysmsizeandcompareswithaspeculatedcriticalsizefromclinicalstatistics,wasdemonstratedinadequatetoforecastingrupture.Here,weproposeanewdetectingstrategythatusesadielectricelastomer(DE)capacitancesensortomonitorthegrowthofsaccularaneurysmsanddeliverboththewallstressandgeometricparameters.Basedontheelasticgrowththeorytogetherwiththefinitedeformationanalyses,thecorrelationbetweenthereal-timeoutputcapacitanceoftheDEsensorandthewallstressand/orgeometryofananeurysmisderived.Comparedtoclinicstatisticsandbiomechanicssimulations,thewallstressandgeometricsizemaybeusedascombinedindicatorstoassesstheruptureriskofasaccularaneurysm.Numericalresultsshowthatanoutputrelativecapacitanceof30indicatesahighriskofrupture.Finally,thesensitivityandresolutionoftheDEsensorareprovedadequatelyhighformonitoringthegrowthstateandevaluatingtheruptureriskofasaccularaneurysm.