简介：AIM:Toestimatethepotentialsystemiceventsduringandafterretinopathyofprematurity（ROP）screening.METHODS:Aprospectiveanddescriptivedesignedstudywasconductedtodetectthephysiologicandpathologicalchanges24hbefore,during,and72hafterROPscreening.Controlbloodpressure（BP）,saturation,pulserate,andbodytemperaturewereroutinelytakenatvarioustimeinternalsbeforeandafterscreening.Adverseeffectspertaintocardiovascularsystem,respiratorysystem,gastricsystem,urinarysystemandnervoussystemwereretrospect0-72hafterROPscreeningata24-hourinterval.RESULTS:Totally1254prematuritybabiesreceivingROPscreeningduringJan.1st2013toDec.31th2013wereenrolledinoursurvey.Comparedtocontrolvitalsigndatatakenbeforetheexamination,therewasafluctuationinthediastolicBPwiththeincreased3.03mmHg（P=0.04）after3dosesofmydriaticdrops.Immediatelyaftertheexamination,therewasafurther12.64mmHg（P<0.01）increaseinsystolicBPanda7.24mmHg（P<0.01）indiastolicBP.Themeanpulserateduringexaminationwas22.4bpm（P<0.01）higherthanthe133.3±9.0bpmcontrollevel.Theoxygensaturationsharedanaveragedropof5%（P<0.01）duringscreening.Inprematuritywithpostconceptionalagelessthan31wk,theincidenceofapnea（23.5%）,necrotizingenterocolitis（NEC）（8.7%）,gastricresidual（25.4%）andupperdigestivetracthemorrhage（6.4%）alsodemonstratedasignificantrise（P<0.01）.CONCLUSION:Inourstudysample,ROPscreeningwasassociatedwithNEC,gastricresidualandupperdigestivetracthemorrhage.Thesegastrointestinalsideeffects,alongwithbreathactivitypatternchangeandvitalsignsindicatorsfluctuation,mayberesultsofadditionalstressresponses.

简介：AIMTo检验light-emitting-diode(带)导致的网膜的neuronal房间损坏和它的波长驱动的病原的mechanisms.METHODSSprague-Dawley老鼠暴露于蓝色LEDs(460nm)，绿LEDs(530nm)，和红LEDs(620nm)。染色的网膜电图描述术(尔格)(H&E)，Hematoxylin和曙红，传播电子显微镜学(TEM)，标记的终端deoxynucleotidyltransferasedUTP刻痕结束(TUNEL)，和染色的immunohistochemical(IHC)，西方的弄污(WB)并且superoxide阴离子的察觉(O2桰獯桰牯汹瑡潩???歁???????????椠浭湵景畬牯獥散据??啓呌？？

简介：DearEditor,IamDr.XiuWang,fromTianjinMedicalUniversityEyeHospital,Tianjin,China.IwritetopresentonecasereportofPosner-Schlossmansyndrome(PSS)inducedlaserinsitukeratomileusis(LASIK)keratectasia.PSSisaconditioncharacterizedbyrecurrent,acuteattacksofmild,unilateral,non-granulomatous,anterioruveitis

简介：AIMTo在氢过氧化物上探索parthenolide的效果(H2在人的透镜的O2)-inducedapoptosis上皮(HLE)apoptoticHLE房间的cells.METHODSThe形态学和数字用光被估计显微镜学和流动cytometry。房间生存能力被山试金测试。另外，相关蛋白质的表示被HLE房间的西方的污点assay.RESULTSApoptosis测量被200导致??丠?????あψ

简介：AIMTo在真菌的部件zymosan在.METHODSHCFs是的有教养的人的角膜的成纤维细胞(HCF)导致的proinflammatorycytokine和chemokine表示上调查triptolide的效果在zymosan或triptolide的缺席或存在有教养。interleukin(IL)的版本-6,IL-8，和进文化上层清液的单核白血球chemoattractantprotein-1(MCP-1)与连接酶的immunosorbent试金被测量。细胞的许多为这些蛋白质的mRNAs被反向的抄写和即时聚合酶链反应分析决定。激活mitogen的蛋白质kinases(MAPK)和内长的原子factor-κ的phosphorylation；B(NF-κ；B)禁止者Iκ；B-α；被immunoblot分析检验。版本喂奶从HCF的脱氢酶(LDH)活动被测量，比色的assay.RESULTSTriptolide禁止了从在一个集中依赖者和时间依赖者举止的HCF的IL-6，IL-8，和MCP-1的导致zymosan的版本。它也在这些房间禁止了IL-6，IL-8，和MCP-1mRNA丰富的导致zymosan的起来规定。而且，triptolide稀释了MAPK的导致zymosan的phosphorylation细胞外的调整信号的kinase(英皇家空军之阶级最低之兵)，c6月NH2-terminalkinase(JNK)，和象Iκ的phosphorylation和降级一样的p38；B-α；。Triptolide没多半展出cytotoxicity因为HCFs.CONCLUSIONTriptolide由暴露于zymosan的HCF禁止了proinflammatorycytokine和chemokine生产，随这个行动被MAPK和NF-κ的抑制调停；B发信号小径。这混合物可能因此被期望限制煽动性的房间的渗入进与真菌的感染联系的角膜。

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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：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。