简介：AIM:ToexplorethemolecularmechanismsinlensdevelopmentandthepathogenesisofPetersanomalyinSmad4defectivemice.METHODS:Le-CretransgenicmouselinewasemployedtoinactivateSmad4inthesurfaceectodermselectively.PathologicaltechniqueswereusedtorevealthemorphologicalchangesoftheanteriorsegmentinSmad4defectiveeye.ImmunohistochemicalstainingwasemployedtoobservetheexpressionofE-cadherin,Ncadherinanda-SMAinanteriorsegmentofSmad4defectivemiceandcontrolmiceatembryonic(E)day16.5.Real-timequantitativepolymerasechainreaction(qPCR)wasperformedtodetecttheexpressionofSnail,Zeb1,Zeb2andTwist2inlensofSmad4defectivemiceandcontrolmiceatE16.5.RESULTS:ConditionaldeletionofSmad4oneyesurfaceectodermresultedincorneaidysplasia,iridocornealangleclosure,corneolenticularadhesionsandcataractresemblingPetersanomaly.LossofSmad4functioninhibitedE-cadherinexpressioninthelensepitheliumcellsandcorneaiepitheliumcellsinSmad4defectiveeye.ExpressionofN-cadherinwasupregulatedincorneaiepitheliumandcorneaistroma.BothE-cadherinandN-cadherinweredown-regulatedatthefuturetrabecularmeshworkregioninmutanteye.TheqPCRresultsshowedthattheexpressionofTwist2wasincreasedsignificantlyinthemutantlens(P<0.01).CONCLUSION:Smad4isessentialtoeyedevelopmentandlikelyacandidatepathogenicgenetoPetersanomalybyregulatingepithelial-mesenchymaltransition.Twist2canberegulatedbySmad4andplaysanessentialroleinlensdevelopment.

简介：Background:Apreviousstudyhasreporteda50%reductionindisuseatrophyofthequadricepsduringthefirst14daysafteranteriorcruciateligament(ACL)reconstruction.Afollow-uptrialisneededtoconfirmthesepromisingresults.ThepresentstudyaimstoinvestigatetheeffectofanocclusionstimulusonquadricepsatrophyafterACLreconstruction.Methods:Atotalof24subjectsparticipatedinthestudy.Theywererandomizedintotwogroups.Startingthe2nddayaftersurgery,theocclusiongroupreceivedanocclusionstimulusfor5min,followedbyremovaloftheocclusivepressurefor3min.Thiswasrepeatedfivetimesinonetrainingsession,twicedaily.Duringtheperiodofocclusivestimulus,thesubjectsperformed20lowloadexercisesforthequadriceps.Thecontrolgroupfollowedthesameexerciseprotocol,butwithouttheocclusionstimulus.Changesinquadricepsanatomicalcrosssectionarea(ACSA)weremeasuredusingaxialmagneticresonance(MR)imagesat40%and50%ofthelengthofthefemur.Results:BothgroupshadasignificantreductionofquadricepsACSAfrom2daysbeforesurgeryto16daysaftersurgery.Duringtheinterventionperiod,theocclusiongrouplost13.8%±1.1%(mean±SEM)andthecontrolgrouplost13.1%±1.0%oftheirquadricepsACSA,respectively.Therewasnosignificantdifferencebetweentheocclusionandcontrolgroupswithregardstoatrophyofthequadricepsmuscles.Conclusion:Inconflictwithotherstudiesusingasimilarprotocol,applicationofbloodflowrestrictionthefirst14daysafterACLreconstructiondidnotreducequadricepsACSAmuscleatrophymeasuredbyMRinapopulationofathletes.