简介：AIM:Toexaminetheintegrityoftheocularsurfacesofsubjectswithandwithoutdiabeteswithnoconjunctivalanddryeyesignsandsymptomsandcompareconjunctivalimpressioncytologyfindingsindiabeticswithnon-proliferativeandproliferativediabeticretinopathy.METHODS:Conjunctivalimpressioncytologywasperformedon43eyesof43subjectswithnonproliferativediabeticretinopathy(NPDR),42eyesof42subjectswithproliferativediabeticretinopathy(PDR),and30eyesof30controlsubjects.Impressioncytologyspecimensofeachgroupweregradedandscoredintherange0-3accordingtoNelson’smethod.RESULTS:Therewere45(52.9%)womenand40(47.1%)men.Themeanageofthepatientswas59.6±9.3y(range,43-76y)inNPDRgroupand58.0±8.8y(range,41-85y)inPDRgroup.CaseswithNPDRandPDRshowedstatisticallysignificanthigherimpressioncytologyscoresthancontrolgroup(P<0.05).TherewasnodifferencebetweentheNPDRandPDRpatientsforimpressioncytologygradingscores.CONCLUSION:ItisdeterminedthatimpressioncytologygradesarealteredinpatientswithNPDRandPDR.Consequently,wesuggestthattheremightbeanassociationbetweentheimpressioncytologygradingscoresandtheseverityofdiabeticretinopathy

简介：Overthepastfewdecades,non-alcoholicfattyliverdisease(NAFLD)hasbecomeone,ifnotthemostcommon,causeofchronicliverdiseaseaffectingbothadultsandchildren.Theincreasingnumberofcasesatanearlyageisthemostworryingaspectofthispathology,sinceitprovidesmoretimeforitsevolution.Thespectrumofthisdiseaserangesfromliversteatosistosteatohepatitis,fibrosisandinsomecases,hepatocellularcarcinoma.NAFLDmaynotalwaysbeconsideredabenigndiseaseandhepatologistsmustbecautiousinthepresenceoffattyliver.Thisshouldprompttheuseoftheavailableexperimentalmodelstounderstandbetterthepathogenesisandtodeveloparationaltreatmentofadiseasethatisdangerouslyincreasing.Inspiteofthegrowingefforts,thepathogenesisofNAFLDisstillpoorlyunderstood.InthepresentarticlewereviewthemostrelevanthypothesesandevidencethataccountfortheprogressionofNAFLDtonon-alcoholicsteatohepatitis(NASH)andfibrosis.TheavailableinvitroandinvivoexperimentalmodelsofNASHarediscussedandrevisedintermsoftheirvalidityintranslationalstudies.Thesestudiesmustbeaimedatthediscoveryofthestillunknowntriggersormediatorsthatinducetheprogressionofhepaticinflammation,apoptosisandfibrosis.

简介：Hearinglossisoneofthemostcommonbirthdefects,withinheritedgeneticdefectsplayanimportantrole,contributingtoabout60%ofdeafnessoccurringininfants.However,hearingimpairmentisgeneticallyheterogeneous,withbothcommonandrareformsoccurringduetomutationsinestimated500genes.Duetothelargenumberandpresumablylowmutationfrequenciesofthosegenes,itwouldbehighlyexpensiveandtime-consumingtoaddressthisissuebyconventionalgene-by-geneSangersequencing.Next-generationsequencingisarevolutionarytechnologythatallowsthesimultaneousscreeningofmutationsinalargenumberofgenes.Itiscosteffectivecomparedtoclassicalstrategiesoflinkageanalysisanddirectsequencingwhenthenumberorsizeofgenesislarge,andthushasbecomeahighlyefficientstrategyforidentifyingnovelcausativegenesandmutationsinvolvedinheritabledisease.Inthisreview,wedescribemajorNGSmethodologiescurrentlyusedforgeneticdisordersandhighlightapplicationsofthesetechnologiesinstudiesofmoleculardiagnosisandthediscoveryofgenesimplicatedinnon-syndromichearingloss.

简介：这篇文章的目的是作为安慰剂针估计临床的证据为或对非渗透的假冒的针的令人目眩的效果。这系统的评论包括了作为安慰剂针拿非渗透的假冒的针灸的针灸的使随机化的控制审判(RCT)。系统的搜索在13个电子数据库被进行直到2012年7月：Medline，PubMed，Cochrane图书馆，CINAHL，EMBASE，一个中国医药数据库。没有语言限制，所有平行或为非渗透的针的令人目眩的效果的针灸的转线路RCT被选择。最后，完全，7RCT满足了包括标准。在结论，我们的系统的评论和元分析证明非渗透的针是为在针灸RCT的安慰剂控制的一台有效仪器。

简介：Purpose:Anumberofdifferentclinicalcharacteristicshavebeenreportedtosinglycorrelatewiththerapeuticactivityofepidermalgrowthfactorreceptor(EGFR)tyrosinekinaseinhibitors(TKIs)inadvancednon-small-celllungcancer(NSCLC).Thisstudyaimedtoidentifypredictivefactorsassociatedwithprognosticbenefitsofgefitinib.Patientsandmethods:EGFRgenetypingin33advancedNSCLCpatientsreceivedgefitinib(250mg/day)wereanalyzedwithmutant-enrichedPCRassay.Gefitinibresponsewasevaluatedwithpotentialpredictivefactorsretrospectively.Results:Theoverallobjectiveresponserate(ORR)andmedianprogression-freesurvival(PFS)inthe33patientstreatedbygefitinibwere45.5%and3.0(2.0-4.0)months.TheORRandmedianPFSinEGFRgenemutationpatientsweresignificantlyhigher/longerthanthoseinEGFRgenewild-typepatients(P<0.01).Similarly,theORRandmedianPFSinnon-smokerpatientsweresignificantlyhigher/longerthanthoseinsmokerpatients(P<0.05,P<0.01,respectively).However,nodifferenceforORRandmedianPFSoccurredbetweenmaleandfemalepatients.LogisticmultivariateanalysisshowedthatonlyEGFRmutatedgenewassignificantlyassociatedwiththeORR(P<0.01).BothEGFRmutatedgeneandnon-smokerwerethemajorfactorsthatcontributedtoPFS(P<0.05).Conclusions:EGFRmutatedgeneandnon-smokerstatusarepotentialpredictorsforgefitinibresponseinNSCLCpatients.

简介：Objective:Toevaluatetherelationbetweenargyrophilicnucleolarorganizerregion(AgNOR)-associatedproteinsandclinicopathologicalparametersandsurvivalinnon-small-celllungcancer(NSCLC).Methods:Atotalof207surgicalspecimensdiagnosedasNSCLCwereincludedinthisstudy.Double-stainingprocedureswereperformedusingantigenKi-67(cloneMIB-1)andsilvernitratebyimmunohistochemicalandAgNOR-stainingmethods.Results:TheAgNORareainMIB-1-positivecellsofNSCLCisrelatedtoclinicopathologicalparametersundertheTNM(tumor,node,andmetastasis)system.ThesurvivalofpatientswithsmallAgNORareainMIB-1-positivecellsisbetterthanthatofpatientswithlargeAgNORarea.Molecular,biological(AgNORareainMIB-1-positivecells),andclinicopathological(greatesttumordimension,metastasestoregionallymphnodes,histology,anddifferentiation)parametersareindependentprognosticfactorsofNSCLC.Conclusion:TheAgNORareainMIB-1-positivecellsisrelatedtoclinicopathologicalparametersandsurvivalinNSCLC.

简介：Objective:Non-smallcelllungcancer(NSCLC)patientswithepidermalgrowthfactorreceptor(EGFR)-activatingmutationshavehigherresponserateandmoreprolongedsurvivalfollowingtreatmentwithsingle-agentEGFRtyrosinekinaseinhibitor(EGFR-TKI)comparedwithpatientswithwild-typeEGFR.However,allpatientstreatedwithreversibleinhibitorsdevelopacquiredresistanceovertime.Themechanismsofresistancearecomplicated.ThelackofestablishedtherapeuticoptionsforpatientsafterafailedEGFR-TKItreatmentposesagreatchallengetophysiciansinmanagingthisgroupoflungcancerpatients.ThisstudyevaluatestheinfluenceofEGFR-TKIretreatmentfollowingchemotherapyafterfailureofinitialEGFR-TKIwithinatleast6monthsonNSCLCpatients.Methods:Thedataof27patientswhoexperiencedtreatmentfailurefromtheirinitialuseofEGFR-TKIwithinatleast6monthswereanalyzed.Afterchemotherapy,thepatientswereretreatedwithEGFR-TKI(gefitinib250mgqdorerlotinib150mgqd),andthetumorprogressionwasobserved.Thepatientswereassessedforadverseeventsandresponsetotherapy.TargetedtumorlesionswereassessedwithCTscan.Results:Ofthe27patientswhoreceivedEGFR-TKIretreatment,1(3.7%)patientwasobservedincompleteresponse(CR),8(29.6%)patientsinpartialresponse(PR),14(51.9%)patientsinstabledisease(SD),and4(14.8%)patientsinprogressivedisease(PD).Thediseasecontrolrate(DCR)was85.2%(95%CI:62%-94%).Themedianprogression-freesurvival(mPFS)was6months(95%CI:1-29).Ofthe13patientswhoreceivedthesameEGFR-TKI,1patientinCR,3patientsinPR,8patientsinSD,and2patientsinPDwereobserved.TheDCRwas84.6%,andthemPFSwas5months.Ofthe14patientswhoreceivedanotherEGFR-TKI,nopatientinCR,6patientsinPR,6patientsinSD,and2patientsinPDwereobserved.TheDCRwas85.7%,andthemPFSwas9.5months.SignificantdifferencewasfoundbetweenthetwogroupsinPFSbutnotinresponserateorDCR.Conclusion:RetreatmentofEGFR-TKIscanbeconsideredano