简介:Objective:Toanalyzetheinfluencingfactorsforradiation-inducedheartdisease(RIHD)inapanelofcaseswithmalignantthymictumorstreatedbyradiotherapy.Methods:52consecutivepatientsweretreatedbyradiotherapyformalignantthymictumor(14atMasaokastageII,23atstageIIIand15atstageIV).Treatmentincludedradical(in20),postoperative(in14),preoperative(in2)andpalliative(in16)radiotherapy.Theconventionaltwo-dimension(2D)radiationtherapywasperformedinforty-sevenpatientsandthree-dimension(3D)conformalradiationtherapyhasbeenusedin5patientssinceOctober2000.Thetotaltumordoserangedfrom10Gyto84.5Gy(medianof55Gy).Chemotherapywasgivenintwenty-fivepatientsbeforeorafterradiotherapy.Theresultsoffollowing-upcouldbeobtainedfromthedatabaseandupdatedwhereappropriated.Thedosevolumehistogram(DVH)ofheartinradiotherapyforallpatientswasanalyzedfortheeffectivevolumedoseofheart.Result:Themedianfollowing-upwas14months(rangedfrom0.6to111.3months)inthestudy.RIHDwasobservedinsevenpatients.CardiactoxicityofthesesevenpatientswereevaluatedasSOMAgrade1-3.Themediantwo-thirdeffectivevolumedoseofheartwas47.2Gy(rangedfrom8.3Gyto70.1Gy)forconventional2Dradiotherapy,whichcorrelatedwiththymictumordose(P<0.0001).Themediantwo-thirdeffectivevolumedoseofheartwas35.3Gy(rangedfrom13Gyto38.7Gy)for3Dconformalradiotherapy.Theeffectivevolumedosesofheartweredecreasedbyusing3Dconformalradiotherapy(P=0.048).Asignificantassociationbetweencardiactoxicityandeffectivevolumedoseofheartwasfoundinthisstudy(P<0.0001).Cardiactoxicityaccountedfor10.4%and4.1%ofpatientsreceivingandnotreceivingadjuvantchemotherapy,respectively,andoccurredearlierinradiochemotherapygroup(P=0.0528).Multivariateanalysissuggestedthatcardiactoxicitywassignificantlyinfluencedbytheeffectivevolumedoseofheartandchemotherapy.C
简介:Objective:Toexploretheeffectofearlyenteralnutrition(EN)onpostoperativenutritionalstatus,intestinalpermeability,andimmunefunctioninelderlypatientswithesophagealcancerorcardiaccancer.Methods:Atotalof96patientswithesophagealcancerorcardiaccancerwhounderwentsurgicaltreatmentinourhospitalfromJune2007toDecember2010wereenrolledinthisstudy.TheyweredividedintoENgroup(n=50)andparenteralnutrition(PN)group(n=46)basedonthenutritionsupportmodes.Thebodyweight,timetofirstflatus/defecation,averagehospitalstay,complicationsandmortalityafterthesurgeryaswellastheliverfunctionindicatorswererecordedandanalyzed.Peripheralbloodsampleswerecollectedonthedays1,4and7aftersurgery.Theplasmadiamineoxidase(DAO)activityandD-lactatelevelweredeterminedtoassesstheintestinalpermeability.TheplasmaendotoxinlevelsweredeterminedusingdynamicturbidimetricassaytoassesstheprotectiveeffectofENonintestinalmucosalbarrier.Thepostoperativebloodlevelsofinflammatorycytokinesandimmunoglobulinsweredeterminedusingenzyme-linkedimmunosorbentassay(ELISA).Results:Afterthesurgery,thetimetofirstflatus/defecation,averagehospitalstay,andcomplicationsweresignificantlylessintheENgroupthanthoseinthePNgroup(P<0.05),whereastheENgrouphadsignificantlyhigheralbuminlevelsthanthePNgroup(P<0.05).Onthe7thpostoperativeday,theDAOactivity,D-lactatelevelandendotoxincontentsweresignificantlylowerintheENgroupthanthoseinthePNgroup(allP<0.05).Inaddition,theENgrouphadsignificantlyhigherIgA,IgG,IgM,andCD4levelsthanthePNgroup(P<0.05)butsignificantlylowerIL-2,IL-6,andTNF-αlevels(P<0.05).Conclusions:Inelderlypatientswithesophagealcancerorcardiaccancer,earlyENaftersurgerycaneffectivelyimprovethenutritionalstatus,protectintestinalmucosalbarrier(byreducingplasmaendoxins),andenhancetheimmunefunction
简介:Objective:Polycystickidneydisease(PKD)isthemajorcauseofkidneyfailureandmortalityinhumans.Ithasalwaysbeensuspectedthatthedevelopmentofcystickidneydiseasesharesfeatureswithtumorigenesis,althoughtheevidenceisunclear.Methods:Wecrossedp53mutantmice(p53N236S,p53S)withWernersyndromemiceandanalyzedthepathologicalphenotypes.TheRNA-seq,ssGSEAanalysis,andreal-timePCRwereperformedtodissectthegenesignaturesinvolvedinthedevelopmentofdiseasephenotypes.Results:Wefoundenlargedkidneyswithfluid-filledcystsinoffspringmicewithagenotypeofG3mTerc-/-WRN-/-p53S/S(G3TM).PathologyanalysisconfirmedtheoccurrenceofPKD,anditwashighlycorrelatedwiththeincidenceoftumorigenesis.RNA-seqdatarevealedthegenesignaturesinvolvedinPKDdevelopment,anddemonstratedthatPKDandtumorigenesissharedcommonpathways,includingcomplementpathways,lipidmetabolism,mitochondriaenergyhomeostasisandothers.Interestingly,thisG3TMPKDandtheclassicalPKD1/2deficientPKDsharedcommonpathways,possiblybecausethemutantp53ScouldregulatetheexpressionlevelsofPKD1/2,Pkhd1,andHnf1b.Conclusions:WeestablishedadualmousemodelforPKDandtumorigenesisderivedfromabnormalcellularproliferationandtelomeredysfunction.TheinnovativepointofourstudyistoreportPKDoccurringinconjunctionwithtumorigenesis.ThegenesignaturesrevealedmightshednewlightonthepathogenesisofPKD,andprovidenewmolecularbiomarkersforclinicaldiagnosisandprognosis.
简介:目的研究C02对宫颈癌Hela细胞株CDK9基因表达的影响,分析其在癌细胞生长与转移中的作用。方法将宫颈癌Hela细胞株随机分为3组:A组Hela细胞株在压力为8mmHg的纯C02下通气4h,培养24h;B组Hela细胞株在压力为8mmHg的纯C02下通气4h,培养120h;C组Hela细胞株未进行C02处理,细胞株置于常规细胞培养箱中培养120h。采用RT-PCR法检测A、B、C组宫颈癌Hela细胞CDK9mRNA的表达。结果A、B组与C组比较,A、B组CDK9mRNA的相对表达量明显下调(P〈0.05);B组与A组比较,B组CDK9mRNA的相对表达量比A组下调更显著(P〈0.01)。结论宫颈癌Hela细胞CDK9基因在C02作用下受抑制出现表达下调,且随C02作用时间越长,CDK9基因相对表达量降低越明显。