英語科研寫作課件

·研寫TheIntroduction?–Whatdidyou·研寫TheIntroduction?–Whatdidyou?Whatdidyou科研論文四部分，主要內容有哪些?Whatdoyourfindings ?–Whydidyoudothe–Whatwasyourhypothesisor本課內·本課內·研寫????Introduction寫作順·研寫inIntroduction寫作順·研寫in·研寫·研寫Settingthe（策略性）長度——10-15%oftheIntroduction包括的內·研Introduction包括的內·研寫GapinHypothesis/purposestatementStrategyfortestinghypothesisorachievingpurpose123,·研·研寫·研寫Gapin·研寫Gapin?從已知到未知強調填補這個gap的重要“However,wedonotknowwhateffectthistreatmentwillhaveonpatientswithstageIV“Whetherthesefindingswilltranslatetotheclinicalsettingisnotknown.”“Paststudiesofthisissuehaveresultedinconflictingfindings.”“Sofar,onlyqualitativefindingshavebeen“However,littleisknownaboutthelong-termimpactoncellfunctionsofraisedlevelsofAlthoughseveralstudieshaveassociatedQRSexpressionwithcolorectaladenocarcinoma,thedirecteffectsofQRSonestablishedcolorectalcancershavenotbeendetermined.AnunderstandingofhowQRScontributestotumorigenicityincolorectalcancercellsmayenableitsuseasaprognosticfactororeventherapeutic???????·研寫·研寫出現(xiàn)的三地方——introduction,abstract,In“WehypothesizedthattheRb-E2F1pathwayisoneofthecriticaltumor-suppressor/oncogenepathwaysinvolvedinregulatingtelomeraseexpressionandactivityinglioblastoma.”In“WefoundthattheRb-E2Fpathwayisinvolvedinregulatingtelomeraseexpressionandactivityincancerandnormalcells...”實驗方實驗方·研寫“WeidentifiedthesequencesdownstreamfromtheTATAboxinbasalHypothesisInthisstudy,wetestedthehypothesisthatvariationsinothermembersoffibulingenefamilyareinvolvedinthepathogenesisofmaculardegenerationbyexaminingthecodingsequencesofthegenesforfibulin1,2,4,5,and6inmorethan400patientswithage-relatedmaculardegeneration.·研寫·研寫Totestthishypothesis,weexaminedB-celllymphomasthatcarriedspecificchromosomaltranslocations.Ineachcase,avaryingproportionofthemicrovascularendothelialcellsofthelymphomaexhibitedthelymphoma-specificgeneticaberration,suggestingacloserelationshipbetweenthetwotypesofcells.·研寫Known·研寫Known(generalto1Includeonlyenoughbackgroundtomakethereasonforthestudy23Organizetheinformationlikeafunnel,fromgeneralto·研寫Gap·研寫Gapin??Untilnow,ithasnotbeenpossibletoHowever,wedonotknowwhateffectthistreatmentwillhaveon...Therehasbeensomedisagreement,however,inthefindingswiththismodel...Sofar,onlyqualitativefindingshavebeenBecauseoftherarityofthiscancer,ithasbeendifficulttodeterminesurvivalrateswithstatisticalcertainty...???·研寫·研寫???Thepurposeofourstudywastodetermine...Wehypothesizedthat...Ourhypothesiswas·研寫·研寫??WetestedourhypothesisbyTodothis,weused...andanalyzed...inaninsitu·研寫·研寫??Overall,ourfindingsthat…Inthisstudy,wefound·研寫TheriskofcancercanbesignificantlyincreasedbydisruptionofgenomicintegrityresultedfromdysfunctionalDNAdamageresponsesignalingand/oraberrantactivityofthekeycomponentsintheDNArepairpathways.TheDNArepairmachineriesworkconstantlytoremovenumerousDNAlesionscausedbychemotherapeuticagentssuchascisplatin,whichcontributestodrugresistanceinmanycancers.Asresistancetostandardcisplatin-basedchemotherapybecomesafrequentphenomenon,cancertreatmenttargetingimportantcomponentsintheDNArepairpathwaysemergestobeanimminentandcompellingtask.RDM1(RAD52motif1,orRDmotif)isinvolvedincellularresponsetocisplatin,andshowssimilaritiestoRAD52,akeyregulatorinDNArecombinationandrepair,wheretheRDmotifofRDM1functionallyresemblestheN-terminalregionofRAD52[1-3].Importantly,RDM1–/–cellsexhibitedincreasedsensitivitytocisplatin[4].Moreinterestingly,ourinitialcomprehensivebioinformaticsexplorationinmultipleOncomineexpressiondatasetshasalsoidentifiedRDM1asoneofthesignificantlyup-regulatedproteinsinhumanlungadenocarcinoma.Despitethesediscoveries,however,todate,littleisknownregardingtheroleofRDM1inhumancancer.GiventhepotentialroleofRDM1intheDNArepairpathwaysthatconstituteanimportantaspectofcancerinitiationandprogression,weproposethatRDM1maydisplayoncogenicpropertiesanddrivetumorigenesis.·研寫Lungcancerisaleadingcauseofcancerdeaths,andremainsoneoftherefractorycancertypes.Adenocarcinomaaccountsfor40%ofalllungcancers.Thefive-yearsurvivalrateoflungcanceristhelowestamongthemajorcancers,includingcolon,breast,andprostatecancers[5].Evenwithmajorclinicalinterventions,suchassurgery,radiationtherapy,chemotherapy,targetedcancertherapy,andimmunotherapy,thesurvivalratehasnotbeenimprovedsignificantly,andlingersatonly15%withinfiveyearsoftreatment[6].TheclinicalstagingoflungcancersfollowstheTNMclassificationsystem,wherethedeterminingfactorsinclude:thesizeoftheprimarytumor(T),theeffectsontheregionallymphnodes(N),andthedistantmetastaticstatus(M).Recentyearshavewitnessedsomesuccessintargetedtherapiesforparticularmutationsinlungadenocarcinoma,suchasthoseinEGFRandALK,andthesestrategieshavebeenapprovedforuseasfirst-linetreatmentinadenocarcinoma[7-9].Conceptually,investigationofthemutationallandscapeinlungadenocarcinomawillhelpidentifynewtargetswhichcanbeenlistedtothegrowingbiomarkerpanelthatmayassistwiththediagnosis.Asaresult,itisimperativetouncovermorenovelmolecules,whichwillbebeneficialtothetreatmentanddiagnosisoflungadenocarcinoma.·研寫Inthisstudy,wefoundthatRDM1isup-regulatedinclinicallungadenocarcinomasamplesasrevealedbyIHCstaining.Significantly,up-regulationofRDM1iscorrelatedwithpoorclinicalcharacteristicsandriskfac