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简介：Thymidinephosphorylase(TP)isakeyenzymethatcontributestothecompositionanddecompositionofpyrimidinenucleotides.TPseemshomologoustoplatelet-derivedendothelialcellgrowthfactor,anditseffectsoninducingvascularizationandanti-apoptosisarecloselyrelatedtogrowthandmetastasisofcolorectalcarcinoma.Inaddition,TPisakeyenzymethatcatalyzesthetransformationfrom5-fluorouracil(FU)prodrugsof5′-deoxy-5-fluorouridine(5′-DFUR)to5-FU.TheactivityofTPiscloselyrelatedtothesensitivityofcolorectalcarcinomacellstofluorouracildrugsandtargetedtherapy.GiventheimportantfunctionsofTPingrowth,metastasis,tumortreatment,andprognosis,determiningitsexpressionmechanismissignificant.ThisarticlesummarizestheresearchdevelopmentofTPexpressionincolorectalcarcinoma,tumorneovascularization,cytotoxicityactivationof5′-DFUR,andcolorectalcarcinomatherapy.

简介：Astochasticsimulationoffluidflowinporousmediausingacomplexvariableexpressionmethod(SFCM)ispresentedinthispaper.Hydraulicconductivityisconsideredasarandomvariableandisthenexpressedincomplexvariableform,therealpartofwhichisadeterministicvalueandtheimaginarypartisavariablevalue.ThestochasticseepageflowissimulatedwiththeSFCMandiscomparedwiththeresultscalculatedwiththeMonteCarlostochasticfiniteelementmethod.InusingtheMonteCarlomethodtosimulatethestochasticseepageflowfield,thehydraulicconductivityisassumedinthreedifferentprobabilitydistributionsusingrandomsamplingmethod.Theobtainedseepageflowfieldisexaminedthroughskewnessanalysis,andtheskeweddistributionprobabilitydensityfunctionisgiven.TheheadmodevalueandtheheadcomprehensivestandarddeviationareusedtorepresentthestatisticsofcalculationresultsobtainedbytheMonteCarlomethod.ThestochasticseepageflowfieldsimulatedbytheSFCMisconfirmedtobesimilartothatgivenbytheMonteCarlomethodfromnumericalaspects.TherangeofcoefficientofvariationofhydraulicconductivityinSFCMislargerthanusedpreviouslyinstochasticseepageflowfieldsimulations,andthecomputationtimeisshort.TheresultsprovedthattheSFCMisaconvenientcalculatingmethodforsolvingthecomplexproblems.

简介：HuipainterandresidentofHami,Xinjiang,LiuYizhong’sfigurepaintingsaboundwithanexpressiveblendofboldandgentlelinesandacollageofcolors,whichcapturethespiritofdiversityandtoleranceunitinghisregion’sethnicmix.Liuendowshissubjects,thepeopleofWesternChina,withasenseofancestry,Conveyingasenseofpovertyanddesperationalongwithhopeandinspiration,heleavesuswithalastingimpressionoftheWesternspirit.Althoughthesurroundinglandscapeisnotdepicted,allusionstotheenvironmentareinherentandreflectthehistoryofstrugglesexperiencedbyitsinhabitants.

简介：Vasa,whichisaconservedmemberoftheDEAD-boxproteinfamily,playsanindispensableroleinprimordialgermcellproliferation.However,theexpressionofvasageneduringthereproductivecycleinovoviviparousfishhasnotbeendocumented.Inthisstudy,thefull-lengthsequenceofvasawasobtainedfromtheovaryofKoreanrockfish(Sebastesschlegeli)usingreversetranscription-PCRandrapidamplificationofcDNAends.TheVasawithamatureproteinof650aminoacidsshowedgreatesthomology(84%)withgiantgourami(Osphronemusgoramy)andPacificbluefintuna(Thunnusorientalis).TheexpressionofvasamRNAinKoreanrockfishwasdetectedingonadsonly,suggestingitsspecificroleingonadaldevelopment.Inaddition,seasonalchangesinthevasaexpressionlevelswereexaminedingonadsbyquantitativereal-timePCR.Thevasatranscriptlevelsinadulttestiswerefoundhigherduringspermatogenesisthanduringspermiation.Thevasatranscriptlevelsremainedrelativelyhighattheearlyovarystagebutdeclinedduringovarymaturationinadultfemalefish.TheseresultssuggestthatthevasageneplayanimportantroleinspermatogenesisandearlyoogenesisduringthereproductivecycleofKoreanrockfish.

简介：Thisstudyaimedtoexploretheroleofmechanicaltensioninhypertrophicscarsandthechangeinnervedensityusinghematoxylin-eosinstainingandS100immunohistochemistry,andtoobservetheexpressionofnervegrowthfactorbywesternblotanalysis.Theresultsdemonstratedthatmechanicaltensioncontributedtotheformationofahyperplasticscarinthebackskinofrats,inconjunctionwithincreasesinbothnervedensityandnervegrowthfactorexpressioninthescartissue.Theseexperimentalfindingsindicatethatthecutaneousnervoussystemplaysaroleinhypertrophicscarformationcausedbymechanicaltension.

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：2013年10月12—13日中国生理学会张锡钧基金会第十二届全国青年优秀生理学学术论文交流会在湖南长沙顺利召开。由各省生理学会推荐的37名参赛选手的论文参与评选，会议展示了选手们近3年来在生理学研究方面所取得的最新研究成果。经过专家对参评者论文和现场报告的综合评判，评出一等奖、二等奖、三等奖、特别奖、最佳表达奖、最佳答辩奖和最佳图标奖共11名。从2013年第6期开始，《生理通讯》将陆续转载获奖者的参评论文各一篇，以飨读者。

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简介：Noise-inducedhearinglossisacommoncauseofacquiredhearinglossintheadultpopulation.Acousticoverstimulationcausescochleardamagethroughmechanicalstresstothetissue.Consequently,complexmolec-ularchangesareinitiated,andthesechangesleadtomorphologicalandbiologicalalterationsinthecochlea,whichinturncompromisethecochlearfunctionandcausehearingloss.Inthepast10years,therehavebeensignificantadvancesinourunderstandingofthemolecularmechanismsofnoise-inducedhearingloss.Theseadvancesareattributed,inpart,tothedevelopmentofhigh-throughputtechnologiesfortheglobalanalysesofmolecularchanges.Inthisreview,webrieflydescribethenewlydevelopedmethodsforinvestigatingthemo-lecularresponsesofthecochleatoacoustictraumaandtheknowledgegeneratedfromthesestudies.Wealsodiscussthestrengthsandlimitationsofeachtechniqueandthemajorchallengestoinvestigatecochleardegen-erationfollowingacousticinjury.

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