简介：AbstractBackground:Hyperbaric oxygen treatment (HBOT) has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids. To explore the mechanism of the effect of HBOT on keloids, tumor immune gene expression and immune cell infiltration were studied in this work.Methods:From February 2021 to April 2021, HBOT was carried out on keloid patients four times before surgery. Keloid tissue samples were collected and divided into an HBOT group (keloid with HBOT before surgery [HK] group, n = 6) and a non-HBOT group (K group, n = 6). Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit. Data were mined with R package. The differentially expressed genes between the groups were compared. Hub genes between the groups were determined and verified with Quantitative Real-time PCR. Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry (IHC).Results:Inflammatory cell infiltration was reduced in the HK group. There were 178 upregulated genes and 217 downregulated genes. Ten hub genes were identified, including Integrin Subunit Alpha M (ITGAM), interleukin (IL)-4, IL-6, IL-2, Protein Tyrosine Phosphatase Receptor Type C (PTPRC), CD86, transforming growth factor (TGF), CD80, CTLA4, and IL-10. CD80, ITGAM, IL-4, and PTPRC with significantly downregulated expression were identified. IL-10 and IL-2 were upregulated in the HK group but without a significant difference. Infiltration differences of CD8 lymphocyte T cells, CD4 lymphocyte T-activated memory cells, and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis. Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.Conclusion:HBOT affected tumor gene expression and immune cell infiltration in keloids. CD4 lymphocyte T cell, especially activated memory CD4+T, might be the key regulatory immune cell, and its related gene expression needs further study.

简介：肿瘤immunoevasion是肿瘤房间在获得能力围绕主人免疫系统并且利用protumorigenic发炎的癌症immunosurveillance的一个先进阶段。T房间免疫球蛋白粘蛋白(提姆)基因家庭成员作为调整多重有免疫力的反应阶段并且维持有免疫力的动态平衡的批评检查点蛋白质出现了。积累的证据证明肿瘤房间利用提姆基因家庭成员躲避immunosurveillance，而提姆基因家庭成员便于发炎相关的肿瘤前进的预防。因此，在肿瘤前进澄清提姆基因家庭成员的相对贡献的全面分析可以阐明在癌症病人的immunosurveillance系统。

简介：Microarraydataareoftenextremelyasymmetricindimensionality,suchasthousandsoreventensofthousandsofgenesbutonlyafewhundredsofsamplesorless.Suchextremeasymmetrybetweenthedimensionalityofgenesandsamplescanleadtoinaccuratediagnosisofdiseaseinclinic.Therefore,ithasbeenshownthatselectingasmallsetofmarkergenescanleadtoimprovedclassificationaccuracy.Inthispaper,asimplemodifiedantcolonyoptimization(ACO)algorithmisproposedtoselecttumor-relatedmarkergenes,andsupportvectormachine(SVM)isusedasclassifiertoevaluatetheperformanceoftheextractedgenesubset.Experimentalresultsonseveralbenchmarktumormicroarraydatasetsshowedthattheproposedapproachproducesbetterrecognitionwithfewermarkergenesthanmanyothermethods.IthasbeendemonstratedthatthemodifiedACOisausefultoolforselectingmarkergenesandmininghighdimensiondata.

简介：AbstractImportance:LIM domain only 1 (LMO1) gene polymorphisms were previously found to be implicated in the risk of several cancers. No available studies were performed regarding the predisposing effect of LMO1 gene single nucleotide polymorphisms (SNPs) on central nervous system (CNS) tumor risk.Objective:We aimed to determine whether the LMO1 gene SNPs were associated with the risk of CNS tumor by applying a case-control study with 191 cases and 248 controls in China.Methods:The contributions of LMO1 gene SNPs to the risk of CNS tumor was evaluated by multinomial logistic regression.Results:Based on the calculations of odds ratio (OR) and 95% confidence interval (CI), we failed to detect a significant relationship between each LMO1 gene SNP (rs110419 A>G, rs4758051 G>A, rs10840002 A>G, rs204938 A>G, and rs2168101 G>T) and CNS tumor risk, respectively. A negative association was also found in the combined effects on these five SNPs and CNS tumor risk. The stratification analysis further demonstrated the individuals with rs204938 AG/GG genotype confer to increased risk of CNS tumor compared with those with an AA genotype in males (OR: 1.74, 95% CI: 1.01-2.98, P = 0.046).Interpretation:We concluded that LMO1 gene SNPs may not strong enough to influence the risk of CNS tumor in Chinese children. More studies are required to verify this association.

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简介：Themoditicationoftumorcellsoreffcorcellsusingcytokinegenesasastrategytoenhancehostantitumorimmunityhasbeenstudiedintensivelyoverthe

简介：Objective:Tostudytherelationshipbetweencyclooxygenase-2(COX-2)expressionandtumorangiogenesisinhumanbreastcancer.Methods:Archivalprimarybreastcarcinomas(n=62),adjacentductalcarcinomainsitu(DCIS,n=13)andDCISalone(n=5)wereanalyzedforCOX-2andVEGFexpressionbyimmunohistochemistryusingspecificmonoclonalantibodies.Microvesseldensity(MVD)wasalsoexaminedtheusingCD34staining.Results:AsignificantcorrelationwasfoundbetweenCOX-2andVEGFexpression(P<0.01).BothCOX-2andVEGFweresignificantlycorrelatedwithMVD(P<0.05)andP<0.01,respectively).COX-2andVEGFgeneswereoverexpressedintumorspecimensascomparedwithnormalepithelia.Conclusion:COX-2isrelatedtotumorangiogenesisinbreastcancer.ItislikelythatVEGFisoneofthemostimportantmediatorsoftheCOX-2angiogenicpathway.

简介：Objective:Toinvestigatethepreparationofthecarboxymethlydextranironoxidemagneticnanoparticles(CDMN)andtheeffectsofCDMNcarriersystemassociatedwithexternalmagneticfieldsonkillingtumorcellsandgenetransfectioninvitro.Methods:Epirubicin-CDMN(EPI-CDMN)andgreenfluorescentprotein(GFP)plasmid-CDMN(GFP-CDMN)werepreparedbytheoxidation-reductionprocedureandtheircharactersweredetected,respectively.TheeffectsofEPI-CDMNassociatedwithexternalpulsedelectromagneticfields(PEMFs)(10mT)onkillinghumanbladdercancerBIU-87cellswerestudiedbyMTTassayandAnnexin-V/PIdouble-labeledflowcytometrytechnique,respectively.AndthetransfectionefficiencyofGFPwhenCDMNwereusedasgenecarrierassociatedwiththeexternalmagneticfieldswasevaluatedunderfluorescencemicroscopeinvitro.Results:ThediameterofEPI-CDMNandGFP-CDMNwereabout8~10nmand5~9nm,respectively,andsaturationmagnetizationwere0.22emu/gand0.26emu/g,respectively.EPI-CDMNassociatedwithPEMFscouldsignificantlyinhibittheproliferationofBIU-87cellsandinducecellsapoptosis,thegrowthinhibitoryrateandapoptosisratewere(21.82(3.18)%and(16.79(3.37)%,respectively.ThetransfectionefficiencyofGFP-CDMNcombinedwithPEMFswassignificanthigherthanthatofGFP-CDMNwithoutPEMFs[(45.70(4.32)%vs(35.85(2.16)%,P<0.05].Conclusion:ItseemedthatEPI-CDMNassociatedwithexternalmagneticfieldscouldsignificantlykilledhumanbladdercancerBIU-87cellsandCDMNcouldeffectivelytransferGFPgeneintotumorscellswiththehelpofexternalmagneticfieldswhichprovidedexperimentalbasisforthemagnetictargetingtherapyoftumor.

简介：工程是调查IL-12基因的反肿瘤效果的这的目的修改了乳房的肉瘤鼠科的房间线，EMT6/IL-12，在里面老鼠模型。在这研究，我们transfectedrecombinant真核细胞的plasmid编码IL-12基因(pcDNA6-p70)进EMT6并且获得了表示EMT6/IL-12的IL-12房间线。当时，EMT6/IL-12房间是接种进老鼠的s.c。recombinant向量处理组被放作为控制。我们然后在象cytotoxicity，splenocytes的增长和连续IFN-水平那样的vivo评估了肿瘤生长和反肿瘤免疫功能的抑制。并且在splenocytes之中生产CD4或CD8T房间的IFN-的百分比也在忍受老鼠的肿瘤被分析。我们的结果证明肿瘤的生长显然在EMT6/IL-12组被禁止。而且，反肿瘤免疫的能力都在与控制相比的EMT6/IL-12组是显著地更高的。现在的调查的结果支持EMT6/IL-12能施加的观点在由改进反肿瘤的肿瘤模型的基因治疗细胞的免疫。

简介：Objective:Toinvestigatethetreatmentofspontaneousmetastaticlungcancerbytumorantigen-pulsed,interleukin-12(IL-12)gene-modifieddendriticcells(DC).Methods:Thespontaneousmetastaticlungcancermodel,preparedbyinjectionofthe3LLLewislungcancercellsintothefootpadsofC57BL/6mice,wastreatedbysubcutaneousvaccinationwithtumorantigenpeptidemut1-pulsed,IL-12gene-modifieddendriticcells(DC-IL-12/mut1)derivedfromthenormalbonemorrow.Aftertreatment,thelungweight,thenumberoflungmetastaticnodesandthesurvivaltimeofthetumor-bearingmicewereobserved,andtheNKandCTLactivityweredeterminedrespectively.Themiceweredividedinto8groupswith12miceineachgroup.Results:Comparedwithmicetreatedwithmut1-pulsed,controlLacZgenemodifiedDCanduntreatedDC,tumor-bearingmicetreatedwithDC-IL-12/mut1hadthelightestlungweights(P<0.01),theleastlungmetastaticnodenumber(P<0.01),thelongestsurvivaltime(P<0.01),alsowiththeinductionofpotentCTLactivity(P<0.01)andNKactivity(P<0.01).Conclusion:Tumorantigen-pulsed,IL-12gene-modifieddendriticcellshavesignificanttherapeuticeffectsonthespontaneousmetastaticlungcancer,providinganewapproachtotreatmentoflungtumors.

简介：正弦电场驾驶的一个蛋白质马达系统被调查。Thesignal-to-noise比率(SNR)在断热的限制被导出。随机的回声的现象被作出对有利的裁决这个蛋白质马达系统。

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简介：Ithasbeendemonstratedthattbecriticalroleofbonemarrowstromalcells(HMSCs)istosustaintheselfrenewalofpluripotenthematopoieticstemcellsandmaintainthehomeostasisofbonemarrowhematopoiesismicroenvironment.BMSCprogenitorcandifferentiateintoseveralclementsincludingmacrophages,endothelialcells,fibroblastsandsomeothercells.Almostall

简介：AsanewmemberofIAP(inhibitorsofapoptosisprotein)family,survivinhaspotentanti-apoptoticactivities,andinvolvesinthemitosisandangiogenesis.Researcheshavedemonstratedthatsurvivingisatumor-specificanti-apoptoticfactor,expressedinfetaltissues,andcommonhumancancers,whilenotinnormal,terminallydifferentiatedadulttissues.Theoverexpressionofsurvivinintumortissuesiscorrelatedwithpoorprognosisofthepatients.Survivincanbeusedasaprognosticfactorandanewtargetintumortargetingtherapy.

简介：Thegeneralprinciplefortumorcellstoescapefromimmunesurveillanceistopreventtumorantigensfrombeingrecognizedbytheimmunesystem.Manymethodshavebeendevelopedtoincreasetheimmunogenecityofthetumorcells.Themostefficientmethodsareabletoforcetumorcellstopresenttheirowntumorantigenstotheimmunesystem.StimulatingThcellsbyconvertingtumorcellsintoMHCclassⅡ+/Ii-antigenpresentingcellsisoneofthemostefficienttechnologies.Usingantisensemethods,wesuppresstheexpressionoftheIiproteinthatnormallyco-expresseswithMHCclassⅡmoleculesandblockstheantigenicpeptidebindingsiteofMHCclassⅡmoleculesduringsynthesisintheendoplasmicreticulum.Insuchtumorcells,the'unprotected'MHCclassⅡmoleculespickupendogenoustumorantigenicpeptides,whichhavebeentransportedintotheERforbindingtoMHCclassⅠmolecules.SimultaneouspresentationoftumorantigensbybothMHCclassⅠandⅡmoleculesgeneratesarobustandlong-lastinganti-tumorimmuneresponse.MHCclassⅡ+/Ii-tumorcellsarepotenttumorcellvaccinesandalsocureasignificantnumberofanimalswithrenalandprostatetumors.Wehavedevelopedanalogoushumangenevectorsthataresuitableformostpatientsandcancers.

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简介：Anexperimentalinvestigationofananosecondpulseddielectricbarrierdischargeinatmosphericairispresented.Inthesetupaquartztubewasinsertedbetweentheconeandplaneelectrodesinthedirectionparalleltotheelectricfield.Itwasshownthattheappearanceandpropertyofthedischargeweresensitivetothesizeandthepositionofthequartztube.Whenthetubewasplacedonthegroundedplaneelectrode,thedischargeintensitywasfoundtoimprovegraduallywiththeincreaseinthediameterofthequartztube.Furthermore,withanappropriatedistancebetweenthebottomedgeofthequartztubeandtheplaneelectrode,thedischargetendedtoexhibitbetterperformanceingeneratinghomogeneousdiffusiveplasma.Thepossiblemechanismisdiscussed.

简介：Tumor-targetingantibodieswereinitiallydefinedasagroupoftherapeuticmonoclonalantibodies(mAb)thatrecognizetumor-specificmembraneproteins,blockcellsignaling,andinducetumor-killingthroughFc-driveninnateimmuneresponses.However,inthepastdecade,ampleevidencehasshownthattumor-targetingmAb(TTmAb)eradicatestumorcellsviaactivationofcytotoxicTcells(CTLs).Inthisreview,wespecificallyfocusonhowTTmAbsinduceadaptiveanti-tumorimmunityanditspotentialincombinationtherapywithimmunecytokines,checkpointblockade,radiation,andenzymetargetedsmallmoleculedrugs.ExploringthemechanismsofthesepreclinicalstudiesandretrospectiveclinicaldatawillsignificantlybenefitthedevelopmentofhighlyefficientandspecificTTmAb-orientedanti-tumorremedies.