简介：这贡献考察Arima和Iachello的交往的波色子模型的对称性质。当动态对称的概念是时现在熟悉的，这未必那么为部分动态对称和伪的扩大观点是动态对称，它能漂亮地在交往的波色子模型的上下文被说明。分析的主要结论是动态对称是少见的当时他们的部分并且伪延期是无所不在的。

简介：Inthispaperaviscous-inviscidinteractingflowtheory(IFT)isdevelopedforanincompressible,two-dimensionallaminarflow.IFT’smainpointsareasfollows.(1)Byintroducingaconceptofinteractionlay-erwherethenormalmomentumexchangeisdominating,anewthreelayerstructureisestablished.(2)Throughtheconventionalmanipulationsandbyintroducinganinteractionmodel,boththestreamwiseandnormallengthscalesareprovedtobefunctionsofasingleparameterm,whichisrelatedtothestreamwisepressuregradientandReynoldsnumber.(3)Theapproximateequationsgoverningtheflowofeachlayeraswellasthewholeinteractionflowarederived.ThepresentIFTisapplicabletobothattachedandattached-separationbubble-reattachedflows,TheclassicalboundarylayertheoryandTriple-decktheoryareshowntobetwospecialcasesofthepresenttheoryunderm=0and1/4,respectively.FurthermoreIFTprovidesnewdistinctionsofboththenormalandstreamwiselengthscalesforflow-fieldnumericalcomputationandalsogivesanewapproachtodevelopingthesimpli-fiedNavier-Stokes(SNS)equations.

简介：象在旋转液体的范围和磁盘一样的身体的相互作用导致新奇流动结构。在环绕的方向的主要打漩流动被一个第二等的运动在南方的飞机附加。流动被在轴的中心通过一个洞介绍墨水设想并且在在交往的身体之间的中央飞机放射状地散布了。流动结构取决于身体，他们的几何安排和旋转速度给的雷纳兹数字的形状。观察流动结构与PIV测量和数字模拟产生了进一步的调查。关键词旋转液体-模式形成-再通行地区-交往的身体-流动可视化CLC数字O351.3

简介：这份报纸为调遣目标追踪学习适应格子和模糊交往的多重模型(AGFIMM)的算法，当集中于固定结构的问题时，不高的多重模型(FSMM)算法费用效率比率和Markov转移交往的概率是困难的确切决定的多重模型(IMM)算法。这个算法认识到适应模型由适应格子调整设定，并且获得由模糊逻辑推理在模型集合匹配度的每个模型。模拟结果证明AGFIMM算法能有效地改进精确性和多重模型算法的费用效率比率，并且对设计应用作为结果合适。

简介：AZener-Strohcrackinteractingwithanedgedislocationisstudied.Thecrackfacesareassumedtobetractionfree.Theapplied'generalizedloading'forcrackistheinitialdisplacementjumpandtheinterventionoftheedgedislocation.Throughdecomposingtheproblemintotwosubsimpleproblems,usingthesuperpositionprinciple,itssolutionisobtained.Todemonstrateboththevalidityofthesolutionanditspotentialapplication,twosimpleexamplesrelatedtothecrackstressintensityfactorsarepre...

简介：

简介：Manynonlinearquantumopticalphysicsphenomenaneedmoreaccuratewavefunctionsandcorrespondingenergyorquasienergylevelstoaccountfor.AnanalyticexpressionofwavefunctionswithcorrespondingenergylevelsforanatomicelectroninteractingwithaphotonfieldispresentedasanexactsolutiontotheSchrSdinger-likeequationinvolvedwithbothatomicCoulombinteractionandelectron-photoninteraction.Thesolutionisanaturalgeneralizationofthequantum-fieldVolkovstatesforanotherwisefreeelectroninteractingwithaphotonfield.ThesolutionshowsthatanN-levelatominlightformstationarystateswithoutextraenergysplittinginadditiontotheFloquetmechanism.Thetreatmentdevelopedherewithcomputingcodescanbeconvenientlytransferredtoquantumopticsinclassical-fieldversionasresearchtoolstobenefitthewholephysicscommunity.

简介：Moleculardynamicssimulationswereperformedtostudytheinteractionbetweenatomichydrogenandsiliconcarbide.Inthepresentstudy,wefocusontheeffectofthesurfacetemperatureonHinteractingwithsiliconcarbide.ThesimulationresultsshowthattheretentionofHatomsinthesampledecreaseslinearlywithincreasingsurfacetemperature.ThedepthprofileanalysisshowsthatthesampleismodifiedbyHbombardment,andthedensityofHatomsisgreaterthanthoseofSiandCatomsneartheinterfaceregionbetweentheH-containingregionandthebulk.However,nearthesurfaceregionthedensitiesofH,SiandCatomsarealmostequivalent.Inthemodifiedlayer,thebondsconsistofSi-CandSi-HandC-H.ThefractionofSi-Cbondsisthegreatest.OnlyafewC-Hbondsarepresent.

简介：Interactingmultiplemodelsisthehotspotintheresearchofmaneuveringtargetmodelsatpresent.AhierarchicalideaisintroducedintoIMMalgorithm.Themethodisthatthewholemodelsareorganizedastwolevelstoco-work,andeachcellmodelisanimproved'current'statisticalmodel.Intheimprovedmodel,akindofnonlinearfuzzymembershipfunctionispresentedtogetoverthelimitationoforiginalmodel,whichcannottrackweakmaneuveringtargetprecisely.Atlast,simulationexperimentsprovetheefficientofthenovelalgorithmcomparedtointeractingmultiplemodelandhierarchicalinteractingmultiplemodelbasedoriginal'current'statisticalmodelintrackingprecision.

简介：

简介：Thispaperpresentsacomputationalmodelforthefluiddynamicsinafracturedductilepipeunderhighpressure.Thepressureprofileinfrontofthecracktip,whichisthedrivingsourceofcrackpropagation,iscomputedusinganonlinearwaveequation.Thesolutioniscoupledwithaonedimensionalchokedflowanalysisbehindthecrack.Thesimulationutilizesahighorderoptimizedprefactoredcompact-finitevolumemethodinspace,andlowdispersionanddissipationRunge-Kuttaintime.Asthepipefracturestherapiddepressurizationtakeplaceinsidethepipeandthepropagationofthecrack-inducedwavesstronglyinfluencestheoutflowdynamics.Consistentwiththeexperimentalobservation,themodelpredictstheexpansionwaveinsidethepipe,andthereflectionandoutflowofthewave.Themodelalsohelpscharacterizethepropagationofthecrackdynamicsandfluidflowsaroundthetipofthecrack.

简介：在为光玻璃BK7的擦伤过程的有弹性塑料的转变政体和易碎可锻的转变政体被分析基于赫兹波方程和被魏建议的压力比率理论。为有变量被有限元素模拟的ABAQUS软件基于精力破裂理论模仿的砂砾间隔距离的光玻璃BK7的交往的擦伤进程。为光玻璃BK7的双砂砾交往擦伤测试在DMG超声的70-5上被执行线性，由哪个有限元素模拟的可靠性被验证。细工品的表面形态学被扫描电子显微镜学(SEM)分析，它证明沟的宽度随擦伤深度和砂砾间隔距离的增加显然增加了。沟的宽度的结果与模拟结果一致。表面下的损坏层被蚀刻的HF酸的方法分析，它证明有交叉的裂缝的一个区域。抓的力量被KISTLER的threedimensional测力计测量，它证明第二抓的力量随抓深度和砂砾间隔距离的增加增加了。在第二处擦伤的力量在第一次是比那小的，它与Griffith破裂理论一致。

简介：Wehaveinvestigatedthelow-lyingcollectivestatesandelectromagnetictransitionsin94Mowithintheframeworkoftheinteractingbosonmodel.Theinfluenceofmodelparametersontheenergylevelsandelectromagneticpropertieshasbeeninvestigated.Theanalysisoftheobtainedresultsandtheparametervaluespredictthatthe23+stateisthelowestmixedsymmetrystatewithpureF=Fmax-1inthisnucleus.Thecalculatedresultspredicatethatthe25+(two-Q-phonon)mixedsymmetrystateisclosedtotheJ=2+at2.870MeVintheexperimentaldata,andthe2.965MeVstateisthelowestmixedsymmetrywithJ=3+.

简介：AbstractBackground:The chaperonin containing t-complex (CCT) proteins play an important role in cell cycle-related protein degradation in yeast and mammals. The role of the chaperonin containing t-complex 4 (CCT4), one subtype of CCT proteins, in the progress of hepatocellular carcinoma (HCC) was not fully elucidated. Here, we aimed to explore the mechanisms of CCT4 in HCC.Methods:In this study, we used the UALCAN platform to analyze the relationship between CCT4 and HCC, and the association of CCT4 with the overall survival (OS) of HCC patients was also analyzed. CCT4 expression in HCC tumor tissues and normal tissues was also determined by western blot (WB) assay. Lentivirus vector was used to knock down the CCT4 expression, and quantitative polymerase chain reaction and WB were used to determine the level of CCT4 in HCC cell lines. Cell counting kit-8 (CCK-8) and 5-ethynyl-2＇-deoxyuridine (EdU) assays were used to detect the cell proliferation, and flow cytometry (FCM) was performed to evaluate the effect of CCT4 on the apoptosis of HCC cells. Co-immunoprecipitation (co-IP) assay and WB were used to explore the mechanisms of CCT4 regulating the growth of HCC. Data were calculated from at least three replicate experiments and expressed as mean ± standard deviation. Student’s t test, paired t test, and Kaplan-Meier analysis were used to compare across different groups.Results:We found CCT4 was upregulated in HCC tissues compared with normal tissues, and its high expression was associated with poor prognosis (P < 0.001). CCT4 was significantly increased in HCC tumor tissues compared with normal tissues (0.98 ± 0.12 vs. 0.23 ± 0.05, t = 7.73, P < 0.001). After being transfected with CCT4 short-hairpin RNA (shRNA), CCT4 was decreased in mRNA level and protein level in both Huh7 (mRNA level: 0.41 ± 0.07 vs. 1.01 ± 0.11, t = 8.09, P = 0.001; protein level: 0.61 ± 0.03 vs. 0.93 ± 0.07, t = 7.19, P = 0.002) and Hep3b cells (mRNA level: 0.55 ± 0.11 vs. 1.04 ± 0.15, t = 4.51, P = 0.011; protein level: 0.64 ± 0.10 vs. 0.95 ± 0.08, t = 4.32, P = 0.012). CCK8 assay indicated that CCT4 knockdown inhibited cell proliferation in both Huh7 (OD value of 3 days: 0.60 ± 0.14 vs. 0.97 ± 0.16, t = 3.13, P = 0.036; OD value of 4 days: 1.03 ± 0.07 vs. 1.50 ± 0.12, t = 5.97, P = 0.004) and Hep3b (OD value of 3 days: 0.69 ± 0.14 vs. 1.10 ± 0.11, t = 3.91, P = 0.017; OD value of 4 days: 1.12 ± 0.12 vs. 1.48 ± 0.13, t = 3.55, P = 0.024) cells. EdU assay showed that CCT4 knockdown inhibited the cell proliferation in both Huh7 (EdU positive rate: [31.25 ± 3.41]% vs. [58.72 ± 3.78]%, t = 9.34, P = 0.001) and Hep3b cells (EdU positive rate: [44.13 ± 7.02]% vs. [61.79 ± 3.96]%, t = 3.79, P = 0.019). FCM assay suggested that CCT4 knockdown induced apoptosis in HCC cells (apoptosis rate of Huh7: [9.10 ± 0.80]% vs. [3.66 ± 0.64]%, t = -9.18, P = 0.001; apoptosis rate of Hep3b: [6.69 ± 0.72]% vs. [4.20 ± 0.86]%, t = -3.84, P = 0.018). We also found that CCT4 could regulate anaphase-promoting complex (APC)Cdc20 activity via interacting with Cdc20. Furthermore, CCT4 knockdown induced securin (0.65 ± 0.06 vs. 0.44 ± 0.05, t = -4.69, P = 0.009) and B-cell lymphoma-2 (Bcl-2) interacting mediator of cell death (Bim; 0.96 ± 0.06 vs. 0.61 ± 0.09, t = -5.65, P = 0.005) accumulation. The upregulation of securin inhibited cell growth by downregulating cyclin D1 (0.65 ± 0.05 vs. 1.04 ± 0.07, t = 8.12, P = 0.001), and the accumulation of Bim inhibited Bcl-2 (0.77 ± 0.04 vs. 0.87 ± 0.04, t = 3.00, P = 0.040) and activated caspase 9 (caspase 9: 0.77 ± 0.04 vs. 0.84 ± 0.05, t = 1.81, P = 0.145; cleaved caspase 9: 0.64 ± 0.06 vs. 0.16 ± 0.07, t = 1.81, P = 0.001), which led to elevated apoptosis.Conclusions:Overall, these results showed that CCT4 played an important role in HCC pathogenesis through, at least partly, interacting with Cdc20.

简介：WithintheframeworkoftheUsdpf(16)interactingbosonmodel(IBM),theeffectsofstrongcorrelationsofthedipole(p--boson)andtheoctupole(f--boson)degreeoffreedomonthepositive-paritystatesofeven-evennucleiinSU(3)limitarediscussed.Itisshownthatconfigurationsofanevennumberofmanyp-andf-bosonscannotonlybeincorporatedintotheusuallow-lyingcollectiverotationalbands,suchasthegroundstateband,β-andγ-vibrationalbands,butalsonaturallyformtheKπ＝1+,3+rotationalbands,etc.TheseresultsaresimilartothatofUsdg(15)-IBMandinagreementwellwiththeexperimentaldataofthe17672Hf104nucleus.Besides,severalintrabandE2transitionprobabilitiesaregiven,whichareconsistentwiththatofUsd(6)-IBM.

简介：Riceblack-streakeddwarfvirus(RBSDV)isarecognizedmemberofthegenusFijivirus,familyReoviridae.Itsgenomehastendouble-strandedRNA(dsRNA)segments(S1-S10),inwhichthefifthgenomesegment(S5)containstwoopenreadingframes(ORFs)withapartiallyoverlappingregion.ThesecondORFofRBSDVS5encodesaviralnonstructuralproteinnamedp5bwithunknownfunction.Torevealthefunctionofp5b,itsgenewasligatedintothebaitplasmidpGBKT7andanexpressionlibrarycontainingricecDNAswasconstructedusingplasmidpGADT7foryeasttwo-hybridassay.Thebaitproteinp5bwasdetectedinyeastbywesternblot,andtheresultofanauto-activationtestshowedthatp5bcouldnotautonomouslyactivatetheexpressionofreportergenesinyeast.Thenthebaitproteinp5bwasusedforscreeningthecDNAexpressionlibrariesofrice.Genefragmentsofsomepivotalenzymesinvolvedinphotosynthesis,respirationandotherimportantmetabolicprocesses,wereidentifiedtointeractwithp5binyeast,suggestingthattheseinteractionsmayplayrolesinsymptomdevelopmentininfectedplants.

简介：由不变的理论使用，我们学习与一块时间依赖者激光地交往的二精力级的Bose-Einsteincondensate，动态、几何的阶段aregiven分别地。Aharonov-Anandan阶段也在轮转的进化下面被获得。

简介：Inthepost-genomicera,variouscomputationalmethodsthatpredictprotein-proteininteractionsatthegenomelevelareavailable;however,eachmethodhasitsownadvantagesanddisadvantages,resultinginfalsepredictions.Herewedevel-opedauniqueintegratedapproachtoidentifyinteractingpartner(s)ofSemaphorin5A(SEMA5A),beginningwithsevenproteinssharingsimilarligandinteractingresiduesasputativebindingpartners.ThemethodsincludeDwyerandRoot-Bernstein/Dillontheoriesofproteinevolution,hydropathiccomplementarityofproteinstructure,patternofproteinfunctionsamongmolecules,informationondomain-domaininteractions,co-expressionofgenesandproteinevolution.AmongthesetofsevenproteinsselectedasputativeSEMA5Ainteractingpartners,wefoundthefunctionsofPlexinB3andNeuropilin-2tobeassociatedwithSEMA5A.WemodeledthesemaphorindomainstructureofPlexinB3andfoundthatitsharessimilaritywithSEMA5A.Moreover,avirtualexpressiondatabasesearchandRT-PCRanalysisshowedco-expressionofSEMA5AandPlexinB3andtheseproteinswerefoundtohaveco-evolved.Inaddition,weconfirmedtheinterac-tionofSEMA5AwithPlexinB3inco-immunoprecipitationstudies.Overall,thesestudiesdemonstratethatanintegratedmethodofpredictioncanbeusedatthegenomelevelfordiscoveringmanyunknownproteinbindingpartnerswithknownligandbindingdomains.

简介：TheexpressionpatternsofOsPIL11,oneofsixputativephytochrome-interactingfactors,wereanalyzedindifferentorgansoftransgenictobacco(Nicotianatabacum).TheexpressionofOsPIL11wasorgan-specificandwasregulatedbyleafdevelopment,abscisicacid(ABA),jasmonicacid(JA)andsalicylicacid(SA).TofurtherexploretheroleofOsPIL11inplantlightsignaltransduction,aplantexpressionvectorofOsPIL11wasconstructedandintroducedintotobacco.Whengrownundercontinuousredlight,OsPIL11-overexpressedtransgenictobaccoexhibitedshorterhypocotylsandlargercotyledonsandleavescomparedtowild-typeseedlings.Whengrownundercontinuousfar-redlight,however,transgenicandwild-typeseedlingsshowedsimilarphenotypes.TheseresultsindicatethatOsPIL11isinvolvedinredlightinducedde-etiolation,butnotinfar-redlightinducedde-etiolationintransgenictobacco,whichlaysthefoundationfordissectingthefunctionofOsPIL11inphytochrome-mediatedlightsignaltransductioninrice.

简介：hPFTAIRE1(PFTK1)，Cdc2相关的蛋白质kinase，高度在人的大脑被表示。它在Hela房间展出细胞质的分发，尽管它在它的N终点包含二个原子本地化信号(NLS)。到为它的底层和规章的部件的搜索，我们由把全身的hPFTAIRE1用作一个诱饵屏蔽了一个二混血儿的图书馆。四14-3-3isoforms(贝它，epsilon，希腊语字母的第七字，字形物)被识别与hPFTAIRE1交往。我们在hPFTAIRE1发现了一个通常认为的14-3-3绑定一致主题(RHSSPSS)，它与它的第二NLS重叠了。RHSSPSS主题的删除或有在保存有约束力的主题的翼的Ser119的替换废除了在hPFTAIRE1和14-3-3蛋白质之间的特定的相互作用。变异的S120AhPFTAIRE1也显示出一个弱相互作用到14-3-3蛋白质。结果建议Ser119为在hPFTAIRE1和14-3-3蛋白质之间的相互作用是关键的。当熔化了到绿荧光灯的蛋白质(GFP)的C终点时，所有hPFTAIRE1异种在Hela房间和人的neuroblastoma房间(SH-SY5Y)的细胞质散布了，显示有14-3-3蛋白质的那绑定不贡献潜水艇hPFTAIRE1的细胞的本地化，尽管绑定可以涉及它的发信号的规定。