简介:<正>Atthe2011NationalFinancialWorkConference,itwasclearlypointedoutthatfinanceshouldcontinuetoservetherealeconomyandthatcapitalshouldbeensuredtobeinputtedintotherealeconomyinabidtoeffectivelysolvetheproblemsthatitwasdifficultandexpensivetofinance
简介:处理的大数据正在成为数据中心计算的固执己见者部分。然而,最近的研究显示了大数据工作量不能充分利用现代记忆系统。我们发现处理的大数据的戏剧的无效从缓存失误的庞大的数量和看情况的存储器存取的货摊。在这篇论文,我们介绍二优化处理这些问题。第一是slice-and-merge策略,它减少种类过程的缓存失误率。第二优化是direct-memory-access,它改革在钥匙/值的存储使用的数据结构。这些优化被评估与微基准并且真实世界的基准HiBench。结果我们的微基准清楚地以硬件事件计数表明我们的优化的有效性;并且HiBench的另外的结果显示出1.21X一般水准加速在上申请级。两结果说明那小心的硬件/软件合作设计将改进大数据处理的存储器效率。我们的工作已经集成于为ApacheHadoop的Intel分发。
简介:Sincethe18thNationalCongressoftheCommunistPartyofChina,GeneralSecretaryXiJinpinghasissuedaseriesofimportantexpositionsonpeaceanddevelopment,whoseimpactisincreasinglyimportantforthecurrentprocessofglobalgovernance.XihaspointedoutthatChinesecivilizationhasupheldharmonyinhandling
简介:One-dimensionalorderedwatermoleculesenteringandexitingfromacarbonnanotubewithanappropriateradiusarestudiedwithmoleculardynamicssimulations.Itcanbefoundthatawatermoleculenearthenanotubeendismorelikelytobeexpelledfromthenanotubeifitsdipoleisalmostperpendiculartothenanotubeaxis.ThekeytothisobservationisthatthosewatermoleculesareclosertothewallofthenanotubeawayfromtheequilibriumpositionoftheLennar-Jones(LJ)potential.Thus,theinteractionenergyforthosewatermoleculesisrelativelyhigh.Therearetwoparticularstructuresoftheperpendicularwatermoleculedependingonthedipoledirectionoftheadjacentwatermoleculeinthenanotube.Althoughtheprobabilitiesofthesestructuresarequitesmall,theircontributionstothenetfluxacrossthenanotubeendareapproximatelyequaltothepredominantstructures.Thepresentfindingsfurthershowthepossibilityofcontrollingthewaterflowbyregulatingthedipoledirectionsofthewatermoleculesinsidethenanochannels.
简介:EliminationoftheCRISPR/Cas9constructsineditedplantsisaprerequisiteforassessinggeneticstability,conductingphenotypiccharacterization,andapplyingforcommercializationoftheplants.However,removaloftheCRISPR/Cas9transgenesbygeneticsegregationandbybackcrossislaboriousandtimeconsuming.WepreviouslyreportedthedevelopmentofthetransgenekillerCRISPR(TKC)technologythatusesapairofsuicidegenestotriggerself-eliminationofthetransgeneswithoutcompromisinggeneeditingefficiency.TheTKCtechnologyenablesisolationoftransgene-freeCRISPR-editedplantswithinasinglegeneration,greatlyacceleratingcropimprovements.Here,wepresentedtwonewTKCvectorsthatshowgreatefficiencyinbotheditingthetargetgeneandinundergoingself-eliminationofthetransgenes.ThenewvectorsreplacedtheCaMV35SpromoterusedinourpreviousTKCvectorwithtworicepromoterstodriveoneofthesuicidegenes,providingadvantagesoverourpreviousTKCvectorundercertainconditions.Thevectorsreportedhereofferedmoreoptionsandflexibilitytoconductgeneeditingexperimentsinrice.
简介:AbstractBackground:Non-coding RNAs have attracted considerable attention for their vital role in cancer. The purpose of this study was to determine the effects of non-coding RNAs on hepatocellular carcinoma (HCC) and reveal their regulatory mechanism in the pathophysiological process.Methods:We measured the expression of mucin 1 (MUC1) and miR-485-5p in tissues from 15 HCC patients and in liver cancer cell lines by quantitative real-time polymerase chain reaction and Western blot, screened for aberrantly expressed microRNAs (miRNAs) by miRNA microarrays. Bioinformatics tools were used to find the miRNA and circular RNA that regulated MUC1, which were validated by RNA immunoprecipitation assay and luciferase reporter assay. Cell counting kit-8, Transwell assays, and flow cytometry were used to conduct functional experiments. Proteins were examined by western blot and immunohistochemical staining assays. Significant differences between groups were estimated using the one-way analysis of variance. A P < 0.05 was considered statistically significant.Results:MUC1 was overexpressed in HCC tissues compared with that in paratumor tissues (normal vs. tumor, 1.007 ± 0.215 vs. 75.213 ± 18.403, t = 18.401, P < 0.001) while miR-485-5p was down-regulated (normal vs. tumor, 4.894 ± 0.684 vs. 1.586 ± 0.398, t= 16.191, P < 0.001). Inhibition of miR-485-5p promoted cell proliferation (73.33% ± 5.13% vs. 41.33% ± 3.51%, t= 8.913, P < 0.001), migration (102 ± 8 cells vs. 46 ± 8 cells, t= 8.681, P < 0.001), invasion (59 ± 7 cells vs. 28 ± 2 cells, t = 8.034, P < 0.01), and suppressed apoptosis (22.64% ± 6.97% vs. 36.33% ± 3.96%, t = 2.958, P < 0.05) of HepG2 cells with which MUC1 is knocked down. Mechanically, miR-485-5p binds to MUC1, while circHECTD1 binds to miR-485-5p, resulting in the indirect up-regulation of the MUC1 level.Conclusions:Our findings reveal that circHECTD1 facilitates HCC progression by sponging miR-485-5p to up-regulate MUC1.