简介:背景概念噪点的名字有很多,也叫噪声或噪音,主要是指感光材料(CCD或CMOS)将光线作为接收信号接收并输出的过程中所产生图像的粗糙部分,也指图像中不该出现的外来像素。噪点通常由电子干扰产生,这样的点一般情况下是随机产生的,也是没有办法避免和消除的。
简介:AsimplePIcontrollertuningmethodforlargedead-timeprocessesispresented.First,afirst-orderplusdeadtimemodelisidentifiedonthebasisofrelayfeedbackexperiments,whichNyquistcurveisveryclosetothatoflargedead-timeprocessesoverawidefrequencyrange.Withthemodelavailable,PIcontrollerisdesignedwithanewrobustspecification.SimulationexamplesshowtheeffectivenessandfeasibilityofthepresentedPItuningmethodforlargedeadtimeprocesses.
简介:Theultrasonicmotor(USM)possessesheavynonlinearitieswhichvarywithdrivingconditionsandload-dependentcharacteristicssuchasthedead-zone.Inthispaper,anidentificationmethodfortherotarytravelling-wavetypeultrasonicmotor(RTWUSM)withdead-zoneisproposedbasedonamodifiedHammersteinmodelstructure.ThedrivingvoltagecontributingeffectonthenonlinearitiesoftheRTWUSMwastransformedtothechangeofdynamicparametersagainstthedrivingvoltage.Thedead-zoneoftheRTWUSMisidentifiedbasedupontheabovetransformation.Experimentresultsshowedgoodagreementbe-tweentheoutputoftheproposedmodelandactualmeasuredoutput.
简介:Theproblemofadaptivefuzzycontrolforaclassoflarge-scale,time-delayedsystemswithunknownnonlineardead-zoneisdiscussedhere.Basedontheprincipleofvariablestructurecontrol,adesignschemeofadaptive,decentralized,variablestructurecontrolisproposed.Theapproachremovestheconditionsthatthedead-zoneslopesandboundariesareequalandsymmetric,respectively.Inaddition,itdoesnotrequirethattheassumptionsthatallparametersofthenonlineardead-zonemodelandthelumpeduncertaintyareknownconstants.Theadaptivecompensationtermsoftheapproximationerrorsareadoptedtominimizetheinfluenceofmodelingerrorsandparameterestimationerrors.Bytheoreticalanalysis,theclosed-loopcontrolsystemisprovedtobesemi-globallyuniformlyultimatelybounded,withtrackingerrorsconvergingtozero.Simulationresultsdemonstratetheeffectivenessoftheapproach.
简介:Background:Aftertheirdeath,Scotspinetreescanremainstandingfordecadesandsometimesupto200years,forminglong-lastingandecologicallyimportantstructuresinborealforestlandscapes.Standingdeadpinesdecayveryslowlyandwithtimedevelopinto‘kelo'trees,whicharecharacterizedbyhardwoodwithsilvery-coloredappearance.Thesekelotreesrepresentanecologicallyimportant,longlastingandvisuallystrikingelementofthestructureofnaturalpine-dominatedforestsinborealFennoscandiathatisnowadaysvirtuallyabsentfrommanagedforestlandscapes.Methods:Weexaminedandmappedtheamount,structuralfeatures,sitecharacteristicsandspatialdistributionofdeadstandingpinetreesoveratenhectareareainanunmanagedborealforestlandscapeintheKalevalaNationalParkinRussianVienaKarelia.Results:Themeanbasalareaofdeadstandingpinetreesintheforestedpartofthelandscapewas1.7m~2?ha~(-1)andtheestimatedvolume12.7m~3?ha~(-1).Fromthetotalnumberofstandingdeadpinetrees65%werekelotrees,withabasalareaof1.1m~2?ha~(-1)andvolumeof8.0m~3?ha~(-1),theremainderconsistingofstandingdeadpinesalongthecontinuumbetweenarecentlydeadtreeandakelotree.Overall,standingdeadpinesweredistributedthroughoutthestudyarea,buttherewasatendencytowardsspatialclusteringupto<100mdistances.Standingdeadpinesweremostcommonlysituatedonflatgroundorinthemidslopeinthelocaltopography.Inaddition,standingdeadpinescontributedtosubstratediversityalsobycommonlyhavingcharredwoodandbrokentops.Basedonthepresenceofdeadpinesnagsindifferentstageoftransitionfromarecentlydeadpinetoakelowithsilverysurface,itseemsevidentthattheprocessofkelorecruitmentwascontinuouslyinactioninthestudiedlandscape.Conclusions:Kelotreesareanomnipresentfeatureinnaturalpine-dominatedforestlandscapeswithimportantcontributiontoforeststructuralandsubstratediversity.Becauseo
简介:摘要目的检测DEAD盒RNA解螺旋酶5(DDX5)和微小RNA-205(miR-205)在前列腺癌(PCa)中的表达情况,并分析二者与PCa预后的关系。方法选取2015年4月至2017年4月于北京市朝阳区双桥医院行前列腺癌根治术或穿刺活检术的86例PCa患者为研究对象,取患者术中切除的癌组织及癌旁组织分别作为PCa组和对照组。采用实时荧光定量PCR(qRT-PCR)法检测组织中DDX5 mRNA、miR-205的水平。采用免疫组化法检测组织中DDX5的表达情况。分析DDX5、miR-205表达水平与临床病理特征的关系。采用Kaplan-Meier生存分析DDX5、miR-205表达水平与PCa患者的预后关系。采用Cox回归分析PCa预后不良的影响因素。结果PCa组的DDX5 mRNA及蛋白表达水平均高于对照组(均P<0.05),miR-205表达水平低于对照组(P<0.05)。PCa患者中DDX5、miR-205表达与肿瘤分期、血清PSA、Gleason评分、肿瘤转移均有相关性(均P<0.05),而与患者年龄、切缘性质均无相关性(均P>0.05)。经Kaplan-Meier生存分析,DDX5阳性表达患者的3年累积生存率低于DDX5阴性表达患者(P<0.05);miR-205高表达患者的3年累积生存率高于miR-205低表达患者(P<0.05)。多因素Cox分析结果显示,DDX5水平偏高、miR-205水平偏低是PCa不良预后的危险因素(HR=2.598、3.342,均P<0.01)。结论在PCa患者癌组织中DDX5高表达,miR-205低表达,二者与PCa的多种临床病理及预后有关,是PCa患者预后不良的危险因素。
简介:摘要目的探讨右美托咪定对SHG-44胶质瘤细胞增殖和凋亡的影响及其机制。方法采用0.1 μmol/L(低浓度组)、1.0 μmol/L(中浓度组)和10.0 μmol/L(高浓度组)右美托咪定处理SHG-44胶质瘤细胞(购自中国科学院细胞库)。将si-DEAD/H盒解旋酶11反义核糖核酸1(DDX11-AS1)和pcDNA-DDX11-AS1分别转染至SHG-44胶质瘤细胞并采用10.0 μmol/L右美托咪定处理。采用噻唑蓝(MTT)法、克隆形成实验、流式细胞仪、实时荧光定量聚合酶链反应(RT-qPCR)和蛋白质印迹法(Western blot)检测各组细胞增殖、克隆形成数、凋亡率、DDX11-AS1、裂解的半胱氨酰天冬氨酸特异性蛋白酶-3(cleaved-Caspase-3)、Caspase-3前体(pro-Caspase-3)表达。采用t检验或单因素方差分析。结果低浓度组、中浓度组和高浓度组SHG-44胶质瘤细胞吸光度(A)490值、克隆形成数、DDX11-AS1和pro-Caspase-3表达依次降低[A490值为1.17±0.05、0.90±0.04、0.55±0.03,克隆形成数为(108.67±3.09)、(82.00±2.45)、(55.00±2.16)个,DDX11-AS1为0.96±0.04、0.68±0.03、0.36±0.02,pro-Caspase-3为0.72±0.04、0.48±0.02、0.24±0.02],凋亡率和cleaved-Caspase-3表达依次升高[凋亡率为(6.38±0.18)%、(16.78±0.71)%、(21.77±0.77)%,cleaved-Caspase-3为0.23±0.01、0.45±0.02、0.64±0.03],差异有统计学意义(F=140.693、198.187、262.395、321.333、611.199、135.429,P<0.05)。si-DDX11-AS1组SHG-44胶质瘤细胞A490值、克隆形成数和pro-Caspase-3表达低于si-NC组SHG-44胶质瘤细胞[0.72±0.03比1.20±0.05、(65.00±2.45)个比(110.33±4.78)个、0.34±0.02比0.73±0.04,t=14.258、14.617、15.105,P<0.05],凋亡率和cleaved-Caspase-3高于si-NC组SHG-44胶质瘤细胞[(18.38±0.53)%比(6.45±0.20)%、0.53±0.02比0.21±0.01,t=36.477、24.787,P<0.05]。高浓度右美托咪定+pcDNA-DDX11-AS1组SHG-44胶质瘤细胞A490值、克隆形成数和pro-Caspase-3表达高于高浓度右美托咪定+pcDNA组[0.98±0.04比0.54±0.03、(93.33±3.09)个比(56.00±2.16)个、0.63±0.03比0.24±0.01,t=15.242、17.150、21.361,P<0.05],凋亡率和cleaved-Caspase-3表达低于高浓度右美托咪定+pcDNA组[(13.93±0.33)%比(21.79±0.72)%、0.34±0.02比0.65±0.03,t=20.189、15.892,P<0.05]。结论右美托咪定通过下调DDX11-AS1表达来抑制胶质瘤细胞增殖并促进其凋亡。