简介:Equivalentsourcelayer(ESL)imagingisanimportantkindofhigh-resolutionelectroencephalogram(EEG)imaging.Itconsistsoftwocategories:equivalentdipolelayer(EDL)andequivalentchargelayer(ECL).Bothofthemareassumedtobelocatedonornearthecorticalsurfaceandhavebeenproposedashigh-resolutionimagingmodalitiesorasintermediatestepstoestimatetheepicorticalpotential.Here,EDLandECLbasedonarealisticheadmodelarepresented,bothsimulationsandrealdataexperimentaredonetocomparethesetwomodels.TheresultsshowthatECLcanprovidehigherspatialresolutionaboutsourcelocationthanEDLdoes.
简介:为了提供,身体上在地区性的规模为风侵蚀研究基于风建模,3D计算液体动力学(CFD)风模型被开发。模型基于海军司烧方程用C语言被规划,并且它作为开放源代码自由地可得到。与空间分析和建模工具(SAMT)综合,风模型举办方便输入准备和强大的产量可视化。为了验证风模型,,一系列实验在一条风隧道被进行。一个堵住的流入实验被设计在基本液体进程的模拟上测试模型的性能。一个圆障碍实验被设计检查模型是否能在风地上模仿障碍的影响。结果证明测量并且模仿的风地有高关联,和风模型能两个都模仿风的基本过程和对风地的障碍的影响。这些结果显示出风模型的高可靠性。一个区域的一个数字举起模型(DEM)(长的3800m和1700m宽)在在内部蒙古的Xilingele草地(自治区域,中国)被用于模型,和一块3D风地成功地被产生了。由风隧道实验的模型和足够的确认的清楚的实现在地区性的规模为风侵蚀的预言和评价打了一个稳固的基础。
简介:APoissonregressionmodelandanegativebinomialregressionmodel(NBmodel)areoftenusedinareassuchasmedicineandeconomy,butrarelyinthedomesticforestrysector,especiallyintheforestfireforecasting.BasedonthedataofforestfireoccurrencesinDaxing’anlingregionin1980-2005,thispaperprofoundlyanalyzestheapplicationconditionsandtestmethodsofthetwomodels.TheAICmethodwasusedtocheckthefittinglevelofthemodelsandthecapabilityofthemodelsforforecastingforestfireswasdiscussed.ThisstudyprovidednecessarytheoreticalbasisanddatasupportfortheapplicationofthetwomodelsinthefieldofforestryinChina.
简介:Thispaperproposesa3-dimensionalcoarsegrainmodelofmicrotubulesandtreatsthetubulinmonomerasasphereofmultiplepatches,withparameterschosentoyieldexperimentalvaluesofbendingandstretchingstiffness.Themodelhasdemonstratedtheabilitytoproducethebistabilityoftubulinsheets,elasticdeformationnearthetip,andcrackingandpeelingofprotofilaments.Thismodelisexpectedtotakeintoaccountthestructuralandmechanicalaspectsunderlyingthephysicalmechanismofpolymerization/depolymerizationanddynamicinstabilityofmicrotubules.
简介:在这份报纸,我们学习交往的散开的线性系统的一个班的一些各态历经的定理,它是一个寓言的安德森模型。首先,在假设下面转变内核=(一(我,j))我,jS是二倍地随机的,我们获得长期的集中到基于自我两重性从围住的一泛音函数h开始的不变的概率措施h性质,然后我们显示出集中到措施h为起始的分布的一个宽广的类保持的不变的概率。秒(一(我,j))我,jS短暂、对称,并且在阀值下面的散开参数c遗体,我们能决定不变的概率与有限的秒测量的extremal的集合时刻。最后,在情况中转变核(一(我,j))我,jS是二倍地随机的并且满足大小写我(看见大小写我在里面[Shiga,T.:在人口遗传的一个交往的系统。J。数学。京都大学,20,213242(1980)]),我们证明这个寓言的安德森模型局部地灭绝独立于散开参数c。
简介:InCAGDandCG,energymodelisoftenusedtocontrolthecurvesandsurfacesshape.Incurve/surfacemodeling,wecangetfaircurve/surfacebyminimizingtheenergyofcurve/surface.However,ourresearchindicatesthatinsomecaseswecan'tgetfaircurves/surfaceusingthecurrentenergymodel.Soanimprovedenergymodelispresentedinthispaper.Examplesarealsoincludedtoshowthatfaircurvescanbeobtainedusingtheimprovedenergymodel.
简介:BackgroundMyocardialfibrosisplaysacriticalroleintheprocessofdiabeticcardiacremolding.MicroRNAs(miRNAs)areendogenous,smallnon-codingRNAsthatnegativelyregulategeneexpressionindiversebiologicalandpathologicalprocesses.However,therolesofmiRNAsinmyocardialfibrosishavenotbeenwellelucidated.Inthepresentstudy,miRNAsprofilesinthefibroticmyocardiumofdb/dbmiceandmiRNAsexpressioninTGF-β1-stimulatedmousecardiacmyofibroblastswasexamined.MethodsHeartfunctionof18-week-olddb/dbmiceanddb/mcontrolmicewasdetectedbyechocardiography.miRNAexpressionprofileindiabeticmyocardiumwasdetectedbymiRNAmicroarray.Quantitativereal-timePCRwasusedtodeterminetheexpressionoffibrosis-relatedgenesandmiRNAprecursorsofinterest.Westernblotwasusedtodetectthelevelsoffibrosis-relatedproteins,activatedSmad3andtotalSmad3.ResultsTheresultofechocardiographyshowedthatleftventricularsystolicanddiastolicfunctionwasimpairedin18-week-olddb/dbmicewithoutsignificantchangeofejectionfraction(EF)andfractionalshortening(FS).Fibrosis-relatedgenesexpressionwasupregulatedandtheamountofphosphorylatedSmad3wasincreasedsignificantlyinthediabeticmyocardium.miRNAsdysregulationwasshownindiabeticmyocardium,sixty-eightmiRNAs,includingmiR-208b,miR-29b,miR-26bandmiR-30e,wereincreasedovertwo-fold,meanwhile,sixty-twomiRNAsweredecreasedmorethantwo-foldinthemyocardiumofdb/dbmicecomparedtodb/mcontrols.InparallelwithasignificantupregulationofCol1a1,Col3a1andCTGFmiRNAexpression,miR-208b,miR-29b,miR-26bandmiR-30eprecursorswerealsoshowntobeupregulatedinTGF-β1-inducedC57bl/6mousecardiacmyofibroblasts.ConclusionsmicroRNAsweredysregulatedindiabeticmyocardium,withtheactivationofTGF-β/smad3pathway,contributingtodiabeticmyocardialfibrosis.