简介:摘要水质和水压是现代供水企业赖以生存和发展的基本服务因素,在水质稳定的前提下,水压的服务质量和能耗是相互制约的两个对立因素。我公司是水厂供水部门,主要供大兴新城沿线各单位生产和生活用水,由于用水的不均匀,每天供水量变化较大,目前日供水量为5万吨,变频调速恒压供水技术其节能、安全、供水高品质比等优点,在供水行业得到了广泛的应用。本文先从变频器的工作原理、变频调速的特性、等出发,结合我厂供水的现状,介绍了变频器在恒压供水控制系统中的应用,大大提高了系统的安全性,保证了供水的稳定性,期望能够大幅度简化供水系统中的变速控制程序,实现系统整合调整后的节能减排效果。
简介:摘要随着我国工业和经济的快速发展,大量的非线性设备投入运行,导致电网中产生大量电力谐波,严重降低了电能的质量,影响用户的安全生产,同时对于电网的稳定运行也产生了较大的威胁。而有源电力滤波器是目前治理配电网谐波的重要手段,但是在其运行中存在能量损耗,导致直流侧电压产生波动,影响谐波补偿性能,为此本文将提出一种模糊PI控制方法,有效提高直流侧电压的稳定性。
简介:Objective:ActivatingKRASmutationsarethemostcommondriversinthedevelopmentofnon-smallcelllungcancer(NSCLC).However,unsuccessoftreatmentbydirectinhibitionofKRAShasbeenproven.DeregulationofPI3KsignalingplaysanimportantroleintumorigenesisanddrugresistanceinNSCLC.TheactivityofPI3Kα-selectiveinhibitionagainstKRAS-mutatedNSCLCremainslargelyunknown.Methods:CellproliferationwasdetectedbysulforhodamineBassay.Cellcycledistributionandapoptosisweremeasuredbyflowcytometry.CellsignalingwasassessedbyWesternblotandimmunohistochemistry.RNAinterferencewasusedtodown-regulatetheexpressionofcyclinD1.HumanNSCLCxenograftswereemployedtodetecttherapeuticefficacyinvivo.Results:CYH33possessedvariableactivityagainstapanelofKRAS-mutatedNSCLCcelllines.AlthoughCYH33blockedAKTphosphorylationinalltestedcells,RbphosphorylationdecreasedinCYH33-sensitive,butnotinCYH33-resistantcells,whichwasconsistentwithG1phasearrestinsensitivecells.CombinedtreatmentwiththeCDK4/6inhibitor,PD0332991,andCYH33displayedsynergisticactivityagainsttheproliferationofbothCYH33-sensitiveandCYH33-resistantcells,whichwasaccompaniedbyenhancedG1-phasearrest.Moreover,down-regulationofcyclinD1sensitizedNSCLCcellstoCYH33.Reciprocally,CYH33abrogatedthePD0332991-inducedup-regulationofcyclinD1andphosphorylationofAKTinA549cells.Co-treatmentwiththesetwodrugsdemonstratedsynergisticactivityagainstA549andH23xenografts,withenhancedinhibitionofRbphosphorylation.Conclusions:SimultaneousinhibitionofPI3KαandCDK4/6displayedsynergisticactivityagainstKRAS-mutatedNSCLC.ThesedataprovideamechanisticrationaleforthecombinationofaPI3KαinhibitorandaCDK4/6inhibitorforthetreatmentofKRASmutatedNSCLC.