简介：Themodulationandcontrolofgecko'sfootmovementswerestudiedelectrophysiologicallyinordertodesignthemotorcontrolsystemofagecko-mimicrobot.Inthisstudy(1)theanatomyoftheperipheralnervescontrollingthegecko'sfootmovementswasdetermined;(2)therelationshipbetweenthelimbnervesofthegeckoanditsfootmotorpatternswasstudied;(3)theafferentimpulsesofthenervesevokedbyrubbingthegecko'stoesandpalmwererecorded;(4)copyingthenaturalpatternsofmovementofthegecko'sfoot(abduction,adduction,flexion,andrevolution)anditslimbnervemodulationandcontrolmechanism,thenerveswerestimulatedundercomputercontrol,andtheresultsrecordedbyCCD.Resultssuggestthatgecko'sfootmovementscanbesuccessfullycontrolledbyartificialelectricalsignals.

简介：InordertoanalyzethemechanismofimmunomodulationbyLPSonmurineperitonealsuppressormacrophages,wehave,usingRNaseprotectionassay,checkedthechangesofmRNAexpressionpatternofseveralcytokinegenesduringtheimmuno-modulation.Ithasbeenfoundthat,aftertreatingperitonealsuppressormacrophageswithLPS,mRNAsofIL-12p35,IL-12p40,IL-6andIFN-γarenewlyappeared,whilethoseofIL-1α，IL-1βandIL-1Raareincreasebandthoseofothercytokines,likeTGF-β1andMIFarenotchangedatall.Itseemscertainthatthosecytokines,whoseexpressionisincreasedbyLPSstimulation,mayberesponsibleforthefunctionalchangesofsuppressormacrophagesduringimmuno-modulation.Amongthesechanges,theappearanceofIL-12mRNAmayplayacriticalrole,and,inthisregard,thesynergeticeffectbetewwnIFN-γandLPSontheincreaseofIL-12p35andIL-12p40mRNAexpressionisaninterestingfinding.

简介：百日咳毒素(PTX)禁止禁止的heterotrimericG蛋白质(G伪_(i./o))的伪-子单元的激活并且调制电压门钠隧道，它可以是pyrethroids的主要目标之一。调查农业害虫抵抗的潜在的机制到pyrethroid杀虫药剂，我们在中央神经原在钠隧道上由PTX检验了调整第三—第4中间形态幼虫cyhalothrin抵抗(Cy-R)并且cyhalothrin易受影响(Cy-S)Helicoverpa有佩带徽章权利的人一旁边整个房间的补丁夹钳技术。孤立的神经原为12是有教养的—在改进L15昆虫培养基与或没有PTX(400ng/mL)的16h。结果证明Cy-R和Cy-S钠隧道展出了快动力学和tetrodotoxin(TTX)敏感。Cy-R钠隧道展出了改变的gating性质不仅包括在电压依赖者激活(V_(0.5act))的8.88-mV权利移动和在在激活(V_(0.5inact))的电压依赖者的6.54-mV权利移动，而且是在钠隧道密度(I_(密度))的duced山峰(那中的55.2%个在Cy-S神经原)。Cy-R钠隧道也显示出低易兴奋性，证实了由恰好在5激活潜力(V_(行为i))变—由20mV的10mV和山峰潜力(V_(山峰))。PTX施加了重要效果onCy-S钠隧道，减少在70.04%的钠隧道密度，由14.41mV的正确的变V_(0.5act)和在9的V_(0.5inact)。38mV。它没引起在Cy-R钠隧道上面提及的参数的任何重要变化。在山峰电压的山峰的从潜伏的激活时间(T_(山峰))并且在激活时间常数快(τ_(在行为))在Cy-S和Cy-R，神经原没被影响。结果建议对pyrethroid杀虫药剂抵抗的棉花一种蛾的幼虫包含不仅变化和电压门钠隧道的紧密相联的位的改变，而且可能含有PTX敏感的Gα_(i./o)的不安联合了发信号的转导小径。

简介：Ionizingradiationisoneofthemosteffectivetoolsincancertherapy.Inapreviousstudy,wereportedthatproteintyrosinekinase(PTK)inhibitorsmodulatetheradiationresponsesinthehumanchronicmyelogenousleukemia(CML)celllineK562.Thereceptortyrosinekinaseinhibitor,genistein,delayedradiation-inducedcelldeath,whilenon-receptertyrosinekinaseinhibitor,herbimycinA(HMA)enhancesradiation-inducedapoptosis.Inthisstudy,wefocusedonthemodulationofradiation-inducedcelldeathbygenisteinandperformedPCR-selectsuppressionsubtractivehybridization(SSH)tounderstanditsmolecularmechanism.Weidentifiedhumanthymidinekinase1(TK1),whichiscellcycleregulatorygeneandconfirmedexpressionofTK1mRNAbyNorthernblotanalysis.ExpressionofTK1mRNAandTK1enzymaticactivitywereparallelintheirincreaseanddecrease.TK1isinvolvedinG1-Sphasetransitionofcellcycleprogression.Incellcycleanalysis,weshowedthatradiationinducedG2arrestinK562cellsbutitwasnotabletosustain.However,theadditionofgenisteintoirradiatedcellssustainedaprolongedG2arrestupto120h.Inaddition,theexpressionofcellcycle-relatedproteins,cyclinAandcyclinB1,providedtheevidencesofG1/SprogressionandG2-arrest,andtheirrelationshipwithTK1incellstreatedwithradiationandgenistein.TheseresultssuggestthattheactivationofTK1maybecriticaltomodulatetheradiation-inducedcelldeathandcellcycleprogressioninirradiatedK562cells.