简介:Afamilyofpiecewiserationalquinticinterpolationispresented.Eachinterpolationofthefamily,whichisidentifieduniquelybythevalueofaparameterαi,isofC2continuitywithoutsolvingasystemofconsistencyequationsforthederivativevaluesattheknots,andcanbeexpressedbythebasisfunctions.InterpolantisofO(hr)accuracywhenf(x)?Cr[a,b],andtheerrorshaveonlyasmallfloatingforabigchangeoftheparameterαi,itmeanstheinterpolationisstablefortheparameter.Theinterpolationcanpreservetheshapepropertiesofthegivendata,suchasmonotonicityandconvexity,andaproperchoiceofparameterαiisgiven.
简介:目的:观察外源给予H2O2对C2C12细胞中UII/UT系统表达的影响。方法:培养小鼠肌原细胞系C2C12细胞株,应用胎盘蓝染色和测定细胞培养液中LDH的含量检测H2O2对细胞损伤的影响,应用放射免疫的方法检测细胞培养液和裂解液中UII的含量,应用RT-PCR法测定C2C12中UTmRNA的表达,应用WesternBlot检测不同浓度H2O2对肌原细胞系C2C12中UT蛋白表达的影响。结果:外源给予不同浓度的H2O2,C2C12细胞裂解液中UII的含量各组间无明显差异,但增加了细胞孵育液中UII的含量,10-4M和10-3M时分别增加了83.1%(p〈0.01)和94.5%(P〈0.01)。低浓度H2O2(0.5×10-6M,10-6M,10-5M,10-4M)刺激明显增加了UTmRNA的表达,而高浓度的H2O2(10-3M)刺激反而使UTmRNA的表达降低。高浓度的H2O2(10-6M,10-5M,10-4M,10-3M)刺激使UT蛋白表达分别增加了200.1%、255.6%、111.1%和100.1%(均p〈0.05)。结论:H2O2作为T2DM发病因素之一的活性氧族,可能是T2DM时骨骼肌组织中UII/UT系统表达增加的一个因素。
简介:采用编织-粉料铺填法制备Cf/ZrB2预制体,经过“浸渍-炭化”制得C/C-ZrB2复合材料,研究材料的微观结构与力学性能、抗氧化性能和抗烧蚀性能。结果表明:ZrB2颗粒由树脂炭包裹,在C/C-ZrB2复合材料内部均匀分布。材料的氧化质量损失率随氧化时间延长呈线性增长,在1100℃温度下氧化10min和60min后质量损失率分别为2.67%和20.47%。该材料的抗弯强度为81.1MPa,氧化10min后抗弯强度仍保持在氧化前的80%,氧化前后均呈假塑性断裂模式。ZrB2粉体的加入可显著改善C/C复合材料的抗烧蚀性能,等离子烧蚀120s后,其质量烧蚀率和线性烧蚀率分别为0.30mg/s和8.75μm/s。玻璃态ZrO2的阻氧作用以及B2O3的挥发吸热是复合材料主要的抗烧蚀机理。
简介:Theroleofpulseparametersonnanoparticlepropertyisinvestigatedself-consistentlybasedonacoupleoffluidmodelandaerosoldynamicsmodelinacapacitivelycoupledparallel-plateacetylene(C2H2)discharge.Inthismodel,themasscontinuityequation,momentumbalanceequation,andenergybalanceequationforneutralgasaretakenintoaccount.Thus,thethermophoreticforceariseswhenagastemperaturegradientexists.Thetypicalresultsofthismodelarepositiveandnegativeiondensities,electronimpactcollisionsrates,nanoparticledensity,andchargedistributions.Thesimulationisperformedfordutyratio0.4/0.7/1.0,aswellaspulsemodulationfrequencyfrom40kHzto2.7MHzforpureC2H2dischargesatapressureof500mTorr.Wefindthatthepulseparameters,especiallythedutyratio,haveagreataffectonthedissociativeattachmentcoefficientandthenegativedensity.Moreimportantly,bydecreasingthedutyratio,nanoparticlesstarttodiffusetothewall.Undertheactionofgasflow,nanoparticledensitypeakiscreatedinfrontofthepulseelectrode,wherethegastemperatureissmaller.
简介:ThefirststarsintheearlyUniversewereformedabout400millionyearsafterthebigbang.VerificationoftheexistenceofthesestarsisimportantforourunderstandingoftheevolutionoftheUniverse[1].IthasbeenpredictedthatforPopulation-IIIstellarproductionyields,theabundancesofodd-Zelementsareremarkablydeficientcomparedtotheiradjacenteven-Zelements[2].Astronomersaresearchingforlong-lived,lowmassstarswiththeuniquenucleosyntheticpatternmatchingthepredictedyields[3].
简介:Zirconiagraphiterefractoryisusedasacore-nozzleinthethin-stripcastingofsteel.Post-mortemanalysisofusedrefractorywasperformedinanefforttoestablishthefailuremechanism.CorrosionbehaviorwasstudiedagainstmoltensteelwithMnO-SiO2basedliquidinclusions.CorrosionofthesematerialsinvolvesdissolutionandoxidationofgraphiteinthematrixfollowedbypenetrationofliquidslagleadingtodegradationofZrO2particles.Thermodynamicequilibriumcalculationswereperformedtostudythiscorrosionmechanism.
简介:摘要目的探讨CYP2C9、CYP2C19基因多态性对心脏瓣膜置换术后患者华法林代谢及个体化用药的影响。方法随机选取2012年1月~2015年1月期间我院收治的风湿性心脏病心脏瓣膜置换术后患者120例,均用PCR-荧光探针法对患者CYP2C9*3(A1075C)基因多态性进行检测,从而辅助临床指导患者个体化华法林的使用;检测CYP2C19*2(G681A)和CYP2C19*3(G636A)基因多态性,通过对患者基因分型检测,判定患者的华法林代谢速率类型,从而合理调整药物剂量,提高药物的有效性。结果CYP2C9、CYP2C19基因多态性对华法林血药浓度具有影响;PM、M与EM标准血药浓度比较,差异明显(P<0.05),具有统计学意义。结论CYP2C9、CYP2C19基因多态性对个体华法林代谢存在一定影响,为提高患者个体用药效果提供参考与借鉴。
简介:目的研究血管紧张素II和坎地沙坦对小鼠骨骼肌细胞(C2C12)胰岛素敏感性的影响及其机制。方法C2C12诱导分化成熟后,分为对照组(C组)、模型组(M组:AngII)、坎地沙坦低剂量组(Can1组:坎地沙坦0.1μM+AngII)、坎地沙坦中剂量组(Can2组:坎地沙坦1μM+AngII)、坎地沙坦高剂量组(Can3组:坎地沙坦10μM+AngII)。各组细胞给予相应药物及胰岛素处理后,检测2-脱氧葡萄糖(2-NBDG)的摄取率,并用RT-PCR法和Western印记法分别检测各组细胞中磷脂酰肌醇3激酶(PI3K)、蛋白激酶B(Akt)和胰岛素受体底物分子-1(ISR-1)的mRNA及蛋白表达水平。结果M组摄取2-NBDG较C组明显降低(P〈0.01),而Can3组摄取2-NBDG则较M明显增加(P〈0.05)。M组ISR-1和Akt的mRNA表达较C组明显降低(P〈0.01),Can2组及Can3组ISR-1、PI3K和Atk的mRNA表达较M组明显升高(P〈0.05)。M组p-ISR-1和p-Akt蛋白表达较C组明显降低(P〈0.01),Can2组及Can3组p-ISR-1和p-Akt较M组明显升高(P〈0.05)。结论AngII通过下调胰岛素信号通路中重要因子ISR-1、Akt的mRNA及蛋白表达抑制胰岛素的生物学效应,引起骨骼肌细胞胰岛素抵抗;而坎地沙坦通过抑制AngII的这种作用改善骨骼肌胰岛素抵抗。
简介:摘要目的C-erbB-2、Pgp蛋白表达与CRC临床病理特征的关系.方法免疫组化检测蛋白表达,SPSS软件分析数据.结果C-erbB-2蛋白表达与临床病理特征均无统计学相关性(P>0.05).Pgp蛋白表达在大体溃疡型(86.88%)与隆起型(75.51%)间统计学差异显著(P<0.05);在肿瘤侵润深度(肠壁浆膜层或累及临近器官90.48%、肠壁全层88.42%、肌层72.22%、粘膜下层60%)间统计学差异显著(P<0.05);在淋巴结有无转移(93.98%,75.91%)间统计学差异特别显著(P<0.01).C-erbB-2与Pgp蛋白表达间无统计学相关性(P>0.05).结论多数CRC可能有原发性多药耐药;Pgp蛋白可作反映CRC生物学行为的标志物,恶性程度较高的CRC可能易出现原发性多药耐药.关键词C-erbB-2Pgp结直肠癌多药耐药TheClinicalSignificanceofC-erbB-2andPgpProteinExpressionsinColorectalCarcinomaAbstractObjectiveExplorethefeasibilitythatC-erbB-2andPgpproteinexpressionsareusedtoassessbiologicalbehaviorsandprognosisofcolorectalcancer.MethGodsImmunohistochemistrywasusedtodetecttheproteinexpressions.SPSSstatisticsoftwarewasusedtoanalyzetherelationshipoftheproteinexpressionstoclinicalpathoGlogicalfeaturesofthecancerandthecorrelationbetweentheproteinexpressions.ResultsTheexpressionofC-erbB-2proteinhadnosignificantrelationstocharacteristicsofthecancers(P>0.05).ThepositiveratesofPgpproteinexpressioningrossshapeofulcerandprotrusionwere86.88%and75.51%andtherewasstatisticalsignificancebetweenthem(P<0.05).Thepositiveratesininvasionstoadjacentorgansorpenetrationserosa,toserosaoradventitia,tomuscleandtosubmucosawere90.48%,88.42%,72.22%and60%respectivelyandtherewerestatisticalsignificancesamongthem(P<0.05).Thepositiveratesintumorwithandwithoutlymphnodemetastasiswere93.98%and75.91%andtherewasstatisticalsignificancebetweenthem(P<0.01).TherewerenostatisticalcorrelationsbetweenexpressionsofC-erbB-2andPgpproteinincolorectalcancer(P>0.05).ConclusionsThemajorcolorectalcancersmighthaveaprimarymultidrugresistance.PgpproteincanbeseenasapotentialmarkerforjudgeGmentmKaelyignWaonrtdsbehaviorofcolorectalcancerandthecolorectalcancerwithhighmalignancymighthavebigchancetobeprimarymultidrugresistance.C-erbB-2PgpCRCmultidrugresistance中图分类号R735.3文献标识码B文章编号1008-6315(2015)12-0375-02