简介：目的：讨抑郁症的神经生物学发病机制，揭示针刺治疗抑郁症的机理。方法：以Wistar大鼠为受试对象，采用给予孤养大鼠以长期不可预见的中等强度刺激的方法建立抑郁大鼠模型，检测应激后造成的抑郁模型大鼠行为学改变、下丘脑垂体肾上腺皮质轴（HPA）的变化，同时观察针刺干预效应及不同针法的疗效比较。结果：型组、生理盐水组血清CORT和ACTH含量明显高于正常对照组（P〈0．05）；手针治疗组、电针治疗组血清CORT和ACTH含量明显低于模型组（P〈0．05）；药物组血清CORT和ACTH含量明显低于生理盐水组（P〈0．05）：手针治疗组、电针治疗组、药物组比较差别无统计学意义。结论：刺百会、太冲具有较明显的抗抑郁效应，其机制可能与针刺对HPA轴的调整有关。

简介：AbstractPolycystic ovary syndrome (PCOS) is a heterogeneous reproductive disease that can cause infertility. The Hippo signaling pathway, a network highly conserved throughout evolution, maintains the balance between follicle proliferation and dormancy. Dynamic changes in primordial follicles cannot occur without the participation of biological signals and mechanical force; however, little is known about the mechanism by which biomechanical signaling triggers PCOS, especially in the context of primordial follicle development. To investigate the contribution of mechanical stress and the Hippo signaling pathway to the onset of PCOS, we searched the literature via the PubMed database, and inclusion and exclusion criteria were established to ensure the rigor of this research. We eventually included 54 publications in which Hippo signaling and mechanical force were suggested to play a vital role in the development of primordial follicles as well as elucidate the pathogenesis of PCOS. The Hippo pathway modulating follicle growth can be perturbed via extracellular mechanical stress caused by the stiff ovarian cortical environment in PCOS. Clinical intervention targeting the Hippo pathway can alter the activity of core Hippo members, such as the Yes-associated protein/transcriptional co-activator PDZ-binding motif complex. In some patients with PCOS, follicle overactivation can be attributed to the dysfunction of Hippo signal transduction. PCOS, a condition with various patterns, cannot be accurately explained by a single, specific mechanism. The present review identifies potential targets and therapeutic strategies for PCOS.

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简介：目的methotrexate(MTX)的最重要的副作用是mucositis。这研究的目的是在收到methotrexate的老鼠在肠的损坏和氧化应力上评估沉金摘录的效果。方法实验在划分成六个组的男Wistar白化体老鼠上被执行。首先组织收到的正常盐口头上地，第二个组收到了沉金摘录(100mg瑡潩?????????????????假吗？？

简介：Freeradicalsinducedbytraumaticbraininjuryhavedeleteriouseffectsonthefunctionandantioxidantvitaminlevelsofseveralorgansystemsincludingthebrain.Melatoninpossessesantioxidanteffectonthebrainbymaintainingantioxidantenzymeandvitaminlevels.Weinvestigatedtheeffectsofmelatoninonantioxidantabilityinthecerebralcortexandbloodoftraumaticbraininjuryrats.Resultsshowedthatthecerebralcortexβ-carotene,vitaminC,vitaminE,reducedglutathione,anderythrocytereducedglutathionelevels,andplasmavitaminClevelweredecreasedbytraumaticbraininjurywhereastheywereincreasedfollowingmelatonintreatment.Inconclusion,melatoninseemstohaveprotectiveeffectsontraumaticbraininjury-inducedcerebralcortexandbloodtoxicitybyinhibitingfreeradicalformationandsupportingantioxidantvitaminredoxsystem.

简介：Interleukin-6(IL-6)-deficientmicearepronetoethanol-inducedapoptosisandsteatosisintheliver;however,theunderlyingmechanismisnotfullyunderstood.Mitochondrialdysfunctioncausedbyoxidativestressisanearlyeventthatplaysanimportantroleinthepathogenesisofalcoholicliverdisease.Therefore,wehypothesizethattheprotectiveroleofIL-6inethanol-inducedliverinjuryismediatedviasuppressionofethanol-inducedoxidativestressandmitochondrialdysfunction.Totestthishypothesis,weexaminedtheeffectsofIL-6onethanol-inducedoxidativestress,mitochondrialinjury,andenergydepletionintheliversofIL-6(-/-)miceandhepatocytesfromethanol-fedrats.Ethanolconsumptionleadstostrongerinductionofmalondialdehyde(MDA)inIL-6(-/-)micecomparedtowild-typecontrolmice,whichcanbecorrectedbyadministrationofIL-6.Invitro,IL-6treatmentpreventsethanol-mediatedinductionofreactiveoxygenspecies(ROS),MDA,mitochondrialpermeabilitytransition(MPT),andethanol-mediateddepletionofadenosinetriphosphate(ATP)inhepatocytesfromethanol-fedrats.AdministrationofIL-6invivoalsoreversesethanol-inducedMDAandATPdepletioninhepatocytes.Finally,IL-6treatmentinducesmetallothioneinproteinexpression,butnotsuperoxidedismutaseandglutathioneperoxidaseinculturedhepatocytes.Inconclusion,IL-6protectsagainstethanol-inducedoxidativestressandmitochondrialdysfunctioninhepatocytesviainductionofmetallothioneinproteinexpression,whichmayaccountfortheprotectiveroleofIL-6inalcoholicliverdisease.

简介：瞄准：为了调查白果树biloba的效果，肺损害上的摘录(EGb761)由肠的ischemia/reperfusion(II/R)导致了。方法：II/R损害的老鼠模型被为灌注为180min跟随的60min夹钳优异mes伤寒动脉生产。老鼠随机被分配进假冒，II/R，和EGb+II/R组。在EGb+II/R组，EGb761(100mg/kg每天)在外科以前经由一个胃的试管被给7连续的天。在II/R和假冒的组的老鼠与EGb761的车辆的相等的体积被对待。肺损害被轻显微镜学，wet-to-dry肺重量比率(W/D)和肺的渗透索引(PPI)估计。malondialdehyde(MDA)和亚硝酸根/硝酸盐的层次(没有(2)(-)/NO(3)(-))，以及超级氧化物歧化酶(草皮)的活动和myeloperoxidase(军邮局)被检验。西方的污点被用来决定可诱导的氮的氧化物synthase(iNOS)的表示。结果：显著地改进的EGb761意味着动脉压和稀释的肺损害，由组织学的变化的改进和肺的W/D和PPI的重要减少表明了(P<0.05或0.01)。而且，EGb761显著地增加了草皮活动，减少的MDA层次和军邮局活动，并且没压制iNOS表示的下面规定伴随的产生(P<0.05或0.01)。结论：结果显示EGb761在II/R导致的肺损害上有保护的效果，它可能与它的抗氧化剂性质和嗜中性的累积的抑制有关并且导致iNOS没有产生。EGb761似乎是为有与II/R有关的呼吸衰竭的非常有病的病人的一个有效治疗学的代理人。

简介：BACKGROUND:Mailuoning,aChineseherb,hasbeenwidelyusedinChinatotreatacuteischemicstroke,andthemajorcomponentexhibitsanti-oxidativeeffects.However,thepreciseanti-oxidationpathwayremainsuncertain.OBJECTIVE:TovalidatetheprotectiveeffectsofMailuoningonH2O2-inducedprimarycorticalneuroninjuryinembryonicmice.DESIGN,TIMEANDSETTING:ComparativeobservationandinvitroexperimentswereperformedattheJiangsuKeyLaboratoryforMolecularMedicinefromJanuary2008toSeptember2009.MATERIALS:Mailuoning(NanjingJinlingMedicalCompany,China),reactiveoxygenspecies(ROS)kit(BeyotimeBiotechnology,China),superoxidedismutase(SOD),Cu/ZnSODkit,malondialdehyde(MDA)kits(NanjingJiancheng,China),mitochondrialmembranepotential(GMS10013.1,GENMED,USA)andcatalaseactivityassaykit(BeyotimeBiotechnology,China)wereutilizedforthepresentstudy.METHODS:MouseembryoniccorticalneuronswereisolatedandculturedwithculturemediumcontainingH2O2(80μmol/L)and/orMailuoning(1.25μg/mL)for24hours.MAINOUTCOMEMEASURES:Neuronalviabilityanddeathweredetectedbymethylthiazolyltetrazdiumandflowcytometry;ROSproductionwasdeterminedbyflowcytometry;mitochondrialmembranepotentialwasdetectedusingfluorescentstaining;SODactivitywasdetectedusingamodifiednitrobluetetrazoliummethod;Cu/ZnSODandcatalaseactivitywasdetectedbyspectrophotometry;andMDAwasdeterminedusingthelipidperoxidationmethod.RESULTS:H2O2increasedROSproductionandMDAconcentration(P<0.05),anddecreasedmitochondrialmembranepotential,SOD,Cu/ZnSODandcatalaseactivity(P<0.05);thenumberofsurvivingneurons(P<0.05)wasalsoreduced.Mailuoningreversedthesechanges.CONCLUSION:MailuoningprotectsH2O2-inducedinjuryincorticalcellsbyinhibitingROSandMDA,increasingdepolarizationofmitochondrialmembrane,andenhancingSODandcatalaseactivity.

简介：Thispaperaimstotheresearchoftheimpactoffluidshearstressontheadhesionbetweenvascularendothelialcellsandleukocyteinducedbytumornecrosisfactor-α(TNF-α)bymicrofliudicchiptechnology.Microfluidicchipwasfabricatedbysoftlithograph;Endothelialmicrofluidicchipwasconstructedbyoptimizingtypesoftheextracellularmatrixproteinsmodifiedinthemicrochannelandcellincubationtime;humanumbilicalveinendothelialcellsEA.Hy926linedinthemicrochannelwereexposedtofluidshearstressof1.68dynes/cm~2and8.4dynes/cm~2respectively.Meanwhile,adhesionbetweenEA.Hy926cellsandleukocytewasinducedbyTNF-αunderaflowcondition.EA.Hy926cellculturedinthestaticconditionwasusedascontrolgroup.Thenumbersoffluorescently-labeledleukocyteinmicrochannelwerecountedtoquantizetheadhesionlevelbetweenEA.Hy926cellsandleukocyte;cellimmunofluorescencetechniquewasusedtodetecttheintercellularadhesionmolecule(ICAM-1)expression.TheconstructedendothelialmicrofluidicchipcanaffordtothefluidshearstressandrespondtoexogenousstimulusofTNF-α;comparedwiththeadhesionnumbersofleukocyteincontrolgroup,adhesionbetweenEA.Hy926cellsexposedtolowfluidshearstressandleukocytewasreducedunderthestimulusofTNF-αataconcentrationof10ng/ml(P<0.05);leukocyteadhesionwithEA.Hy926cellsexposedtohighfluidshearstresswasreducedsignificantlythanEA.Hy926cellsincontrolgroupandEA.1Hy926cellsexposedtolowfluidshearstress(P<0.01);theregulationmechanismoffluidshearstresstotheadhesionbetweenEA.Hy926cellsandleukocyteinducedbyTNF-αwasthroughthewayofICAM-1.Theendothelialmicrofluidicchipfabricatedinthispapercouldbeusedtostudythefunctionsofendothelialcellinvitroandprovideanewtechnicalplatformforexploringthepathophysiologyoftherelatedcardiovascularsystemdiseasesunderaflowenvironment.

简介：Angiogenesis在出生后的生命期间在胚胎的脉管的树的发展以及处于几个正常、病理学的条件起一个基本作用。Bloodsupply，由neovascularization建立了，在愈合弯屈期间为histogenesis是必要的以及变长的手足在骨胳的损伤sequalae的治疗广泛地适用。Butlittle注意对这个区域被给予了。这评论试图在机械应力下面总结angiogenesis规定，在愈合的创伤中的angiogenesis的过程和angiogenesis，特别地与紧张压力原则联合。

简介：介绍Cystone是为各种各样的尿混乱在印度使用的同意的Ayurvedicpolyherbal专卖药品，包括urolithiasis。试图在urolithiasis把Cystone的保护的效果与导致hyperoxaluria的氧化应力和钙盐水晶免职作比较。方法乙烯乙二醇(例如)(0.75%，V/V)在喝，水被给老鼠28天与Cystone(500和750mg/kg身体重量)的同时的处理导致urolithiasis，并且urolithiasis的各种各样的尿风险因素和抗氧化剂标记被估计。例如结果处理导致增加的尿体积和降低的尿pH与盐的增加的尿排泄一起，在未经治疗的动物的钙和磷酸盐。这些变化在未经治疗的老鼠的肾引起了广泛的钙盐水晶免职，增加的类脂化合物peroxidation和抗氧化剂酶(草皮，过氧化氢酶和GPx)的减少的活动。Cystone阻止了这些hyperoxaluric表明并且在两剂量在对待的老鼠禁止了钙盐水晶免职。结论Cystone治疗由改进肾的织物抗氧化剂地位和多尿对导致hyperoxaluria的氧化应力和钙盐水晶免职提供保护。

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简介：AbstractOxidative stress is caused by the imbalance between the generation of free radicals/reactive oxygen species (ROS) and the antioxidant defense systems, which can activate various transcription factors and affect their transcriptional pathways. Oxidative stress plays an important role in the occurrence and development of leukemia and is closely related to the treatment and prognosis of leukemia. The standard chemotherapy strategies for the pre-treatment of leukemia have many drawbacks. Hence, the usage of antioxidants and oxidants in the treatment of leukemia is being explored and has been preliminarily applied. This article reviews the research progress of oxidative stress and leukemia. In addition, the application of antioxidants treatment in leukemia has been summarized.

简介：Plantcelllinesdifferredgreatlyintheabilitytowithstandshearstresses.Usingto-baccocellsandlicoricecellsasmodelplantcells,westudiedtheeffectsofshearstressesonthevi-abilityofplantcells.OurexperimentswerecarriedoutonahighshearrateCouetterheometerprovidinghomogeneousandconstantshearstressesoflaminarflow.TheviabilitywasdeterminedbyTTC（2,3,5-Triphenyltetrazoliumchloride）.Theresultswereasfollows.（1）Theviability（V）droppedexponentiallywithtime（t）,namelyV=Exp（-kt）,（k>oisaconstant）.Thismeantthetenabilityofstatisticalhomogeneity.（2）Thevalueofkwasafunctionofplantcells’mechanicalpropertiesandtheshearstressactingontheplantcells.Theshearratecorrespondingtok=owasthecriticalshearratethattheplantcellscouldwithstand.Itcanbeeasilydetermindedbyextrapo-lation.For7-day-oldtobaccocells,itwas1090s-1andfor9-day-oldlicoricecells,itwas6566s-1.（3）Theplantcellsuspensionswerepseudoplasticfluidsfittingτ=Kγn.Forthetobaccocellsus-pensiontested,n=O.73,andforthelicoricecellsuspensiontestedn=0.7.Thusthecriticalshearstressforthetobaccocellswas25dynes/cm2andforthelicoricecellsitwas80dynes/cm2.（4）Oneoftheirreasonsforlicoricecellstohavegreatertolerancetoshearstressesthantobacaccocellsmaybethegeometricfeaturesofthecellsandthesizesofthecells.Thelicoricecellswererod-shaped,butthetobaccocellsweresphericalandlargerthanthelicoricecells.

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.

简介：AbstractObjective:To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model.Methods:Pregnant rats (n=60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups),and were studied on the 17th, 19th, and 21st gestational days (GD) (n=5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons.Results:A significant difference was found in placenta weight (F=8.10, P<0.05), fetal rat weight (F=40.86, P<0.05), fetal rat length (F=61.61, P<0.05), and fetal rat tail length (F=55.63, P<0.05) among four groups on the 17th ,19th , and 21st GD.What’s more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant (F=2.48, P<0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46±0.15 vs. 0.24±0.09, P<0.05), EE (0.46±0.15 vs. 0.17±0.04, P>0.05), and IR (0.46±0.15 vs. 0.22±0.15, P>0.05) groups at 19th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42±0.05 vs. 0.58±0.12, P<0.05), UCN (0.43±0.01 vs. 0.47±0.16, P>0.05), and WFS1 (0.57±0.07 vs. 0.74±0.12, P>0.05) protein in the EE-IR group was subsided compared to the IR group at 17th GD.Conclusion:Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.

简介：Objective:ToinvestigatethedynamicsofplasmacAMP/Cgmpinpatientsduringcardiacsurgery,anditsrelationshiptotraumaticstress.Methods:Sixteenpatients,aged19.31years±10.4years,whounderwentanopenheartoperationwithcardiopulmonarybypass(CPB)andhypothermiawereservedassubjects.Thearterialplasmaconcentrationsofcyclicadenosinemonophosphate(Camp)andcyclicguanosinemonophosphate(Cgmp)weremeasuredbyradioimmunoassay2hoursbeforeoperation,afterheparinization,20minutesfollowingCPB,attheendoftheoperation,and24and72hourspostoperatively,respectively.Thepatients'preoperativebloodsampleswereheparinizedandthevenousbloodsamplesof30healthyblooddonorsweretakentomeasurethelevelsofCampandcGMPasheparinandnormalcontrolsseparately.Results:Therewerenostatisticaldifferenceamongtheheparincontrol,preoperativelevelandnormalcontrol.ThepeakvaluesofCampandCgmpoccurredduringCPBandplasmaCamplevelschangedsynchronouslywithintensitiesofoperativestimulustohumanbody.HowevercGMPlevelwasmainlyrelatedtotheoperativestimulustotheheartandCPB.TheCampvaluewaspositivelycorrelatedwiththeCgmpvalue(r=0.6313,P＜0.001).Conclusions:Dynamicvariationofplasmacyclicribonucleotidecanbeconsideredasareferenceparameterforintensityoftraumaticstress.

简介：Depression/anxiety-relateddisordersandpsychosocialstresshavebeenimplicatedascardiovasculardisease(CVD)riskfactors.Womenareatconsiderableriskforaffectivedisordersandreportgreaterseverityfrompsychosocialstress,comparedtomen.Affectivedisordersandcardiovasculardiseaselikelyshareunderlyingpathophysiologicalmechanismsthatarepotentiatedamongwomen–especiallyyoungerwomen.Environmentalstressorsthatthreatenthesafety,security,andstatusofanindividualareappraisedbythebrain,producingacascadeofevokedphysiologicalandcognitiveresponses.Intheshortterm,theseprocessesovercomestressors,butcomewithlong-termhealthimplications.Chronicpsychosocialstressleadstoadysregulationofthestressresponsesystemsthatcanleadtoaheightenedstressappraisalschemacalledtheunpredictabilityschema,aconstructthatmightarguablyplacewomenatheightenedriskforCVD.

简介：客观：为了在臀部以后学习大腿骨的新潮的修复术的压力分发，连接代替。方法：在新潮的联合代替以后，腿节和修复术什么时候完美地被认为柱体同样同心与banded接口，模仿界面的压力转移的一个相对完美的理论模型被建立。结果：最大值界面砍应力发生在Z=0。在大腿骨的颈的剖面图，界面砍应力随Z的增加指数地减少了。砍应力在Z0.1m变得很小，它意味着在大腿骨的新潮的修复术的远目的shear压力是很小的。为了避免压力集中和大腿骨的新潮的修复术，下沉、界面的应力必须在Z=0仍然保持与压力负担不变、平衡。大腿骨的新潮的修复术的半径随着变化了界面砍应力。半径的最大的价值发生在Z=0，然后，它在m减少了。特殊，在Z=10公里的a=18.2公里，在Z=98公里的a=5.36公里，这些是理想的半径。结论：模仿界面的压力的一个理论模型被证实腿节和修复术是否被认为柱体同样同心。分布界面砍并且有轴的位置的光线的压力被获得。为修复术的设计的一本理论参考书被提供。

简介：AbstractBackground:The detrimental outcomes of right ventricular pacing on left ventricular electromechanical function ultimately result in heart failure, a phenomenon termed pacing-induced cardiomyopathy (PICM) in clinical research. This study aimed to validate prognostic factors that can be used to identify patients with higher susceptibility to progress to the stage of cardiomyopathy before pacemaker implantation.Methods:This observational analysis enrolled 256 patients between January 2013 and June 2016, 23 (8.98%) of whom progressed to PICM after 1 year of follow-up. A Cox proportional hazard model was used to analyze the prognostic factors associated with PICM. Dose-response analysis was used to evaluate the relationship between significant indicators in multifactor analysis and PICM.Results:The mean values of left ventricular ejection fraction before and after pacemaker implantation in 23 patients diagnosed with PICM were 62.3% and 42.7%, respectively. Univariate analysis showed that sex, atrio-ventricular block, paced QRS duration, and ventricular pacing percentage were significantly associated with PICM. In the multivariate analysis, male sex (hazard ratio: 1.20, 95% confidence interval [CI]: 1.09-1.33, P < 0.005), paced QRS duration (hazard ratio: 1.95 per 1 ms increase, 95% CI: 1.80-2.12, P < 0.001), and ventricular pacing percentage (hazard ratio: 1.65 per 1% increase, 95% CI: 1.51-1.79, P < 0.001) were independent prognostic factors associated with the development of PICM. The ventricular pacing percentage and paced QRS duration level defined by the dose-response analysis were positively associated with PICM (P < 0.05).Conclusions:Our findings indicated that paced QRS duration and ventricular pacing percentage were the most sensitive prognostic factors for PICM.