简介:马自达公司将MX-Crossport概念车投入量产,新车名为CX-7,量产版马自达CX-7继承了MX-Crossport概念车中大部分的设计理论,具备优异的性能,驾乘者将会体验到无尽的操控乐趣。
简介:摘要CX3CL1亦称分形趋化因子,是趋化因子CX3C亚类中的唯一成员,通过与其特异性受体CX3CR1结合,在多种中枢神经系统疾病和缺血性脑血管病中发挥重要作用。近年来,大量研究对CX3CL1/CX3CR1的具体作用和相关分子机制进行了探讨。本文就CX3CL1/CX3CR1在缺血性脑血管病中的作用和相关分子机制进行综述,旨在拓展对CX3CL1/CX3CR1作用机制的认识,为缺血性脑血管病的预防、诊断及治疗提供新的思路与干预靶点。
简介:摘要目的评价再灌注房性心律失常大鼠心房肌电传导降低与缝隙连接蛋白40(Cx40)和Cx43的关系。方法取成功建立的Langendorff离体灌注模型的心脏16个,采用随机数字表法分为对照组(C组)和缺血再灌注组(IR组),每组8个。根据是否发生再灌注房性心律失常将IR组分为再灌注非房性心律失常亚组(R-NAA组)和再灌注房性心律失常亚组(R-AA组)。C组使用37 ℃K-H液平衡灌注120 min。IR组使用37 ℃K-H液平衡灌注30 min,停止灌注后注射4 ℃ Thomas液20 ml/kg使心脏停搏60 min,心脏周围用4 ℃Thomas液保护,停搏30 min时复灌4 ℃Thomas液10 ml/kg,然后再次灌注37 ℃K-H液30 min。于平衡灌注120 min或再灌注30 min时,测定右心房有效不应期(ERP)和传导速度(CV),采用Western blot法检测右心房肌Cx40和Cx43的表达,计算Cx40/Cx40+Cx43比值和Cx43/Cx40+Cx43比值。结果IR组再灌注房性心律失常发生率为38%。与C组比较,R-NAA组和R-AA组ERP延长,CV降低,Cx40和Cx43表达下调,Cx40/Cx40+Cx43比值升高,Cx43/Cx40+Cx43比值降低(P<0.05);与R-NAA组比较,R-AA组ERP延长,CV降低,Cx40和Cx43表达下调,Cx40/Cx40+Cx43比值升高,Cx43/Cx40+Cx43比值降低(P<0.05)。结论再灌注房性心律失常大鼠心房肌电传导功能降低可能与Cx40和Cx43表达下调有关。
简介:Objective:ToinvestigatethemembranelocalizationfunctionoftheCX26proteinwhenits86thaminoacidisThr,SerorArg,anditsrelationstodeafness.Methods:CX26-GFPproteinwitheitherThr,SerorArgasthe86thaminoacidwasexpressedinmouseSGNcellsviatheGFPfusiontypelentivirusexpressionsystem.Themembranelocalizationofthefusionproteinwasobservedunderafluorescencemicroscope.Results:ThemutatedproteinofCX26T86Swaslocalizedtocellmembraneandformgapconjunctionstructures,showingnodifferencetothewildtypeCX26protein(withThrasthe86thaminoacid).However,thegapconjunctionstructuredisappearedwhenthemutationwasCX26T86A.Conclusion:TheseresultsindicatethattheCX26T86Rmutationmaybeacauseofhearingloss,butCX26T86Sasanon-pathogenicpolymorphismmutationdoesnotaffectfunctionsoftheCX26protein.Theresultsareinaccordancewiththeresultsofclinicalscreening.
简介:AbstractBackground:Microglia plays an indispensable role in the pathological process of sleep deprivation (SD). Here, the potential role of microglial CX3C-chemokine receptor 1 (CX3CR1) in modulating the cognition decline during SD was evaluated in terms of microglial neuroinflammation and synaptic pruning. In this study, we aimed to investigat whether the interference in the microglial function by the CX3CR1 knockout affects the CNS’s response to SD.Methods:Middle-aged wild-type (WT) C57BL/6 and CX3CR1-/- mice were either subjected to SD or allowed normal sleep (S) for 8 h to mimic the pathophysiological changes of middle-aged people after staying up all night. After which, behavioral and histological tests were used to explore their different changes.Results:CX3CR1 deficiency prevented SD-induced cognitive impairments, unlike WT groups. Compared with the CX3CR1-/- S group, the CX3CR1-/- SD mice reported a markedly decreased microglia and cellular oncogene fos density in the dentate gyrus (DG), decreased expression of pro-inflammatory cytokines, and decreased microglial phagocytosis-related factors, whereas increased levels of anti-inflammatory cytokines in the hippocampus and a significant increase in the density of spines of the DG were also noted.Conclusions:These findings suggest that CX3CR1 deficiency leads to different cerebral behaviors and responses to SD. The inflammation-attenuating activity and the related modification of synaptic pruning are possible mechanism candidates, which indicate CX3CR1 as a candidate therapeutic target for the prevention of the sleep loss-induced cognitive impairments.