The increasing demand for industrial automation and intelligence has put forward higher requirements for the reliability of industrial wireless communication technology.As an international standard based on 802.11,Wir...The increasing demand for industrial automation and intelligence has put forward higher requirements for the reliability of industrial wireless communication technology.As an international standard based on 802.11,Wireless networks for Industrial Automation-Factory Automation(WIA-FA)greatly improves the reliability in factory automation scenarios by Time Division Multiple Access(TDMA).However,in ultra-dense WIA-FA networks with mobile users,the basic connection management mechanism is inefficient.Most of the handover and resource management algorithms are all based on frequency division multiplexing,not suitable for the TDMA in the WIA-FA network.Therefore,we propose Load-aware Connection Management(LACM)algorithm to adjust the linkage and balance the load of access devices to avoid blocking and improve the reliability of the system.And then we simulate the algorithm to find the optimal settings of the parameters.After comparing with other existing algorithms,the result of the simulation proves that LACM is more efficient in reliability and maintains high reliability of more than 99.8%even in the ultra-dense moving scenario with 1500 field devices.Besides,this algorithm ensures that only a few signaling exchanges are required to ensure load bal-ancing,which is no more than 5 times,and less than half of the best state-of-the-art algorithm.展开更多
目的:探讨丁苯酞对缺血性脑卒中大鼠海马神经元凋亡和p38 丝裂原活化蛋白激酶(p38MAPK)信号通路的影响,阐明丁苯酞对缺血性脑卒中的作用机制。方法: 102只雄性SD大鼠随机分为假手术组、模型组和丁苯酞组,每组34只。模型组和丁苯酞组大...目的:探讨丁苯酞对缺血性脑卒中大鼠海马神经元凋亡和p38 丝裂原活化蛋白激酶(p38MAPK)信号通路的影响,阐明丁苯酞对缺血性脑卒中的作用机制。方法: 102只雄性SD大鼠随机分为假手术组、模型组和丁苯酞组,每组34只。模型组和丁苯酞组大鼠采用改良Zea-Longa法制备局灶性脑缺血大鼠模型,丁苯酞组大鼠建模后给予丁苯酞(4.5 mg·kg^-1 )治疗,假手术组大鼠每天相同时间点腹腔注射等量生理盐水。采用HE染色观察大鼠海马神经元细胞形态表现,原位末端转移酶标记(TUNEL)染色观察大鼠海马神经元凋亡情况, Western blotting法测定大鼠海马组织中激活型caspase-3(cleaved caspase-3)、B淋巴细胞瘤-2(Bcl-2)、 Bcl-2 相关X蛋白(Bax)、p38、磷酸化p38(p-p38)和分裂原激活的蛋白激酶(MAPK)蛋白表达水平,逆转录-聚合酶链反应(RT-PCR)测定大鼠海马组织中cleaved caspase-3、Bax、Bcl-2、p38和MAPK mRNA表达水平。结果:假手术组大鼠海马CA1区神经元排列整齐,细胞核和细胞膜正常;模型组大鼠海马CA1区神经元排列紊乱,细胞肿胀破裂,细胞核固缩;丁苯酞组大鼠海马CA1区部分神经细胞结构恢复正常。与假手术组比较,模型组大鼠海马CA1区神经元数量明显降低( P <0.01),神经元凋亡指数明显增加( P <0.01);与模型组比较,丁苯酞组大鼠海马CA1区神经元数量明显增加( P <0.01),神经元凋亡指数明显降低( P <0.01)。与假手术组比较,模型组大鼠海马组织中cleaved caspase-3、Bax、p-p38和MAPK蛋白表达水平明显升高( P <0.01),Bcl-2蛋白 表达水平明显降低( P <0.01);与模型组比较,丁苯酞组大鼠海马组织中cleaved caspase-3、Bax、p-p38 和MAPK蛋白表达水平明显降低( P <0.01),Bcl-2蛋白表达水平明显升高( P <0.01)。与假手术组比较,模型组大鼠海马组织中cleaved caspase-3、Bax和MAPK mRNA表达水平明显升高( P <0.01),Bcl-2 mRNA 表达水平明显降低( P <0.01);与模型组比较,丁苯酞组大鼠海马组织中cleaved caspase-3 、Bax和MAPK mRNA表达水平明显降低( P <0.01),Bcl-2 mRNA表达水平明显升高( P <0.01)。结论:丁苯 酞可通过抑制海马组织p38 MAPK信号通路抑制缺血性脑卒中大鼠海马神经元凋亡。展开更多
基金supported by NSFC project(grant No.61971359)Chongqing Municipal Key Laboratory of Institutions of Higher Education(grant No.cquptmct-202104)+1 种基金Fundamental Research Funds for the Central Universities,Sichuan Science and Technology Project(grant no.2021YFQ0053)State Key Laboratory of Rail Transit Engineering Informatization(FSDI).
文摘The increasing demand for industrial automation and intelligence has put forward higher requirements for the reliability of industrial wireless communication technology.As an international standard based on 802.11,Wireless networks for Industrial Automation-Factory Automation(WIA-FA)greatly improves the reliability in factory automation scenarios by Time Division Multiple Access(TDMA).However,in ultra-dense WIA-FA networks with mobile users,the basic connection management mechanism is inefficient.Most of the handover and resource management algorithms are all based on frequency division multiplexing,not suitable for the TDMA in the WIA-FA network.Therefore,we propose Load-aware Connection Management(LACM)algorithm to adjust the linkage and balance the load of access devices to avoid blocking and improve the reliability of the system.And then we simulate the algorithm to find the optimal settings of the parameters.After comparing with other existing algorithms,the result of the simulation proves that LACM is more efficient in reliability and maintains high reliability of more than 99.8%even in the ultra-dense moving scenario with 1500 field devices.Besides,this algorithm ensures that only a few signaling exchanges are required to ensure load bal-ancing,which is no more than 5 times,and less than half of the best state-of-the-art algorithm.
文摘目的:探讨丁苯酞对缺血性脑卒中大鼠海马神经元凋亡和p38 丝裂原活化蛋白激酶(p38MAPK)信号通路的影响,阐明丁苯酞对缺血性脑卒中的作用机制。方法: 102只雄性SD大鼠随机分为假手术组、模型组和丁苯酞组,每组34只。模型组和丁苯酞组大鼠采用改良Zea-Longa法制备局灶性脑缺血大鼠模型,丁苯酞组大鼠建模后给予丁苯酞(4.5 mg·kg^-1 )治疗,假手术组大鼠每天相同时间点腹腔注射等量生理盐水。采用HE染色观察大鼠海马神经元细胞形态表现,原位末端转移酶标记(TUNEL)染色观察大鼠海马神经元凋亡情况, Western blotting法测定大鼠海马组织中激活型caspase-3(cleaved caspase-3)、B淋巴细胞瘤-2(Bcl-2)、 Bcl-2 相关X蛋白(Bax)、p38、磷酸化p38(p-p38)和分裂原激活的蛋白激酶(MAPK)蛋白表达水平,逆转录-聚合酶链反应(RT-PCR)测定大鼠海马组织中cleaved caspase-3、Bax、Bcl-2、p38和MAPK mRNA表达水平。结果:假手术组大鼠海马CA1区神经元排列整齐,细胞核和细胞膜正常;模型组大鼠海马CA1区神经元排列紊乱,细胞肿胀破裂,细胞核固缩;丁苯酞组大鼠海马CA1区部分神经细胞结构恢复正常。与假手术组比较,模型组大鼠海马CA1区神经元数量明显降低( P <0.01),神经元凋亡指数明显增加( P <0.01);与模型组比较,丁苯酞组大鼠海马CA1区神经元数量明显增加( P <0.01),神经元凋亡指数明显降低( P <0.01)。与假手术组比较,模型组大鼠海马组织中cleaved caspase-3、Bax、p-p38和MAPK蛋白表达水平明显升高( P <0.01),Bcl-2蛋白 表达水平明显降低( P <0.01);与模型组比较,丁苯酞组大鼠海马组织中cleaved caspase-3、Bax、p-p38 和MAPK蛋白表达水平明显降低( P <0.01),Bcl-2蛋白表达水平明显升高( P <0.01)。与假手术组比较,模型组大鼠海马组织中cleaved caspase-3、Bax和MAPK mRNA表达水平明显升高( P <0.01),Bcl-2 mRNA 表达水平明显降低( P <0.01);与模型组比较,丁苯酞组大鼠海马组织中cleaved caspase-3 、Bax和MAPK mRNA表达水平明显降低( P <0.01),Bcl-2 mRNA表达水平明显升高( P <0.01)。结论:丁苯 酞可通过抑制海马组织p38 MAPK信号通路抑制缺血性脑卒中大鼠海马神经元凋亡。
