地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

社区失能老年人照护服务需求调查研究

[目的]了解社区失能老年人基本情况及照护服务需求现状,为政府及社区制定完善的失能老年人长期照护政策提供有力支撑。[方法]采用方便抽样法,对北京市海淀区两个社区的220名失能老年人进行问卷调查。[结果]220名失能老年人中,轻度失能105人(47.73%)、中度失能60人(27.27%)、重度失能55人(25.00%);10项身体照顾服务需求中排序前5位的是：散步、聊天,使用生活辅助用具,翻身、叩背,服药,更换衣服;9项家务及日常生活照顾服务需求中排序前5位的是送餐服务、陪同就医或联络医疗机构、家务助理、家庭访视、陪同或代购;11项居家护理服务需求中排序前5位的是输液、抽血化验、雾化吸入、更换胃管、伤口换药;13项其他服务需求中排序前5位的是定期查体、医护人员上门服务、照护者指导、紧急救援、康复训练与指导。[结论]社区失能老年人对照护服务表现出非常迫切的需求,政府及相关部门应以失能老年人主观需求为基本导向,结合客观评估,制定更加规范的照护标准,提供行之有效且针对性强的长期照护服务,提高失能老年人生存质量。     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

目的 探讨地塞米松对布比卡因诱导小鼠神经母细胞瘤株(N2a)细胞毒性的影响.方法 N2a细胞悬液(105/ml)随机分为4组:对照组(C组)、布比卡因组(Bup组)、地塞米松组(Dex组)和地塞米松+布比卡因组(Dex+Bup组).各组N2a细胞分别接种于24孔培养板(0.5 ml/孔)和直径10 cm的培养皿中(7 ml/皿),每组24孔和4皿.C组不行干预;Bup组加入含900μmol/L布比卡因的MEM培养基500μl;Dex组加入含1μmol/L地塞米松的MEM培养基500μl;Dex+Bup组加入含1/μmol/L地塞米松的MEM培养基500μl孵育12 h后加入布比卡因900 μmol/L.于24孔板中孵育5 h时,测定线粒体跨膜电位(△Ψm);于24孔板中孵育9 h时观察细胞形态,并计算LDH释放率和细胞核固缩率;于培养皿中孵育5 h时测定磷酸化蛋白激酶B(p-Akt)和磷酸化胞外信号调节激酶(p-ERKs)的表达.结果 C组细胞多边形,胞体折光性强,突触伸展良好;Dex组细胞形态学与C组相似;Bup组细胞扁平,突触缩短或断裂,胞体折光性弱;Dex+Bup组扁平细胞减少,突触缩短或断裂减少,胞体折光性略低.与C组比较,Bup组LDH释放率和细胞核固缩率升高,△Ψm降低,p-ERKs和p-Akt表达下调,Dex+Bup组细胞核固缩率升高,△Ψm降低,p-ERK表达下调,p-AKt表达上调,Dex组p-ERKs和p-Akt表达上调(P<0.01).与Bup组比较,Dex+Bup组LDH释放率和细胞核固缩率降低,△Ψm增加,p-ERKs和p-Akt表达上调(P<0.01).结论 地塞米松可减轻布比卡因诱导N2a细胞毒性,其机制可能与恢复线粒体膜电位、抑制Akt和ERKs脱磷酸化有关.     

异丙肾上腺素对大鼠盐酸吸入性肺损伤动脉氧分压的影响

目的研究异丙肾上腺素对盐酸吸入诱导的急性肺损伤的动脉氧分压(PaO2)的影响。方法 SD大鼠全麻气管插管纯氧机械通气下随机分为三组,生理盐水对照组(NS组);盐酸致急性肺损伤组(ALI组);异丙肾上腺素治疗组(ISO组)。ISO组在气管内注入盐酸后1min静脉注入异丙肾上腺素,其余两组在相同时间点注射等量生理盐水。观察各组在气管内盐酸注入后10分钟,30分钟的PaO2值。结果与NS组比较,ALI组和ISO组在气管内注入盐酸后10分钟和30分钟的PaO2明显下降(P<0.01),但ISO组PaO2较ALI组相同时间点明显上升(P<0.01)。结论异丙肾上腺素在一定程度上能减轻盐酸吸入性肺损伤的程度。     

三阶段激励护理方案对淋巴瘤患者希望水平、家庭复原力及锻炼依从性的影响

目的:探讨三阶段激励护理方案对淋巴瘤患者希望水平、家庭复原力及锻炼依从性的影响。方法:选取2018年1月1日~2019年12月31日收治的59例淋巴瘤患者为研究对象,采用随机数字表法分为对照组29例和观察组30例。对照组给予常规护理,观察组在对照组基础上给予三阶段激励护理;比较两组化疗后希望水平[采用Herth希望量表(HHI)]、家庭复原力、锻炼依从性。结果:观察组HHI评分及等级、家庭复原力评定量表总分及亚量表评分、锻炼依从性与对照组比较差异均有统计学意义(P<0.05,P<0.01)。结论:三阶段激励护理方案可提升淋巴瘤患者希望水平、家庭复原力及锻炼依从性,提高其生活质量。