Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

西洛他唑抗动脉粥样硬化的作用机制

目的观察西洛他唑对兔动脉粥样硬化斑块组织的影响,进一步探讨西洛他唑抗动脉粥样硬化作用及其可能机制。方法将30只新西兰雄性白兔随机分为正常对照组、高脂饮食组和西洛他唑组。酶法检测血脂,免疫沉淀法测定血清C反应蛋白水平,免疫组织化学检测基质金属蛋白酶9和核因子κB的表达,病理形态学分析各组主动脉内膜厚度和斑块面积,逆转录聚合酶链反应检测血管组织单核细胞趋化蛋白1mRNA的表达。结果实验第12周末,西洛他唑组总胆固醇、甘油三酯和低密度脂蛋白胆固醇水平低于高脂饮食组,但高于正常对照组(P均<0.01);西洛他唑组主动脉内膜厚度和斑块面积低于高脂饮食组,但大于正常对照组(P均<0.01);西洛他唑组核因子κB、单核细胞趋化蛋白1和基质金属蛋白酶9的表达弱于高脂饮食组,但强于正常对照组(P均<0.01)。结论西洛他唑有抗动脉粥样硬化作用,其作用机制可能与下调核因子κB、单核细胞趋化蛋白1及基质金属蛋白酶9的表达有关。     

兔左室楔形心肌组织块对药物致心律失常作用评估的价值

目的探讨冠状动脉灌流的兔左室楔形心肌组织块模型对药物致心律失常作用评价的价值。方法对6种临床上致心律失常发生率已知的药物,应用冠状动脉灌流的兔左室楔形心肌块对其致心律失常危险度进行评价。采用浮置玻璃微电极法同步记录心内膜、心外膜心肌细胞跨膜动作电位及跨室壁心电图。观察记录QT间期、复极离散度和心律失常来量化每种药物的相对危险度。结果临床上无致心律失常作用的药物其危险度评分小于等于0.1,临床上有致心律失常作用的药物其危险度评分介于1.2至9.8之间。结论应用冠状动脉灌流的兔左室楔形心肌组织块模型评价药物致心律失常作用具有较高的价值。     

雷诺嗪:抗慢性心绞痛药物新成员

雷诺嗪是哌嗪类衍生物,多个临床试验证实其有确切的抗心绞痛作用和良好的耐受性及安全性,而对血流动力学无影响,2006年已被批准与其它抗心绞痛药物联合治疗慢性心绞痛,其作用机制可能与部分抑制脂肪酸氧化、抑制晚钠电流从而减轻细胞内钙超载有关。现综述了雷诺嗪的药代动力学特征、可能的作用机制及治疗心绞痛的相关临床试验。     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

心房颤动与炎症和氧化应激

许多证据表明心房颤动中存在炎症和氧化应激,炎症和氧化应激可导致心房重构,包括电重构和结构重构,提示炎症和氧化应激可能在心房颤动的发生和维持中起着一定作用。抗炎和抗氧化治疗可减少心房颤动的发生和复发,这为干预心房颤动的发生和复发提供了新思路。     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

对公众参与基本公共卫生服务的思考

揭示了基本公共卫生服务中公众参与的内涵;分析了公众参与基本公共卫生服务的必要性;总结了当前我国公众参与基本公共卫生服务中存在的问题,包括:公众参与意识不强、医疗卫生机构不恰当的引导、非政府组织(NGO)在基本公共卫生服务中的缺乏、公众对非政府组织的信任缺失。提出了相对应的政策建议:如加强健康教育宣传力度、充分推进社区参与、大力发挥非政府组织(NGO)的作用、利用新闻媒介广泛宣传等。     

老年慢性病住院患者多重用药的影响因素研究

目的：通过问卷调查研究影响慢性病住院患者多重用药行为的影响因素,提出针对性的建议以控制多重用药。方法：通过文献研究及专家咨询等方法设计调查问卷,采用整群抽样的方法,选取武汉市6家三甲医院,进行问卷调查,利用SPSS软件进行单因素分析及二分类Logistic回归分析。结果：共收集到60岁及以上老年慢性病患者问卷388份,结果显示患者的年收入、是否患有糖尿病、是否患有心脏病、是否患有肾脏疾病、药龄和周围人群有无不良反应以及自感疾病控制情况对患者是否多重用药具有显著影响。结论：我国老年患者多重用药情况严重,发生多重用药行为与患者个人自身健康素养及疾病治疗情况有关,同时发现医疗机构对慢性病患者健康管理作用不显著,未来需从普及合理用药知识与加强各级医疗机构对慢性病健康管理入手,以促进患者合理用药,避免不合理多重用药。     

学术型临床医学博士生科研能力与综合素养影响因素分析——基于院校影响因素理论模型

目的基于院校影响因素理论模型,探究影响学术型临床医学博士生科研能力与综合素养的关键影响因素。方法采用定性与定量结合的研究模式,对某“双一流”建设高校附属医院256名学术型临床医学博士生展开调查。结果通过回归分析,发现课程和科研训练、情感支持、导师指导、学术生态硬环境和学术生态软环境对博士生能力与素养产生显著性影响关系(F=45.83,P<0.001),学术型临床医学博士生的科研能力与综合素养在年级、性别、年龄、生源、培养类型、培养环境等不同特征下差异均有统计学意义(P<0.01)。结论基于培养过程视角设立的5个影响因素维度是影响学术型临床医学博士生科研能力与综合素养的关键因素,有助于提升临床医学博士生的培养质量。