冠心病患者血清脂蛋白(a)水平临床分析

目的:评价血清脂蛋白(a)[Lp(a)]在冠心病(CHD)诊疗中的地位和作用。方法:取250例患者血清进行测定Lp(a)和总胆固醇(TC)、甘油三脂(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),其中正常组63例,冠心病组89例,高血压病组52例,其它类心脏病组46例。结果:①冠心病组血清Lp(a)较其他3组均显著升高(P<0.01),高血压组和其它类心脏病组与正常组Lp水平比较,无显著统计学差异(P>0.05);②冠心病单支病变组、2支病变组、2支以上病变组各组间血清Lp(a)水平比较差异均有统计学意义;③冠心病非急性心肌梗死患者与急性心肌梗死患者血清Lp(a)浓度无明显差异(P>0.05);④多因素逐步回归分析表明,Lp(a)与TG、TC、HDL-C之间无显著相关。结论:高Lp(a)水平是冠心病的独立危险因子,对于预测冠心病的发生有一定的价值,但对于预测冠心病急性心血管病事件的发生却未见明显的优势。     

锁定钢板治疗复杂肱骨外科颈骨折的临床应用

目的:探讨并分析锁定钢板治疗复杂肱骨外科颈骨折的应用优势及临床疗效. 方法:经切开复位后,利用锁定钢板固定治疗复杂肱骨外科颈骨折患者26例. 结果:26例骨折患者手术后,随访8~12个月,平均10.2个月,按照CSS评分标准,观察患者术后肩关节功能恢复状况. 其中优20例,良4例,可1例,优良率为92.3%. 结论:在肱骨近端利用锁定钢板治疗复杂肱骨外科颈骨折,具有手术操作简便易行,固定后牢固稳定,连接可靠,术后出现的并发症极少,骨折愈合率高,肩关节功能恢复好等优点,是一种治疗复杂肱骨外科颈骨折的理想方法,值得在临床应用并推广.     

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.     

促红细胞生成素通过PI3-K/Akt信号通路抑制血管紧张素II诱导的新生大鼠心脏成纤维细胞增殖

目的： 探讨促红细胞生成素（EPO）对血管紧张素Ⅱ(Ang Ⅱ)诱导的心脏成纤维细胞（CFs）增殖的影响,以及磷脂酰肌醇-3-激酶/蛋白激酶B（PI3-K/Akt）信号途径和一氧化氮合酶（NOS）的作用。方法: 应用胰酶和胶原酶双酶和差速贴壁法分离培养新生大鼠CFs细胞,应用EPO、Ang Ⅱ、PI3-K抑制剂LY294002、NOS抑制剂L-NAME不同因素干预。细胞计数和MTT法作出CFs的生长曲线,检测CFs的增殖。化学酶法检测CFs培养液中的一氧化氮（NO）浓度以及总NOS和其亚型的活性。Western blotting检测Akt、p-Akt、内皮型一氧化氮合酶（eNOS）和诱生型一氧化氮合酶（iNOS）蛋白的表达。结果: Ang Ⅱ促CFs增殖的作用显著。EPO剂量依赖性的增加CFs培养液中的NO浓度,同时剂量依赖性的抑制Ang Ⅱ诱导的CFs增殖。在给药后第4 d,和单纯的Ang Ⅱ相比,浓度为5×103 U/L、1×104 U/L和2×104 U/L EPO对CFs增殖的抑制率分别达到了24.4％、41.5%和50.5%。EPO显著提高Akt的磷酸化水平,促进eNOS蛋白的表达。应用PI3-K抑制剂LY294002和NOS抑制剂L-NAME均能使培养液中的NO浓度也随之下降,EPO抑制Ang Ⅱ诱导CFs增殖的作用均被阻断。但LY294002同时阻断了eNOS蛋白表达,而L-NAME对eNOS没有影响。结论: EPO可剂量依赖性的抑制Ang Ⅱ诱导的新生大鼠CFs的增殖。其作用机制是通过激活PI3-K/Akt信号途径促使CFs中eNOS表达来促进NO的生成,从而抑制CFs的增殖。     

促红细胞生成素通过P13-K／Akt信号通路抑制血管紧张素Ⅱ诱导的新生大鼠心脏成纤维细胞增殖

目的：探讨促红细胞生成素（EPO）对血管紧张素11（AngⅡ）诱导的心脏成纤维细胞（CFs）增殖的影响,以及磷脂酰肌醇-3-激酶／蛋白激酶B（P13-K／Akt）信号途径和-氧化氮合酶（NOS）的作用。方法：应用胰酶和胶原酶双酶和差速贴壁法分离培养新生大鼠CFs细胞,应用EPO、AngⅡ、P13-K抑制剂LY294002、NOS抑制剂L—NAME不同因素干预。细胞计数和MTT法作出CFs的生长曲线,检测CFs的增殖。化学酶法检测CFs培养液中的-氧化氮（NO）浓度以及总NOS和其亚型的活性。Western blotting检测Akt、P—Akt、内皮型-氧化氮合酶（eNOS）和诱生型-氧化氮合酶（iNOS）蛋白的表达。结果：AngⅡ促CFs增殖的作用显著。EPO剂量依赖性的增加CFs培养液中的NO浓度,同时剂量依赖性的抑制AngⅡ诱导的CFs增殖。在给药后第4d,和单纯的AngⅡ相比,浓度为5&#215;10。U／L、1&#215;10^4U／L和2&#215;10^4U／LEPO对CFs增殖的抑制率分别达到了24．4％、41．5％和50．5％。EPO显著提高Akt的磷酸化水平,促进eNOS蛋白的表达。应用P13-K抑制剂LY294002和NOS抑制剂L—NAME均能使培养液中的NO浓度也随之下降,EPO抑制AngⅡ诱导CFs增殖的作用均被阻断。但LY294002同时阻断了cNOS蛋白表达,而L—NAME对cNOS没有影响。结论：EPO可剂量依赖性的抑制AngⅡ诱导的新生大鼠CFs的增殖。其作用机制是通过激活P13-K／Akt信号途径促使CFs中eNOS表达来促进NO的生成,从而抑制CFs的增殖。     

上肢骨折病人服的制作和应用

<正>在临床上,很多上肢骨折病人肢体肿胀或手术后有外固定的钢板,穿脱衣服不方便,不能满足个人卫生要求;由于自身不便,病人穿脱袖子需由陪护人员进行,病人无法配合,非常痛苦;医护人员检查、治疗时也不方便。为保持病人的患肢处于功能位,使患肢制动,现在一般采用三角巾对病人的患肢予以固定,使用三     

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.     

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.     

高脂蛋白a血症对冠状动脉支架术后再狭窄的影响

目的 探讨高血清脂蛋白(a)[LP(a)]血症与冠状动脉支架植入术后支架内再狭窄的关系.方法 对152例成功在我院行经皮冠状动脉成形术(PTCA)+支架植入术并于术后行冠状动脉造影随访的患者进行回顾性分析.分为再狭窄组(29例)和无再狭窄组(123例),检测患者血LP(a)水平,对其一般临床资料也进行调查分析.统计学采用Logistic多因素逐步回归分析.结果 2组患者在高LP(a)血症、吸烟、糖尿病比例方面差异均有统计学意义(P均<0.05).Logistic多因素逐步回归分析显示:LP(a)水平是支架术后支架内再狭窄发生的独立危险因素,RR为2.648,95%CI为1.066～6.575,P<0.05.其他因素如吸烟(P=0.023)、糖尿病(P=0.036)、支架类型(P=0.011)也与支架内再狭窄发生有关(P均<0.05).结论 高LP(a)血症是发生冠状动脉支架术后再狭窄的独立危险预测因素.