目的 探索慢性肾脏病维持性血液透析患者的有效管理模式.方法 采取自身前后对照研究,筛选血磷≥1.78 mmol/L的规律透析患者入组,组建医护患质量改善团队,采取责任护士分组管理,运用五"E"模式通过鼓励、教育、运动、工作、评价5项措施干预18个月,并评价患者自我管理能力和血磷水平改善情况.结果 五"E"模式干预18个月后,患者自我管理各维度及总分较干预前明显提高,血磷平均值由(2.15±0.32)mmol/L下降至(1.78±0.42)mmol/L(t=6.249,P<0.01),血磷<1.78 mmol/L的比例提升60.32％;NT-proBNP平均值下降幅度43.24％.结论 运用五"E"模式对透析患者进行全程管理,形成以护士为主导的医护患多团队协作一体化闭环管理架构,可以提高患者自我管理能力,有利于患者的预后及提高生活质量.

Unsafe injection has become a serious public health safety problem. Intravenous infusion therapy is the most common injection operation in clinical practice. Many details of drug handling, device selection, and intravenous infusion therapy operations are related to safe injection. This article introduces the definition of safe injection, and briefly describes the impact of unsafe injection behaviors on patients and medical staff during static therapy from the perspectives of patients and medical staff, and analyzes the risky links of unsafe injection during intravenous therapy. It also points out that to reduce the cross-infection of blood-borne infectious diseases caused by unsafe injections to patients, it is necessary to formulate industry standards and operating procedures, establish and improve infection prevention and control training systems, carry out risk assessment and quality management, and build an effective safety barrier for both doctors and patients by strengthening the management in top-level design, medical staff training, and occupational exposure prevention support systems.

Objective To study the role of TLR4 in angiotension Ⅱ(AngⅡ)-induced vascular remodeling of hypertensive mice.Methods Eighteen wild C57 mice were divided into control group,AngⅡgroup and TLR4 group(6 in each group).The mice were infused with AngⅡfor 7 days and injected with TLR4 through the tail vein to neutralize antibodies 2 days before AngⅡinfusion and 7 days after AngⅡinfusion.Expressions of ET-1,α-SMA,PCNA,ICAM-1 and CD69 were detected by immunohistpchemistry and flow cytometry,respectively.Results The blood pressure and expression levels of ET-1,ICAM-1 and CD69 were significantly higher whereas the expression level of α-SMA was significantly lower in AngⅡgroup than in control group(P<0.05,P<0.01).The blood pressure and expression levels of ET-1,PCNA,ICAM-1 and CD69 were significantly lower whereas the expression level of α-SMA was significantly higher in TLR4 group than in AngⅡgroup(P<0.05,P<0.01).Conclusion TLR4 participates in AngⅡ-induced vascular remodeling of hypertensive mice by mediating inflammatory reactions.

Objective To study the role of TLR4 in angiotension II(Ang II )-induced cardiac fibrosis in hypertensive mice.Methods Eighteen male wild-type mice were divided into blank control group,Ang II group,and TLR4 blocking group(6 in each group).A hypertension model was established by Ang II perfusion with a micropump.Blood pressure was measured in mice through the tail artey cuff and heart function of the mice was tested by echocardiacgraphy after injection of TLR4 neutralizing antibodies through the tail artery.Cardiac fibrosis in the mice was observed with immunohistochemical and Masson staining.Expressions of myocardial interleukin 1(3 and mononuclear cell chemotactic protein 1 mRNA were detected by RT-PCR.Results The blood pressure was lower,the left ventricular wall was thinner,the inner diameter of left ventricule at the end-diastolic phase was larger,the number of infiltated Mac-2 positive macrphygocytes was less,the expression level of interleukin 1βand mononuclear cell chemotactic protein 1 mRNA was lower,and the fibrosis of myocardial interstitium and peripheral blood vessels was milder in TLR4 blocking group than in Ang U group(P<0.05).Conclusion TLR4 participates in Ang II -induced cardiac fibrosis in hypertensive mice by mediating inflammatory reactions.