目的 探讨血清降钙素原(PCT)、白细胞介素-6(IL-6)和高敏肌钙蛋白T(hsTnT)在急性胰腺炎病人中的动态变化及其对病情变化的预测价值.方法 选取符合条件的轻度急性胰腺炎(MAP)病人42例、中度急性胰腺炎(MSAP)病人39例和重症急性胰腺炎(SAP)病人41例,分别于入院第1、3、7天采集静脉血测定血清PCT、IL-6和hsTnT水平,同时对所有病人进行急性生理和慢性健康评分系统Ⅱ(APACHEⅡ)评分和Balthazar CT严重指数(CTSI)评分.根据是否发生感染性胰腺坏死,将41例SAP病人分为感染组(23例)和未感染组(18例).比较不同组间病人血清PCT、IL-6和hsTnT水平,并用ROC曲线分析3个指标对SAP的预测能力.结果 胰腺炎病人血清PCT、IL-6、hsTnT水平于入院第3天达到高峰,之后逐渐下降,但第7天的水平仍高于第1天.SAP病人入院第1、3、7天血清PCT、IL-6、hsTnT水平均高于MAP及MSAP病人,差异有统计学意义(F=2.359～74.066,P＜o.05).Pearson相关分析显示,SAP病人血清PCT、IL-6水平及APACHEⅡ、CTSI评分与血清hsTnT水平均呈正相关(r =0.673～0.787,P＜0.05).感染组各时间点血清PCT、IL-6、hsTnT水平均显著高于未感染组(F=11.072～126.414,P＜0.05).ROC曲线分析显示,hsTnT对SAP的预测能力最强(AUC=0.892),1L-6对SAP的预测能力最弱(AUC=0.782),上述3个指标联合检测比传统指标联合检测对SAP有更高的预测能力(AUC=0.935 vs AUC=0.917).结论 血清PCT、IL 6、hsTnT水平的动态监测有助于对急性胰腺炎病情严重程度的判断和预后的评估.

目的 探讨miR-373-3p是否参与对血管紧张素Ⅱ(AngⅡ)诱导的血管平滑肌细胞(VSMC)迁移的调控.方法 采用Lipofectamine 2000将miR-373-3p agomir(agomir-373-3p)和negative control agomir(NC)转染至人VSMC,并根据转染及是否加AngⅡ将VSMC分为NC组(A组)、AngⅡ+NC组(B组)、agomir-373-3p组(C组)和AngⅡ+agomir-373-3p组(D组).采用划痕实验观察细胞迁移的情况,采用qRT-PCR法检测VSMC中miR-373-3p以及合成表型标志物骨桥蛋白(OPN)和收缩表型标志物α平滑肌肌动蛋白(α-SMA)的表达量.结果 在经AngⅡ诱导的VSMC模型中,miR-373-3p的表达量随着AngⅡ浓度的增加而下调.与B组相比,D组细胞的迁移率降低(t=5.33,P＜0.05).与A组相比,C组细胞α-SMA的表达量增加,OPN的表达量减少,差异有统计学意义(t=17.06、9.64,P＜0.05);与B组相比,D组细胞α-SMA的表达量增加,OPN的表达量减少,差异有统计学意义(t=14.78、5.38,P＜0.05).结论 MiR-373-3p的过表达能抑制AngⅡ诱导的VSMC迁移和表型转化.

目的:探究β受体阻滞剂的应用在 STEMI患者 PCI术后冠脉再灌注中的相关性研究,观察β受体阻滞剂的应用对冠脉无复流的影响.方法:选取 2016 年 2月至 2017 年 6 月青岛大学附属医院急诊科收治的急性心肌梗死患者行 PCI治疗后冠脉再灌注患者 116 例为研究对象,分为服用长效β受体阻滞剂的 A组(23 例),服用短效β受体阻滞剂的 B组(33 例)与未服用β受体阻滞剂的C组(60 例),比较组间患者复流率和3 月、6 月及 12 月后的终点事件发生率.结果:A、B、C组患者未复流率为26.09％、33.33％、38.33％,组间比较差异显著(P<0.05),A、B、C组终点事件发生率为 4.35％、9.09％、13.33％,组间比较,A组、B组较 C 组终点事件发生率略低(P<0.05),A组与B组终点事件发生率(P>0.05)无统计学意义.结论:分析STEMI患者行PCI术后冠脉再灌注与β受体阻滞剂的应用存在密切联系,且在急性心肌梗死发病前长期应用β受体阻滞剂可降低 PCI术后再灌注后的未复流风险,同时患者术后终点事件发生率均有所降低.

Objective Doxorubicin (DOX) as a chemotherapeutic drug is widely used to treat a variety of human tumors. However,a major factor limiting its clinical use is its cardiotoxicity. The molecular components and detailed mechanisms regulating DOX-induced cardiotoxicity remain largely unidentified. Thus, we explores the effect of the long non-coding RNA (lncRNA) on DOX-induced cardiotoxicity and its possible mechanisms. Meth-ods LncRNAs expression profles in 2 μmol/L DOX-induced cell samples compared with control group samples were studied by high-throughput microarray. The significantly differentially expressed lncRNAs were verifed by real-time quantitative PCR. Six healthy male 8-week old mice,produced the model of cardiotoxicity in mice by DOX (model group);six healthy C57BL/6J mice were fed with basal diet as control group. Neonatal mouse cardiomyo-cytes were divided in negative control,pcDNA3.1(-)-lncRNA group and si-LnRNA group by their different trans-fection. Cardiotoxicity model and control mice were used to determine the MIEF1 expression using fluorescence quantitative PCR method. Results ①According to the microarray analysis,results of RT-qPCR revealed that one lnc-RNA,we named cardiac apoptosis factor (CAF) was up-regulated significantly in the DOX group (n=4; t=7.79,P<0.01). ②DOX-induced mouse cardiotoxicity model was successfully built. The fluorescence quantitative PCR results showed that compared with the control group,the expression of MIEF1 mRNA in model group was de-creased signifcantly (n=3;t=14.978,P<0.01). The higher the concentration of DOX,the expression of MIEF1 mRNA was signifcantly decreased (n=4; t2 μmol/L=33.423, P<0.01; t4 μmol/L=36.120, P<0.01; t6 μmol/L=40.205,P<0.01). MIEF1 was down-regulated in the CAF-siRNA group (n=4;t=12.909,P<0.01) and up-regulated in the CAF group (n=4;t=33.634,P<0.01). ③Western Blot results showed a significant down regu-lation of expression of MIEF1(n=4;P<0.01) in CAF group and a significant upregulation of expression of MIEF1 (n=4;t=4.892, P<0.01) in CAF-siRNA group compared with negative control group. Conclusion LncRNA CAF is down regulated in the cardiomyocyte and mouse heart in response to DOX treatment. The expression level of MIEF1 was significantly decreased after treatment with DOX. LncRNA CAF directly targets mitochondrial dynamics protein of 51kDa(MIEF1) and suppresses its expression at transcriptional level. Our study identified a novel path-way composed of lncRNA CAF and MIEF1 that mediates DOX cardiotoxicity. This discovery provides a promising therapeutic strategy for cardioprotection.