Objective To investigate the effects of valsartan on experimental left cardiac function and the vasoactive substance in rats with acute myocardial infarction (AMI).Methods Seventy Wistar rats were randomly divided into 6 group:①Sham groups: including Sham 1(n=5) and Sham 4(n=5).The pericardium of rats in Sham groups were cut open and sutured immediately.The rats were routinely breeded for 1 week and 4 weeks,1.5 mL saline was poured into stomach once a day.②Control groups: AMI 1 (n=10) and AMI 4 (n=10).Anterior descending branches of coronary artery of Wistar rats were ligated to establish models of AMI.The rats with AMI were poured into stomach with 1.5 mL saline once a day after AMI for 1 week and 4 weeks.③Valsartan groups: VAS 1 (n=10) and VAS 4 (n=10).The rats with AMI were poured into stomach with valsartan 10 mg?kg-1 and 1.5 mL saline for 1 week and 4 weeks(once a day).Cardiac function was assayed by arterial cannulatio.Angiotensin Ⅱ(Ang Ⅱ),aldosterone (ALD),endothelin (ET),thromboxane A2(TXA2) and prostacyclin I2 (PGI2) in serum were measured by radioimmunoassay.Results ① Valsartan could evidently improve cardiac function on the 1st and 4th week after experimental AMI.+dp/dtmax and-dp/dtmax were both increased on the 1st and 4th week and more evidently on the 4 week.②Compared with control groups,valsartan decreased the levels of ALD,ET and TXA2 in plasma and increased the levels of AngⅡ and PGI2 in plasma.Conclusion Valsartan could improve left cardiac function on late stage of infarction,the effect improve not only systolic function,but also diastolic function.

Objective To investigate the effect of oxygen free radicals on the myocardial injury in acute MODS.Methods Thirty-six SD rats were randomly divided into two groups.The rats of experimental group were peritoneally injected with the suspension of zymosan-parogen.The rats of control group were injected with steriled saline at the same volume.The dynamtic change of LPO,SOD,myocardial enzyme in plasma and MDA,SOD in myocardial tissue at different time point were detected.The pathologic change of myocardial tissue by HE staining was observed.Results Compared with the control group,the LPO,MDA,CKMB,LDH,GOT in plasma and myocardial tissue increased at 6 hours (P

Objective To study the morphological changes of diaphragm of rats with omethoate poisoning and the protection of penehyclidine hydrochloride.Methods The experimental model of Wistar rats was made by eliac injection ofomethoate,96 rats was divided randomly into four groups in average:the hrinematched control group (Group NO);the omethoate intoxication matched control group (Group PO);atropine and pralidoxime chloride cure group (Group AC); penehyclidine hydrochlofide and pralidoximc chloride cure group (Group PC).The whole blood cholinesterase (ChE) and creatinekinase (CK) activtitise were measured 2 h after poisoning.To observe the morphological changes of diaphragmat different time from 1 to 7 days.Results All the poisoned rats showed that the diaphragmatic histologic damage of the penehyclidine hydrochloride and pralidoxime chloride cure group was slighter than that of atropine cure group.Conclusion A possible reasons of the respiratory muscle paralysis conduced by AOPP was the putrescence of diaphragm muscle fiber, and penehyclidine hydrochloride could definitely protect the diaphragm of rats with omethoate poisoning,and we could deduce that it prevented from intermediate myasthenia syndrome.

Objective To discuss the effects of carvedilol on the heart function and glucolipometabolism in elder patients with diastolic heart failure.Methods 76 elder patients with diastolic heart failure were randomly divided into treatment group(n=34) and control group(n=42),all the patients were given routine treatment of diastolic heart failure,the patients in treatment group were given carvediol in addition( from little dose to more ),the course of treatment was 3-6 months.The parameters of the diastolic function of heart before and after treatment in two groups were determined by ultrasonic cardiogram and uninjured cardiodynamic machine.And the levels of fasting blood glucose,triacylglucerol(TG),cholesterol in two groups were detected.Results After treatment the total effective rate in treatment group was higher than that in control group( P

Aim To study protective effects of ulinastatin on injury of organs in rats induced by endotoxin.Methods 36 Wistar rats were divided into 3 groups: control group,model group and treatment group.The model of injury of organs were induced by injecting lipopolysaccharide(LPS) through the sublingual vein into rats.Ulinastatin was injected into the sublingual vein of rats in treatment group,LPS was injected into rats in the same way after 10 minutes.At the second hour or the sixth hour after treatment,serum and lung,liver and renal samples were cellected from rats to determine levels of TNF-?,IL-6,IL-1?and iNOS by RIA.Pathologic changes of lung,liver and renal organ were examined.Results Levels of TNF-?,IL-6,IL-1?,iNOS of serum and renal organs in treatment group were obviously reduced than those in model group(P

[摘 要] 目的：检测miR-452-5p在食管鳞状细胞癌（ESCC）中的表达，并探讨其异常表达对食管癌KYSE-150细胞增殖、侵袭能力和EMT进程的影响及其分子机制。方法：收集2012年3月至2015年12月在河北医科大学第四医院就诊的86名ESCC患者的癌组织样本和对应的癌旁组织，用qPCR法检测miR-452-5p及其他相关基因在ESCC组织和细胞中的表达；向KYSE-150细胞中分别转染miR-452-5p mimic或pcDNA3.1-SOX7构建过表达的细胞株。分析miR-452-5p表达与ESCC病理特征和患者5年OS的关系。用MTS、Tanswell法检测miR-452-5p过表达对食管癌KYSE-150细胞增殖、侵袭能力和EMT进程的影响；用双荧光素酶报告基因实验及TOP/FOP报告基因系统检测miR-452-5p与SRY盒转录因子（SOX7）3'UTR区的结合作用及对Wnt/β-catenin通路活化水平的影响。结果：miR-452-5p在ESCC组织中呈明显高表达（P<0.01），并与ESCC患者的淋巴结转移、TNM分期及5年OS密切相关（均P<0.01）。miR-452-5p过表达明显促进食管癌KYSE-150细胞的增殖、侵袭能力及EMT进程（P<0.05或P<0.01）。SOX7是miR-452-5p的直接靶基因，miR-452-5p通过对SOX7的负向调控影响了Wnt通路活化水平（P<0.05或P<0.01），同时，miR-452-5p表达也受Wnt通路活化水平的影响（P<0.05或P<0.01），其可能为Wnt通路下游靶基因。结论：miR-452-5p通过miR-452-5p/SOX7/Wnt/miR-452-5p正反馈环路提高Wnt/β-catenin通路活化水平，进而促进ESCC KYSE-150细胞的增殖、侵袭能力及EMT进程，miR-452-5p有望成为ESCC患者靶向治疗的潜在靶点及预后评估的新型分子标志物。

[摘 要] 目的： 探讨长链非编码RNA（lncRNA）LINC01140在食管鳞状细胞癌（esophageal squamous cell carcinoma，ESCC）组织及细胞中的表达及其对Eca109细胞增殖与侵袭的影响及其分子机制。方法：选取2012年3月至2015年5月河北医科大学第四医院收治的133例ESCC患者的临床资料和GEPIA数据库中收集的182例ESCC组织及286例食管正常黏膜组织的LINC01140表达数据，以及ESCC细胞系Kyse150、Eca109和TE13。用qPCR法检测癌组织和细胞中LINC01140的表达水平，分析其表达水平与患者临床病理特征及预后的关系。分别将pcDNA3.1-LINC01140、阴性对照（pcDNA3.1-NC）或miR-452-5p mimic及阴性对照（miR-NC）转染到Eca109细胞，MTS、Transwell实验分别检测细胞的增殖与侵袭能力。用双荧光报告基因实验及TOP/FOP报告基因系统检测LINC01140与miR-452-5p的靶向结合作用及LINC01140对Wnt/β-catenin通路活化水平的影响。结果：LINC01140在ESCC组织和细胞中表达均显著下调（均P<0.01），LINC01140低表达与ESCC患者年龄、淋巴结转移、TNM分期及OS密切相关（均P<0.05）。LINC01140过表达明显抑制Eca109细胞的增殖及侵袭能力（均P<0.01）。机制研究表明，LINC01140可能通过竞争结合miR-452-5p影响Wnt/β-catenin信号通路的活化水平继而调控Eca109细胞的恶性生物学行为。结论：LINC01140通过靶向miR-452-5p/Wnt/β-catenin轴促进ESCC细胞的增殖与侵袭能力，其有望成为ESCC患者靶向治疗的潜在靶点及预后评估的标志物。