自发性高血压大鼠肾脏血管紧张素转换酶2 mRNA转录及其蛋白表达

目的 观察不同月龄自发性高血压大鼠(SHR)肾脏血管紧张素转换酶2(ACE2)mRNA转录及其蛋白表达,初步探讨ACE2在高血压发生、发展过程中的可能作用.方法 雄性SHR 1月龄组(S1)、2月龄组(S2)、3月龄组(S3)、6月龄组(S6)和9月龄组(S9)共5组,每组各6只,各组均有相应月龄匹配的Wistar-Kyoto(WKY)大鼠作对照.采用RBP-Ⅰ型大鼠血压心率测定仪测量大鼠尾动脉收缩压(SBP);逆转录聚合酶链式反应(RT-PCR)法检测肾脏ACE2 mRNA的转录水平;免疫组化染色结合计算机图像分析方法 测定肾脏ACE2蛋白的表达水平.结果 1)SHR的SBP随着月龄的增加而上升,6月龄后趋于稳定.2)SHR和WKY肾脏ACE2蛋白和mRNA水平均随着月份的增加而增加,3月龄时达高峰,6月龄后趋于稳定;且SHR肾脏ACE2蛋白和mRNA水平均低于同龄的WKY.S1肾脏髓质内侧部ACE2免疫染色阳性面积百分比较皮质和髓质外侧部高,与1月后的分布相反.结论 1)SHR肾脏ACE2 mRNA和蛋白的表达水平比WKY大鼠低.2)大鼠肾脏ACE2 mRNA和蛋白的表达具有时间和部位分布上的差异.     

Effect of Trimetazidine on Regressione of Ischemic Dysfunction of Myocardium After Coronary Bypass Surgery on Beating Heart

AIM: To study effect of trimetazidine on restoration of hibernating myocardium after myocardial revascularization on beating heart. MATERIAL: Patients with ischemic heart disease subjected to direct myocardial revascularization on beating heart: 25 patients received trimetazidine (60 mg/day) in pre and postoperative periods and 30 patients did not. METHODS: Echocardiography, veloergometry, 6 minute walk test, myocardial scintigraphy with Tl-199. RESULTS: Course (35 days) treatment with trimetazidine provided significant decrease of frequency and severity of episodes of angina, reduction of nitrate consumption, enhancement of tolerance to physical exercise, improvement of myocardial perfusion manifested as significant decrease of mean size of transient perfusion defects. CONCLUSION: These results demonstrate efficacy and expediency of trimetazidine use in therapy of reversible myocardial dysfunction in patients with ischemic heart disease subjected to direct myocardial revascularization.     

隐性高血压病人中心动脉压及增强指数

目的探讨“隐性高血压”与中心动脉压及动脉硬化的关系。方法采用脉搏波分析仪记录89例临床诊断为血压正常(偶测血压<140/90 mm Hg)及75例高血压(偶测血压≥140/90 mm Hg或正在服用降压药物者)患者的桡动脉脉搏波,经计算机自动转换为相应的中心动脉脉搏波,并分析中心动脉压力及反映全身动脉硬化的增强指数(AIx)。结果小样本人群中,隐性高血压的患病率为15.7%。与血压正常(偶测血压<140/90 mm Hg及白昼动态血压<135/85 mm Hg)组相比,隐性高血压组的血浆总胆固醇及低密度脂蛋白胆固醇浓度、饮酒的比例显著增高;中心动脉收缩压、舒张压、收缩末期压及中心动脉增强压分别增加14.8 mm Hg(CI5.6~24.0 mm Hg)、9.1 mm Hg(CI3.1~15.1 mm Hg)、14.0mm Hg(CI5.8~22.2)及4.2(CI0.6~7.8 mm Hg),增强指数增加11.9%(CI2.8%~20.9%)。虽然隐性高血压组的偶测血压显著低于高血压组,经年龄、性别及身高调整后,两组的白昼动态血压、中心动脉收缩压、舒张压、增强压及增强指数均无显著差异。结论隐性高血压患者的中心动脉压力及增强指数升高,提示动脉顺应性下降,动脉硬化。这些血液动力学的改变可能增加心血管病危险,对其进行评价有助于偶测血压正常者的危险分层。     

PDGF-CC induces tissue factor expression: role of PDGF receptor α/β

Tissue factor (TF) is the principal trigger of the coagulation cascade and involved in arterial thrombus formation. Platelet-derived growth factor CC (PDGF-CC) is a recently discovered member of the PDGF family released upon platelet activation. This study assesses the impact of PDGF-CC on TF expression in human cells. PDGF-CC concentration-dependently induced TF expression by 2.5-fold in THP-1 cells, by 2.0-fold in human peripheral blood monocytes, by 1.4-fold in vascular smooth muscle cells, and by 2.6-fold in microvascular endothelial cells, but did not affect TF expression in aortic endothelial cells. A similar pattern was observed with PDGF-BB. In contrast, PDGF-AA did not alter TF expression in THP-1 cells. TF whole cell activity was induced following stimulation with PDGF-BB and PDGF-CC in THP-1 cells. Real-time polymerase chain reaction revealed that PDGF-CC induced TF mRNA. PDGF-CC transiently activated p42/44 MAP kinase [extracellular signal-regulated kinase (ERK)], while phosphorylation of the MAP kinases c-Jun NH₂-terminal kinase (JNK) and p38 remained unaffected. PD98059, a specific inhibitor of ERK phosphorylation, but not the p38 inhibitor SB203580 or the JNK inhibitor SP600125 prevented PDGF-CC induced TF expression in a concentration-dependent manner. The effect of PDGF-CC was antagonized by both PDGF receptor α and PDGF receptor β neutralizing antibodies; in contrast, PDGF-BB was only inhibited by PDGF receptor β blocking antibody. PDGF receptor α and PDGF receptor β inhibition prevented PDGF-CC-induced ERK phosphorylation. PDGF-CC induces TF expression via activation of α/β receptor heterodimers and an ERK-dependent signal transduction pathway.     

普通窄带成像内镜对结直肠增生性息肉和腺瘤的鉴别诊断价值

目的 分析普通窄带成像(NBI)内镜下结直肠增生性息肉与腺瘤腺管及微血管特征的差异,评价NBI的鉴别诊断价值.方法 将普通内镜下诊断结直肠息肉、病理检查证实为增生性息肉或腺瘤者纳入研究并进行NBI内镜检查.将腺管形态参照改良的工藤分型法分为A型和B型.将微血管形态分为3型,无微血管判为Ⅰ型,微血管沿腺管开口排列、粗细均匀判为Ⅱ型,微血管粗细不均、排列紊乱判为Ⅲ型.比较增生性息肉和腺瘤NBI图像中腺管形态和微血管形态特征的差异,同时对无放大NBI图像观察者间的一致性进行评价.结果 共87例患者的107个息肉(腺瘤73个、增生性息肉34个)进行普通NBI内镜检查.腺瘤组息肉最大径和表面分叶者比例明显高于增生性息肉组(P值分别=0.0023和0.0047).腺瘤组中B型腺管形态[86.3％(63/73)]及Ⅱ或Ⅲ型微血管形态[82.2％(60/73)]者较多.以B型腺管形态、Ⅱ型或Ⅲ型微血管中任一特征诊断腺瘤的敏感度、特异度、准确率分别为97.3％、82.4％、92.5％.以B型腺管形态联合Ⅱ型或Ⅲ型微血管诊断腺瘤的敏感度、特异度、准确率分别为71.2％、91.2％、77.6％.观察者间一致性评价平均Kappa值为0.761.结论 普通NBI内镜下结直肠腺瘤和增生性息肉的微血管特征和腺管特征存在差异,依据以上两方面可在NBI内镜下实时初步鉴别腺瘤和增生性息肉.     

Molecular analysis of the Turkish form of deletion-inversion (δβ)° thalassaemia

Two unrelated (δβ)°-thalassaemia patients from Southern Turkey are presented. DNA studies indicated that both of them are homozygous for the Turkish type of (δβ)°-thalassaemia characterized by one large deletion of 11.5 kb including the δ and β globin genes at the 5' end and one small deletion of 1.6 kb at the 3' end, which are separated by an inverted 7.6 kb long DNA segment that includes L1 repetitive sequence. In the present study a PCR-based method was performed to produce a unique deletion-specific product and subjected to sequence analysis for the determination of the breakpoint. DNA polymorphisms in the β-globin gene cluster of deletion-inversion type of (δβ)°-thalassaemia, IVS-I-6 and β-39 globin genes were examined. Analysis of sequence variations in regulatory regions including the 5' hypersensitive site-2 of the locus control region (LCR), the δ, ^Gγ and ^Aγ 5' flanking regions and the second intervening sequence (IVS-II) of ^Aγ and ^Gγ genes indicated the presence of close similarities between the chromosome carrying the Turkish form of deletion-inversion δβ)°-thalassaemia and the chromosome associated with β-39 nonsense mutation in haplotype II. These two chromosomes are characterized by the presence of a 4 base pair deletion in the ^Aγ^T globin gene promoter. A C → T alteration at position −199 5' to the δ gene was also found to be associated with the Turkish type of (δβ)°-thalassaemia and β-39 chromosome.     

老年缺血性脑血管病血瘀证患者的红细胞变形性及一氧化氮水平的检测及其意义

目的 :探讨老年缺血性脑血管病血瘀证患者的红细胞变形性及一氧化氮 ( NO)水平的变化。方法 :检测 5 5例老年缺血性脑血管病血瘀证患者的红细胞变形指数和 NO的水平。其中短暂性脑缺血发作 ( TIA) 2 5例 ,脑梗死 3 0例 ;另设 2 6例正常对照组作对比观察。结果 :血瘀证 TIA患者红细胞变形指数 ( 0 .4 67± 0 .14 5 )显著低于正常对照组 ( 0 .5 0 8± 0 .14 1) ,P<0 .0 5 ,脑梗死患者红细胞变形指数 ( 0 .4 43± 0 .15 6)降低更为明显( P<0 .0 1) ;NO水平 ,TIA患者与正常对照组比较无显著性差异 ( 79.10± 15 .3 7比 76.70± 17.10 ) ,而脑梗死患者 ( 88.5 0± 13 .68)显著升高。结论 :红细胞变形性改变及 NO水平升高在一定程度上均参与了老年缺血性脑血管病血瘀证的发生发展     

Paclitaxel enhances thrombin-induced endothelial tissue factor expression via c-Jun terminal NH2 kinase activation

Paclitaxel is used on drug-eluting stents because it inhibits proliferation of vascular cells. Stent thrombosis remains a concern with this compound, particularly with higher dosages. This study investigates the effect of paclitaxel on tissue factor (TF) expression in human endothelial cells. Paclitaxel enhanced thrombin-induced endothelial TF protein expression in a concentration- and time-dependent manner. A concentration of 10(-5) mol/L elicited a 2.1-fold increase in TF protein and a 1.6-fold increase in TF surface activity. The effect was similar after a 1 hour as compared with a 25-hour pretreatment period. Real-time polymerase chain reaction revealed that paclitaxel increased thrombin-induced TF mRNA expression. Paclitaxel potently activated c-Jun terminal NH2 kinase (JNK) as compared with thrombin alone, whereas the thrombin-mediated phosphorylation of p38 and extracellular signal-regulated kinase remained unaffected. Similar to paclitaxel, docetaxel enhanced both TF expression and JNK activation as compared with thrombin alone. The JNK inhibitor SP600125 reduced thrombin-induced TF expression by 35%. Moreover, SP600125 blunted the effect of paclitaxel and docetaxel on thrombin-induced TF expression. Paclitaxel increases endothelial TF expression via its stabilizing effect on microtubules and selective activation of JNK. This observation provides novel insights into the pathogenesis of thrombus formation after paclitaxel-eluting stent deployment and may have an impact on drug-eluting stent design.