Objective To investigate the effects of cilazapril on heart rate corrected QT interval disoersion (QTcd) and ventricular arrhythmia (VA) in patients with essential hypertension. Methods 96 hypertensive patients with LVH were divided randomly into two groups. 48 patients in lercanidipine group were treated routinely plus lercanidipine. 48 patients in cilazapril group were treated with routine drugs plus cilazapril. QTcd of 12-lead sur-face ECC and VA malignant degree recorded by Holter were analyzed before therapy and 6 mgnths after therapy. Re-suits In the cilazapril group,the QTcd was different before and after the therapy ((76±12) ms vs (65±9) ms, P<0.05 ). In the lercanidipine group, the QTcd was not significantly different ((76±13 ) ms vs (74±12) ms, P > 0.05). QTed and the malignant degree of VA between the two groups were significantly different after the therapy. Conclusions Treatment with cilazapril can reduce the QTcd and the malignant degree of VA in hypertensive patients with LVH.

Objective To evaluate the value of suprasternal long axis view in echocardiography for right pulmonary artery (RPA) lesions.Methods Echocardiography was performed in 31 patients with clinical suspicion of pulmonary vascular disease.Through suprasternal long axis view,RPA,right superior pulmonary artery and right inferior pulmonary artery were identified,and the vessel wall,intraluminal echoes,and location of the lesion were obtained.Blood flow in pulmonary artery was detected with color Doppler flow imaging.The results of echocardiography were compared with those of computer tomography of pulmonary angiography (CTPA) and clinical diagnosis.Results With suprasternal notch echocardiography,RPA lesions were identified in 27 patients.H owever,RPA could not be clearly identified in four patients.There were 22 patients with moderate or low echo mass in RPA,and five patients with intimal thickening and artery stenosis/obliteration.In the 27 patients with detected lesions,20 lesions were located in RPA,seven lesions were located in distal RPA or its branches.Among the results obtained with echocardiography,25 were in accordance with CT results,6 were not in accordance with CT results.Conclusions The suprasternal long axis view of RPA can be an important alternative imaging modality in identification of pulmonary vascular diseases.

Objective To investigate the correlation between the levels of placenta growth factor (PLGF),soluble angiopoietin receptor-2 (sTie-2) and critical coronary artery plaque imaging morphology of coronary borderline lesions in patients with coronary heart disease (CHD).Methods In three consecutive years from April 2007 to September 2009,a cohort of 719 patients with borderline coronary lesions with stenosis in three main vessels with lumen diameter reduction varied all the way from more than 20％ to less than 70％ and with greater than 2.25 mm of the inner diameter were selected in this study from 4 teaching hospitals of tertiary class A in Beijing.These patients fell into three categories:unstable angina pectoris (UAP,n =292),stable angina pectoris (SAP,n =219) and coronary arteriosclerosis (AS,n =208).The vessels involved were analyzed using quantitative coronary angiography (QCA).Plasma levels of PLGF and sTie-2 were measured by using protein chip.The relationship between plasma levels of vascular factors,sTie-2,PLGF and coronary artery plaque imaging morphology among three groups were analyzed.Results (1) Plasma level of PLGF was 80.33 ng/L in the UAP group,which was significantly higher than 54.29 ng/L in the SAP group and 45.16 ng/L in AS group (both P ＜0.05).Plasma level of sTie-2 was 1353.06 ng/L in the UAP group,which was significantly higher than 1308.28 ng/L in the AS group (P =0.008).(2) There was significantly statistical differences in QCA between the SAP group and the UAP group as well as the AS group (both P ＜ 0.05) in terms of the minimal lumen diameter,diameter stenosis rate,minimal lumen cross-sectional area and cross-sectional area of stenosis.The plaque area in the UAP group was larger than that in the AS group (P =0.013).(3) The relationship between vascular factors and plaque imaging morphology was analyzed.There was significantly statistical difference in the involved lesions among the three groups (P ＜ 0.01).(4) There was a positive correlation between plasma level of PLGF and minimal lumen cross-sectional area (r =0.493,P =0.009).Conclusions The plasma levels of PLGF and sTie-2 reflect the level of neo-vascularization in the plaque,and could be taken as predictive factors for potential pathogenesis of coronary plaque.

Objective To investigate the effects of an adeno-associated virus(AAV2)vector expressing secretory transforming growth factor-β(TGF-β)type Ⅱ receptor(sTβRⅡ)extracellular domain-IgG2a Fc fusion protein(sTβRⅡ-Fc)on proliferation and migration of triple-negative murine breast cancer 4T1 cells in mice.Methods The pAAV-sTβRⅡ-Fc vector expressing sTβRⅡ-Fc fusion protein constructed by molecular cloning,the capsid protein-expressing vector pAAV2 and the helper vector were co-transfected into HEK 293T cells to prepare the recombinant AAV2-sTβRⅡ virus,which was purified by density gradient centrifugation with iodixanol.Western blotting was used to examine the effects of AAV-sTβRⅡ virus on Smad2/3 phosphorylation in 4T1 cells and on expression levels of E-cadherin,vimentin and p-Smad2/3 in 4T1 cell xenografts in mice.BALB/c mice bearing subcutaneous xenografts of luciferase-expressing 4T1 cells received intravenous injections of AAV-sTβRⅡ virus,AAV-GFP virus or PBS(n=6)through the tail vein,and the proliferation and migration of 4T1 cells were analyzed with in vivo imaging.Ki67 expression in the tumor tissues and sTβRⅡ protein expressions in mouse livers were detected with immunohistochemistry and immunofluorescence staining,and tumor metastases in the vital organs were examined with HE staining.Results The recombinant pAAV-sTβRⅡ-Fc vector successfully expressed sTβRⅡ in HEK 293T cells.Infection with AAV2-sTβRⅡ virus significantly reduced TGF-β1-induced Smad2/3 phosphorylation in 4T1 cells and effectively inhibited proliferation and lung metastasis of 4T1 xenografts in mice(P<0.05).In the tumor-bearing mice,intravenous injection of AAV-sTβRⅡ virus significantly increased E-cadherin expression,reduced vimentin and Ki67 protein expressions and Smad2/3 phosphorylation level in the tumor tissues(P<0.05 or 0.01),and induced liver-specific sTβRⅡ expression without causing body weight loss or heart,liver,spleen or kidney pathologies.Conclusion The recombinant AVV2 vector encoding sTβRⅡ extracellular domain is capable of blocking the TGF-β signaling pathway to inhibit the proliferation and lung metastasis of 4T1 cells in mice.

Objective To investigate the effects of an adeno-associated virus(AAV2)vector expressing secretory transforming growth factor-β(TGF-β)type Ⅱ receptor(sTβRⅡ)extracellular domain-IgG2a Fc fusion protein(sTβRⅡ-Fc)on proliferation and migration of triple-negative murine breast cancer 4T1 cells in mice.Methods The pAAV-sTβRⅡ-Fc vector expressing sTβRⅡ-Fc fusion protein constructed by molecular cloning,the capsid protein-expressing vector pAAV2 and the helper vector were co-transfected into HEK 293T cells to prepare the recombinant AAV2-sTβRⅡ virus,which was purified by density gradient centrifugation with iodixanol.Western blotting was used to examine the effects of AAV-sTβRⅡ virus on Smad2/3 phosphorylation in 4T1 cells and on expression levels of E-cadherin,vimentin and p-Smad2/3 in 4T1 cell xenografts in mice.BALB/c mice bearing subcutaneous xenografts of luciferase-expressing 4T1 cells received intravenous injections of AAV-sTβRⅡ virus,AAV-GFP virus or PBS(n=6)through the tail vein,and the proliferation and migration of 4T1 cells were analyzed with in vivo imaging.Ki67 expression in the tumor tissues and sTβRⅡ protein expressions in mouse livers were detected with immunohistochemistry and immunofluorescence staining,and tumor metastases in the vital organs were examined with HE staining.Results The recombinant pAAV-sTβRⅡ-Fc vector successfully expressed sTβRⅡ in HEK 293T cells.Infection with AAV2-sTβRⅡ virus significantly reduced TGF-β1-induced Smad2/3 phosphorylation in 4T1 cells and effectively inhibited proliferation and lung metastasis of 4T1 xenografts in mice(P<0.05).In the tumor-bearing mice,intravenous injection of AAV-sTβRⅡ virus significantly increased E-cadherin expression,reduced vimentin and Ki67 protein expressions and Smad2/3 phosphorylation level in the tumor tissues(P<0.05 or 0.01),and induced liver-specific sTβRⅡ expression without causing body weight loss or heart,liver,spleen or kidney pathologies.Conclusion The recombinant AVV2 vector encoding sTβRⅡ extracellular domain is capable of blocking the TGF-β signaling pathway to inhibit the proliferation and lung metastasis of 4T1 cells in mice.