Influence of granulocyte colony-stimulating factor on cardiac function in patients with acute myocardial infarction and leukopenia after revascularization / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Granulocyte colony-stimulating factor (G-CSF) seems to improve cardiac function and perfusion when used systemically through mobilization of stem cells into peripheral blood, but results of previous clinical trials remain controversial. This study was designed to investigate safety and efficacy of subcutaneous injection of G-CSF on left ventricular function in patients with impaired left ventricular function after ST-segment elevation myocardial infarction (STEMI).</p><p><b>METHODS</b>Thirty-three patients (22 men; age, (68.5 +/- 6.1) years) with STEMI and with comorbidity of leukopenia were included after successful primary percutaneous coronary intervention within 12 hours after symptom onset. Patients were randomized into G-CSF group who received G-CSF (10 microg/kg of body weight, daily) for continuous 7 days and control group. Results of blood analyses, echocardiography and angiography were documented as well as possibly occurred adverse events.</p><p><b>RESULTS</b>No severe adverse events occurred in both groups. Mean segmental wall thickening in infract segments increased significantly at 6-month follow up compared with baseline in both groups, but the longitudinal variation between two groups had no significant difference (P > 0.05). The same change could also be found in longitudinal variation of wall motion score index of infarct segments (P > 0.05). At 6-month follow-up, left ventricular end-diastolic volume of both groups increased to a greater extent, but there were no significant differences between the two groups when comparing the longitudinal variations (P > 0.05). In both groups, left ventricular ejection fraction measured by echocardiography ameliorated significantly at 6-month follow-up (P < 0.05), but difference of the longitudinal variation between two groups was not significant (P > 0.05). When pay attention to left ventricular ejection fraction measured by angiocardiography, difference of the longitudinal variation between groups was significant (P = 0.046). Early diastolic mitral flow velocity deceleration time changed significantly at 6- month follow-up in both groups (P = 0.05).</p><p><b>CONCLUSIONS</b>Mobilization of stem cells by G-CSF after reperfusion of infarct myocardium is safe and seems to offer a pragmatic strategy for recovery of myocardial global function.</p>

Relationship between hs-CRP, proMMP-1, TIMP-1 and coronary plaque morphology: intravascular ultrasound study / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Rupture of unstable plaque with subsequent thrombus formation is the common pathophysiological substrate of the acute coronary syndrome (ACS). It is of potential significance to explore the blood indexes predicting plaque characteristics. Little studies have focused on this field. Therefore we investigated the relationship between hypersensitive C-reactive protein (hs-CRP), pro-matrix metalloproteinase-1 (proMMP-1), tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) and coronary plaque morphology.</p><p><b>METHODS</b>Intravascular ultrasound (IVUS) examination was done in 152 patients with confirmed coronary heart disease before percutaneous coronary intervention from February 2003 to July 2005. Plasma samples of arterial blood were collected prior to the procedure. The level of hs-CRP, proMMP-1 and TIMP-1 were respectively measured by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>Unstable and ruptured plaque were found more frequently in patients with acute myocardial infarction and unstable angina. External elastic membrane cross-sectional area (EEM CSA), plaque area, lipid pool area and plaque burden were significantly larger in ruptured and unstable plaque group. Positive remolding, thinner fabric-cap, smaller minimal lumen cross-sectional area (MLA), dissection and thrombus were significantly more frequent in ruptured and unstable plaque group. The levels of plasma hs-CRP, proMMP-1 and TIMP-1 were higher in ruptured plaque group. hs-CRP > 8.94 mg/L was used to predict ruptured plaque with a ROC curve area of 0.76 [95% confidence interval (CI), 67.0% - 85.8%], sensitivity of 71.8%, specificity of 77.0% and accuracy of 69.2% (P < 0.01), similarly for proMMP-1 > 0.12 ng/ml with a ROC curve area of 0.69 [95% CI, 58.2% - 80.2%], sensitivity of 69.2%, specificity of 75.2% and accuracy of 66.2% (P < 0.01), and TIMP-1 > 83.45 ng/ml with a ROC curve area of 0.67 [95% CI, 56.2% - 78.3%], sensitivity of 66.7%, specificity of 61.9% and accuracy of 66.2% (P < 0.01).</p><p><b>CONCLUSION</b>The plaque characteristics correlate with the clinical presentation. The elevation of hs-CRP, proMMP-1 and TIMP-1 are related to the plaque instability and rupture.</p>

Puerarin suppresses the proliferation of vscular smooth muscule cells and c-fos and bcl-2 protein expression / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the role of puerarin on the proliferation of vascular smooth muscle cells(VSMC) induced by thrombin (T) and the effect of puerarin on the c-fos and bcl-2 protein expression.</p><p><b>METHOD</b>Cell number and cell cycle analysis using flow cytometry were adopted as two different indicators of effects on proliferation of VSMC. Western blot was used to indicate the changes of c-fos and bcl-2 protein after 24 h of treatment of T and puerarin.</p><p><b>RESULT</b>1.5 x 10(-5) - 1.5 x 10(-3) mol x L(-1) puerarin could significantly suppress this stimulation of VSMC proliferation and DNA synthesis induced by T. Western blot demonstrated that after 24 hour of treatment with T and puerarin, T could significantly increase c-fos and bcl-2 protein and 1.5 x 10(-5) - 1.5 x 10(-3) mol x L(-1) puerain could significantly suppress this increase.</p><p><b>CONCLUSION</b>puerarin can suppress the proliferation and DNA synthesis of VSMC promoted by T. This inhibitory effects of puerarin are closely related with the suppression of c-fos and bcl-2 protein.</p>

Immortalization of human umbilical vein endothelial cells by transfected with hTERT and SV40LT / 中华心血管病杂志

<p><b>OBJECTIVE</b>To immortalize human umbilical vein endothelial cells (HUVECs) by ectopic expression of the telomerase reverse transcriptase enzyme (hTERT), and by Simian Virus 40 Large T (SV40LT) antigen without malignant transformation.</p><p><b>METHODS</b>Two different retroviruses that contained hTERT/SV40LT cDNA fragment and drug resistance gene were constructed, and were used to transfect normal primary HUVECs. The transfected cells were screened with 500 microg/ml G418 and 4 microg/ml puromycin. Drug resistance cell clones were selected 3 days after transfection and cultured for further studies. An under inverted microscope and a scanning electron microscope were used to observe the morphology and growth of the cells. The expression of VIII factor and transfected DNA fragments were detected for identification of the endothelial origin and successful transfection. And the expression of E-selectin and endothelial lipase with or without the stimulus of TNF-alpha were also assayed to analyze the biological activity of the transfected cells.</p><p><b>RESULTS</b>The cells were homogenous, closely apposed, large, flat, and polygonal, displayed a characteristic ovoid nucleus with one or two nucleoli and formed monolayer with polygonal shape without overlapping. Immunocytochemical staining showed the existence of VIII factor. SV40LT/hTERT antigen expressed by the transfected cells was detected, while the contrasts had non-expression. Telomerase activity of the cell was detected in the transfected cells, which was 0.36 at 12 th passage and 0.38 at 50 th passage. However, the activity in the normal HUVECs was 1.12 at the first passage and 0.06 at the third passage assayed by PCR-ELISA. Both E-selectin and endothelial lipase were all specific in endothelial cells. The expressions of these two were also detected. And the expression of E-selectin can be up-regulated with the stimulus of TNF-alpha, while the expression of endothelial lipase was not unregulated significantly.</p><p><b>CONCLUSION</b>Ectopic expression of hTERT and SV40LT can effectively immortalize HUVECs without tumorigenesis.</p>

Immortalization of human umbilical vein endothelial cells with telomerase reverse transcriptase and simian virus 40 large T antigen / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

<p><b>OBJECTIVE</b>To establish normally conditionally-immortalized human umbilical vein endothelial cells (HUVECs) by ectopic expression of the human telomerase catalytic enzyme (hTERT) and simian virus 40 large T (SV40 LT) antigen.</p><p><b>METHODS</b>Primary HUVECs were transfected with recombinant retrovirus containing hTERT or SV40 LT respectively. Subsequently drug resistant cell clones were screened and expanded for further studies. Endothelial cell biomarkers were confirmed by examination.</p><p><b>RESULTS</b>The morphological phenotype of the transfected cells was similar to the non-transfected cells. Von Willebrand factor, hTERT and SV40 LT could be detected in transfected HUVECs. Moreover, higher telomerase activity in transfected cells was maintained for over 50 population doublings compared with only low level of endogenous telomerase transiently at early population doublings in primary HUVECs. When exposed to TNF-alpha (tumor necrosis factor-alpha), the expression of E-selectin in transfected cells was significantly up-regulated, but no alteration of endothelial lipase was found.</p><p><b>CONCLUSION</b>Ectopic coexpression of hTERT and SV40 LT can effectively immortalize HUVECs without tumorigenicity in vitro. Immortalized HUVECs may be an ideal target of further molecular function studies.</p>

The evaluation on stent implantation efficacy of myocardial bridge and severe atherosclerosis lesions in the segments proximal to the myocardial bridge / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess long term stent implantation efficacy of myocardial bridge and severe atherosclerosis lesions in the segments proximal to the myocardial bridge.</p><p><b>METHODS</b>The study population consisted of 3 groups (103 patients). Group A included 28 patients with severe atherosclerosis lesion of luminal narrowing of > or = 70% in the segments proximal to the myocardial bridge. Group B included 16 patients with symptomatic myocardial bridge lesion of systolic luminal narrowing of > or = 95%. Group C included 59 patients with severe atherosclerotic lesion of luminal narrowing of > or = 70%. All lesions were successfully treated with stent by standard interventional techniques. Quantitative coronary angiography was performed before and immediately after stent deployment. Follow-up Quantitative coronary angiography was performed at six months or later. Clinical evaluation was done at 20 months after PCI.</p><p><b>RESULTS</b>There was no significant difference in luminal diameter and stent diameter among 3 groups immediately after stent implantation (P > 0.05). At six months, restenosis occurred in 4 patients in Group A (14.3%), in 7 patients in Group B (43.7%), and in 8 patients in Group C (14.8%), respectively. The rate of restenosis was significantly lower in group A and C than in group B (P < 0.05). No significant difference was found between group A and C. Additional balloon dilating of stent were performed in all restenosis patients. Clinical evaluation at 20 months showed that all patients remained free of angina and cardiac events.</p><p><b>CONCLUSION</b>The efficacy of intracoronary stent implantation in treating severe atherosclerosis lesion in the segments proximal to the myocardial bridge is not affected by abnormal haemodynamic changes of myocardial bridges. The rate of restenosis in intracoronary stent implantation of myocardial bridges is higher than that of atherosclerotic lesions in the segments proximal to myocardial bridge.</p>