SONG Ming-Bao , HUANG Lan , YU Xue-Jun , ZHU Guang-Xu , ZHANG Po , YU Shi-Yong , DONG Hong-Mei
Abstract:Aim To explore the effect of the blocker of gap junction on phenotypic transition in cultured rat vascular smooth muscle cells. Methods Rat aortic smooth muscle cells (SMC) were cultured by explanted rat aortic wall tissue. Cell immunofluorescence staining was applied to detect the expressions of connexin (Cx)43 in rat aortic SMC. Fluorescence redistribution after photobleaching (FRAP) was used to measure the communications between cells via gap junctions. MTT and RT-PCR were hired to measure the proliferative capability of rat aortic SMC and the expression of smooth muscle (SM) α-actin respectively. Meanwhile, 18α-glycyrrhetinic acid (18α-GA), a specific blocker of gap junction, was administered to observe its effect on the contents above. Results At 3rd day after cultured, Cx43 was expressed in rat aortic SMC. Fluorescent dye could only be transferred between conjugated cells, and mean fluorescence recovery rate in isolated cells were significantly lower compared with that in conjugated cells (7.30%±0.58% vs 80.61%±6.57%, P<0.01). Compared to control group, mean fluorescence recovery rate in 18α-GA group were significant lower (61.43%±7.62% vs 80.61%±6.57%, P<0.05). Therefore, 18α-GA could inhibit dye transfer between conjugated cells. 18α-GA could also inhibit the proliferation of rat aortic SMC and promote the expression of SM α-actin in cultured rat aortic SMC. Conclusions The blocker of gap junction could promote the phenotypic transition rat aortic SMC from the synthetic to the contractile phenotype, which suggested that gap junction played a role on the phenotypic modulation in cultured rat aortic MSC.
ZHOU Yan-Fang , ZHENG Xiao-Wei , QI Guo-Xian
Abstract:Aim To investigate the effects of hyperglycemia on normoxia and hypoxia apoptosis in primary neonatal rat cardiac myocytes. Methods To culture the primary neonatal rat cardiac myocytes and exposure to normoxia and hypoxia environment in medium containing 33 mmol/L glucose and 5.5 mmol/L glucose (control). The hypoxia environment was achieved by treating cells with cobalt chloride. Cell viability was measured by Trypan blue staining. Cardiomyocyte apoptosis was detected with terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling and Annexin V/PI binding assay. Results In 33 mmol/L glucose group cell survival rate was lower (P<0.01) and apoptosic rate was higher (P<0.01) than those in 5.5 mmol/L glucose group in normoxia condition. However, in hypoxia condition, cell survival rate was higher (P<0.01) and apoptosic rate was lower (P<0.05) in 33 mmol/L glucose group than those in 5.5 mmol/L glucose group. Conclusion In cultured primary neonatal rat cardiac myocytes, hyperglycemia induced apoptosis in normxia condition. However, hyperglycemia plays an anti-apoptotic protective role in cobalt chloride mimic chemical hypoxia condition.
WANG Lian-Sheng , YANG Yong-Zhen , Li Jie , YANG Zhi-Jian , HUANG Jun
Abstract:Aim Glutathione-S-transferases (GST), enzymes with antioxidant activity, have been shown to play a protective role against oxidative stress for many cell types including human vascular smooth muscle cells, but their role in nitroglycerin (NTG) tolerance specifically has not been demonstrated. In this study, we tested the role of hGSTA4-transfection in conferring resistance to the development of tolerance on human fetal aortic smooth muscle cells (FASMC) treated with NTG. Methods A stable transfection of FASMC with cDNA of hGSTA4-4 was established. Western blot analysis, immunocytochemistry assay, MTT cytotoxicity assay and NO assay were used. Results FASMC overexpressing with the hGSTA4-4 were significantly more resistance to cytotoxic injury by NTG, assessed at 24 hours (P<0.05). NO release was higher in hGSTA4-transfected cells during NTG nontolerance and tolerance treatment compared with those in wild-type and vector-transfected FASMC (P<0.01). Conclusions This study demonstrates that hGSTA4-4 can protect smooth muscle cells from the cytotoxicity of NTG and may have a role in smooth muscle cell tolerance to NTG.
WANG Qun , LU Qing-Hua , JIANG Wei-Dong , DU Yi-Meng , WANG Xin , HAO Lin , DONG Zhao-Qiang , XU Dong-Ling , SHENG Lin
Abstract:Aim To clone human Cystatin C gene and construct its eukaryotic expression vector to observe the expression in the human vascular smooth muscle cells (VSMC). Methods Cystatin C gene was obtained from human endothelial cells by reverse transcription-polymerase chain reaction (RT-PCR). Molecular cloning technique was used to construct this kind of eukaryotic expression vector. pCDNA3.1-Cystatin C was identified by restriction enzyme and PCR. Using liposome-mediated transfection, the eukaryotic expression vector pCDNA3.1-Cystatin C was transfected into human VSMC and proved by RT-PCR and Western blot. Results The eukaryotic expression vector pCDNA3.1-Cystatin C was constructed correctly and was highly expressed in human VSMC. Conclusion Cystatin C was cloned successfully, its eukaryotic expression vector was constructed correctly and was expressed highly in human VSMC.
YUAN Zhong-Hua , JIA Wei , Xi-Lin NIU , HUANG An-Fei , LIU Lu-Shan , YI Guang-Hui , WANG Zuo , REN Zhong , TANG Chao-Ke , TIAN Guo-Ping , YANG Yong-Zong
Abstract:Aim To investigate whether overexpression adipophilin induces acyl-coenzyme A∶cholesterol acyltransferase 1 (ACAT1) high expression and lipid accumulation in THP-1 macrophages. Methods The THP-1 cells were differentiated to macrophages through incubation with 160 nmol/L phorbol 12-myristate 13-acetate (PMA) for 24 h. To make overexpressed adipophilin macrophages, the pcDNA3.1-HA-adi constructed was transfected to THP-1 macrophages. Then, cells were incubated with or without oxidized low density lipoprotein (ox-LDL) and/or S-58035 for different time. ACAT1 and adipophilin expression were investigated with reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Oil red O staining and high perfomance liquid chromatography (HPLC) were used to analyze the cellular cholesteryl ester accumulation. Results With the increasing incubated concentration of ox-LDL, both adipophilin and ACAT1 mRNA up-regulated obviously. The upregulated expression of ACAT1 induced by ox-LDL was inhibited by S-58035, and intracellular lipid droplets also decreased. Compared with control, transfecting pcDNA3.1-HA-adi increased adipophilin protein level in THP-1 macrophages. Overexpression adipophilin cells significantly upregulated ACAT1 expression and promoted intracellular lipid accumulation. Ox-LDL synergized the effect of ACAT1 high expression. But the effect could be inhibited by S-58035. Conclusion Overexpression adipophilin can upregulate the ACAT1 expression in THP-1 macrophages, and increase cellular cholesteryl ester. It suggested that adipophilin accumulated cellular cholesteryl ester by ACAT1 in THP-1 macrophages.
LIN Shi-Rong , CHEN Liang-Long
Abstract:Aim To construct lentiviral vector carrying the connexin43 (Cx43) gene, and make it express in the rat bone mesenchymal stem cells (BMSC). Methods The cDNA of human Cx43 gene was obtained with reverse transcription polymerase chain reaction (RT-PCR). The Cx43 gene was recombined to construct the transfer plasmid FUGW-Cx43 by infusion technique. The three-plasmid system of lentiviral vector was consisted of FUGW, the packaging plasmid, and the envelope plasmid VSVG, which were cotransfected to 293T cells mediated by lipofectamin 2000 to produce lentiviral particles. The rat BMSC were infected by obtained lentiviral particles. The expression of Cx43 protein was observed with fluorescent microscope. Results The result of sequencing showed that the cloned Cx43 gene was consistent with the sequence reported in GeneBank. The insertion of Cx43 gene in viral genome was confirmed by PCR. The FUGW-Cx43 plasmid was identified to have correct sequence. After the three plasmids of lentiviral vectors were cotransfected to the 293T cells, the supernatant was collected and concentrated, the titer of the lentiviral vector particles was found to be 1×1011 TU/L. Cx43 gene-modified rat BMSC show linear and stippled patterns of Cx43 expression on cell membrane. Conclusion Lentiviral vector carrying Cx43 gene has been successfully constructed. The infected rat BMSC are able to express the Cx43 protein. This will facillitate the following exploratory development of Cx43 gene modified stem cell-based cardiac repair.
WANG Zhe , LIU Zheng-Cao , CUI Dan , YANG Xiang-Hong
Abstract:Aim To explore the effect of advanced glycation end products (AGE) on injuring of rat renal microvascular endothelial cells (RMEC) and protective effect of probucol. Methods Microvascular endothelial cells isolated and cultured from rat renal were divided into 3 groups: normal control group, AGE group and probucol group. The levels of malondialdehyde (MDA) and nitric oxide (NO) were determined by the assay TBA and nitrate reductase method respectively. The expression of endothelial nitric oxide synthase (eNOS) mRNA and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase protein was detected by reverse transcription polymerase chain reaction (RT-PCR) and Western-blot respectively. The intracellular disposition of nuclear factor kappa B (NF-κB) was observed by immunostaining microscopy. Results In AGE group, the level of MDA increased but the expression of NADPH oxidase protein and eNOS mRNA decreased compared with control. The level of NO in culture medium was increased after exposure to AGE-BSA for 30 min and 6 h,but after 12 h, NO level was decreased. MDA level and the expression of NADPH oxidase protein were decreased but the expression of eNOS mRNA and NO level were upregulated by probucol with a dose-dependent effect in the concentrations of 10, 20, 50, 100 μmol/L. The localization of NF-κB shifted from cytoplasm to nucleus after microvascular endothelial cells were exposed to AGE-BSA. After exposed for 30 min, the expression in nucleus reached the peak and then maintained high level. Conclusion AGE can cause the injury and dysfunction of RMEC via the following possible mechanisms: ①inducing lipid preoxidation; ②activating NADPH oxidase and increasing the production of reactive oxygen species (ROS); ③abnormal expression of eNOS mRNA and further affecting NO production; ④activatin of NF-κB. Probucol can protect microvascular entothelial cells probably via antagonisting the lipid preoxidation, activating of NF-κB and NADPH oxidase,and increasing the AGE-induced abnormal expression of eNOS caused by AGE.
ZHOU Ying , BAI Xiao-Juan , WANG Bo
Abstract:Aim To investigate the possibility of survival, differentiation of bone marrow mesenchymal stem cells (BMMSC) of rats in host myocardium and the effect on left ventricular function in doxorubicin-induced heart failure. Methods 55 female Wistar rats were separated randomly into four groups: normal control group (n=10), heart failure group (n=15), heart failure plus BMMSC transplantation group (n=15), heart failure plus induced BMMSC transplantation (n=15). Male Wistar rats BMMSC were isolated and induced by 10 μmol/L 5-aza for 4 weeks after first generation; then the cells were transplanted into rat heart by doxorubincin-induced heart failure after DAPI-labelled. After 4 weeks, left ventricular function were measured and the heart were checked by immunofluroscopy. Results BMMSC can survive and differentiate in host myocardium; the left ventricular function were significantly improved in BMMSC transplantation group compared with heart failure group, there was no difference between the two BMMSC transplantation groups. Conclusion BMMSC can survive in host myocardium after 4 weeks transplantation and can improve the left ventricular function of doxorubincin-induced dilated cardiomyopathy heart failure.
WANG Jian-Fei , LI Tian-De , ZHENG Xian-Dong
Abstract:Aim To evaluate the efficacy and safty of combination therapy with atorvastatin and fenofibrate in rats with mixed hyperlipidemia. Methods 60 Wistar rats were randomized into normal group, control group, atorvastatin group, AFH group and AFF group. The groups were fed with high fatty foods, except Normal group fed with common foods. At the end of the fourth week, Atorvastatin group [Atorvastatin 1.8 mg/(kg·d)], AFH group [Atorvastatin 0.9 mg/(kg·d)+ Fenofibrate 18 mg/(kg·d), together], and AFF group [Atorvastatin 0.9 mg/(kg·d) + Fenofibrate 18 mg/(kg·d), respectively] were administrated drugs. TC, TG, LDLC, HDLC, ALT, AST and hs-CRP were measured at the end of the fourth and the eighth week. Results The level of TC, LDLC, TG in normal group, atorvastatin group, AFH group and AFF group were obviously lower than control group (P<0.01); That of HDLC in AFH group and AFF group were higher than atorvastatin group(P<0.01). The level of hsCRP in control group, atorvastatin group, AFH group and AFF group were obviously increased than normal group(P<0.05). Compared with Atorvastatin group, the level of hsCRP in AFH group and AFF group were lower. 3.The level of ALT and AST in control group, atorvastatin group, AFH group and AFF group were obviously higher than normal group (P<0.01). Those in Atorvastatin group and AFF group were lower than Control group(P<0.01) and AFH group(P<0.05). Conclusions Combination therapy of fenofibrate plus atorvastatin can strengthen the effects on decreasing lipids and the level of hs-CRP. The negative effects of combination therapy are related to the doses of fenofibrate and atorvastatin, so administrating drugs from low doses and at different time are very important to reduce hepatic damage.
LI Xian-Xia , CHEN Shuang-Xiu , CAO Wei
Abstract:Aim To explore whether Cariporide exerts beneficial effect on impaired vascular endothelial function elicited by exogenous advanced oxidation protein products (AOPP), and to investigate the potential mechanisms. Methods Male SD rats were killed by exsanguination after anesthesia with pentobarbital sodium (30 mg/kg, IP). The thoracic aorta was immediately isolated and was cut into 3 ~ 4 mm rings. AOPP was prepared according to the methods of article. Rat aortic isolated rings were incubated with AOPP (1, 2, 3 mmol/L) and Cariporide (0.01~1 μmol/L) for 90 min. Endothelium-dependent relaxation (EDR) induced by acetylcholine (Ach), endothelium-independent relaxation induced by sodium nitroprusside (SNP), superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) were measured in rat isolated aorta. Results Co-incubation of aortic rings with AOPP-BSA (3 mmol/L) for 90 min resulted in a significant inhibition of EDR response to Ach. Cariporide (0.01~1 μmol/L) groups were significantly attenuated the inhibition of EDR response induced by AOPP-BSA. Conclusion Cariporide was able to protect against vascular endothelial dysfunction caused by AOPP-BSA. The mechanisms may be involved in antioxidative stress and increasing the synthesization and release of NO.
WANG Yue , CHEN Lian-Feng , WANG Jin-Feng , FANG Quan , YAN Xiao-Wei ; Hospital , PUMC , Chinese Academy of Medical Sciences , Beijing , China)
Abstract:Aim To investigate the role of macrophage lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) in the process of atherosclerosis inflammation, the effects of C-reactive protein (CRP) or high density lipoprotein (HDL) on LOX-1 mRNA and protein expression, and on intracellular cholesterol content in THP-1 derived macrophages were investigated. Methods THP-1 cells were differentiated into macrophages with PMA. THP-1 derived macrophages were incubated with CRP or HDL of different concentration in vitro. The expressions of LOX-1 antigen and mRNA were determined by ELISA and RT-PCR. Cellular cholesterol contents were measured before and after CRP or HDL treatments with HPLC. Results Compared with control group, both CRP and HDL can increase the expression of LOX-1 protein and mRNA significantly (P<0.05) in a dose dependent manner on THP-1 derived macrophages. CRP promoted cellular cholesterol accumulation (P<0.01), while HDL decreased intracellular cholesterol content significantly (P<0.01). Conclusions LOX-1 expression in THP-1 derived macrophages can be promoted by either pro-inflammatory factor CRP or anti-inflammatory factor HDL, which suggested that LOX-1 may not play a critical role in the inflammatory process of macrophages.
YANG Li-Xia , SHEN Zhu-Fu , GUO Rui-Wei , YANG Dong , QI Feng , SHI Yan-Kun
Abstract:Aim To study the role of bcl-2 in endothelial cells apoptosis induced by ceramide. Methods Human umbilical vein endothelial cells were cultured in vitro and treated with ceramide at various levels. TUNEL was employed to determine the apoptosis of the cultured endothelial cells. The bcl-2 mRNA and protein levels were evaluated by RT-PCR and Western blotting. Results Ceramide induced apoptosis of endothelial cells in a dose-dependant manner (P<0.05). The percentage of the apoptotic endothelial cells were 2.13%±0.12%, 13.24%±1.32%, 29.67%±2.32%, 34.43%±3.36% and 38.56%±2.21% respectively after treatment with ceramide at various concentrations (5, 12.5, 25 and 50 μmol/L)for 24 hours. The expression of bcl-2 mRNA and protein in endothelial cells treated with ceramide significantly depressed (P<0.05). Conclusion Ceramide may induce apoptosis of endothelial cells through down-regulating the bcl-2 mRNA and protein expression.
LUO Yang-Ping , ZHAO Shui-Ping , NIE Sai
Abstract:Aim To observe the effect of benzafibrate on serum paraoxonase-1 (PON-1) activity in mice during the acute phase response and to investigate the mechanism of anti-oxidation effect. Methods 32 male C57BL/6 mice were randomly divided into 4 groups: in the control group mice were fed with ordinary dietary for 8 weeks; in the benzafibrate group mice were fed with benzafibrate [150 mg/(kg·d)]for 8 weeks; in the lipopolysaccharide (LPS) group mice received intraperitoneal injection of LPS (25 μg) and serum was collected 24 hours later; in the benzafibrate plus LPS group mice were fed with benzafibrate [150 mg/(kg·d)]for 8 weeks and then received an intraperitoneal injection of LPS (25 μg). Serum PON-1 activity was assessed by use of phenylacetate (arylesterase) as substrate and were determined with spectrophotometer. Results Serum PON-1 activity treated with benzafibrate were higher than those in the control group [120.97±39.83 μmol/(min·L) vs 32.71±4.40 μmol/(min·L), P<0.01]. LPS decreased serum PON-1 activity compared with the control group [3.23±0.76 μmol/(min·L) vs 32.71±4.40 μmol/(min·L), P<0.01]. There was no difference between the benzafibrate plus LPS group and the control group. Serum PON-1 activity was positively correlated with high density lipoprotein cholesterol (HDLC) levels (r=0.538, P=0.001). Conclusions Serum PON-1 activity decreased during the acute inflammation phase induced by LPS. Bezafibrate can increase the PON-1 activity, which may be related to its anti-oxidation effect. The effect of benzafibrate may be associated with the increment of HDLC.
DING Feng-Hua , LU Lin , PU Li-Jin , ZHANG Jian-Sheng , ZHANG Rui-Yan , HU Jian , ZHANG Qi , YANG Zheng-Kun , CHEN Qiu-Jing , SHEN Wei-Feng
Abstract:Aim To investigate the relationship between the serum level of glycated albumin (GA) and the presence and severity of coronary artery disease (CAD) in patients with type 2 diabetes mellitus. Methods The serum levels of GA and glycosylated hemoglbin A1c (HbA1c) were measured in 349 consecutive diabetic patients and 340 normal controls. Diabetic patients were further divided into patients without significant coronary stenosis (n=166) and patients with significant coronary stenosis defined as luminal diameter narrowing ≥70% (n=183). Multivariate analysis was performed to determine independent risk factors for significant CAD in patients with type 2 diabetes mellitus. Results The serum GA level was significantly higher in patients with significant coronary stenosis than patients without significant coronary stenosis and controls (P<0.01), and correlated significantly with the number of diseased coronary arteries (r=0.19, P<0.01), whereas no obvious difference was found in HbA1c between the groups. Multivariate analysis revealed that older age, male gender, serum level of GA, lipoprotein (a) and hypertension were independent risk factors for significant CAD in diabetic patients. Conclusions The serum level of GA is associated with the presence and severity of CAD in patients with type 2 diabetes mellitus.
WU Su-Hua , MA Hong , LIU Jun , DU Zhi-Ming , HE Jian-Gui , LI Yi , HU Cheng-Heng , LIAO Xin-Xue , LUO Chu-Fan , WU Xin , HE Wen , DONG Yu-Gang
Abstract:Aim To assess the prognostic significance of ST-segment elevation in lead aVR for patients with first non ST-Segment elevation acute myocardial infarction. Methods Initial ECG in 426 patients with a first acute myocardial infarction without ST-segment elevation in leads other than aVR or V1 were analyzed. Results The rates of in-hospital death in patients without (n=281) and with 0.05 to 0.1 mV (n=68) or ≥0.1 mV (n=77) of ST-segment elevation in lead aVR were 1.8%, 7.4% and 15.6%, respectively (P<0.001). After adjustment for the baseline clinical predictors and for ST-segment depression on admission, the odds ratios of death in the last 2 groups were 4.2 (95% CI was 1.4 to 13.5; P<0.001) and 6.1 (95% CI was 2.4 to 17.3) (P<0.001), respectively. The rates of recurrent ischemic events and heart failure during in-hospital increased in a stepwise fashion among the groups, whereas creatine kinase (CK) and MB isoenzyme of creatine kinase (CK-MB) levels were similar. The prevalence of left main or 3-vessel coronary artery disease in the 3 groups was 16.9%, 37.1% and 56.2%, respectively (P<0.001). Conclusions Lead aVR has short-term prognostic significance in patients with a first non ST-segment elevation acute myocardial infarction. Because the poorer outcome predicted by ST-segment elevation in lead aVR seems to be related to a more severe coronary artery disease, an early invasive approach might be especially beneficial in patients presenting with this finding.
SUN Lian-Qing , SUN Yang , ZHENG Wei
Abstract:Aim To investigate the changes of vascular endothelial function and carotid artery intima-media thickness (IMT) in patients with diabetic arterial occlusion of lower extremities (DAO). Methods Using high resolution ultrasound, endothelium-dependent dilation (EDD), endothelium-independent dilation (EID) and IMT were measured in 60 patients with DAO (20 of 1st stage, 20 of 2nd stage and 20 of 3rd stage). 20 healthy people were respectively observed as the control group. Changes of vascular tension factors as endothelin-1 (ET-1), thromboxane B2 (TXB2), nitric oxide (NO) and 6-keto-prostaglandin F1α(6-Keto-PGF1α) were also be studied. Results The results show that EDD of the branchial artery in patients with DAO was reduced significantly compared with those healthy control and EDD has significantly characteristic changes in different stage (8.39%±1.62%, 6.22%±1.27%, and 4.02%±2.35% vs 10.58%±2.92%, P<0.01). EID of the branchial artery in patients of 3rd stage was also lower than those control (9.07%±6.36% vs 15.17%±2.71%, P<0.01). IMT of patients of 2nd and 3rd stage were significantly higher than those of healthy control group (1.06±0.06 mm and 1.12±0.04 mm vs 0.87±0.04 mm, P<0.01). Vascular contractile factors as ET-1 and TXB2 levels were higher than those in healthy control (P<0.01), while vascular dilatory factors as NO and 6-Keto-PGF1α were declined significantly than those in healthy control (P<0.01). Conclusions Vascular endothelial dysfunction may play an important role in the pathogenesis of DAO. Vascular endothelial function and IMT can be used to monitor patients condition.
GAO Ming-Yu , QI Guo-Xian , SUN Xue-Yan , JIA Da-Lin
Abstract:Aim To study the effect of survival time of the patients who had non-ST-segment elevation acute coronary syndrome with different treatments. Methods Patients suffered successively from non-ST-segment elevation acute coronary syndrome were chosen initially in 14 third-class or second-class hospitals in 10 cities of Liaoning, with questionaire filled in and follow-up when the patients discharged from hospital after 30 days, 90 days, and 180 days, to get 900 complete data. All patients were divided into interventional therapy group and drug treatment group. Observational target included the patients' characters of base line, clinical interference measure and end point events. Results Mean age of patient was 61.1±10.7 years in the interventional therapy group and 65.9±10.8 years in the drug treatment group, history of congestive cardiac failure and smoking in the past and incidence of cerebral accident in the interventional therapy group were fewer than those in the drug treatment group (P<0.05). The incidence rate of reangina pectoris attacks, congestive cardiac failure, rate of death in follow-up 90 and 180 days, nonfatal myocardial infarct, congestive cardiac failure in the interventional therapy group was fewer than that in the drug treatment group(P<0.05). Using drug in follow-up 90 and 180 days, the rate of using drug, such as aspirin, clopidogrel, low molecular heparin, stain, calcium antagonist in the interventional therapy group was higher than that in the drug treatment group. Survival rate in interventional therapy group was higher than that of the drug treatment group, but there was no significant difference between the interventional therapy group and drug treatment group (P>0.05). Conclusion Interventional therapy can reduce incidence rate of myocardial infarct in period of hospital and follow-up 180 days.
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