Objective To observe the efficiency of clopidogrel combined with emergency corona interventional therapy for non-ST segment elevation myocardial infarction.Methods A total of 112 patients with non-ST segment elevation myocardial infarction who were admitted in our hospital from February 2004 to November 2007 were divided into 2 groups at random with 56 patients in each,the experimental group and the control group.All patients were treated with emergency corona interventional therapy and the other routine standard therapies.The experimental group was treated with clopidogrel(75 mg,once per day for 8 weeks),and the control group administered ticlopidine(250 mg,twice per day for 8 weeks).The two group were followed up for a time of half a year.Results The TIMI(thrombolysis in myocardial infarction) myocardial-perfusion grade 3 angiographic flow was achieved in 91.1% of the experimental group,higher than that of the control group(87.5%),but there was no significant difference between them.What's more,there was no obvious difference between the 2 group in cardiac functional grading and life-threatening bleeding.The experimental group had significantly lesser hyporrhea,and lower platelet degradation and total white blood cells counts in comparison to the control group.After the followed-up of half a year,there was significant difference between them in combination-end point.Conclusion Addition of clopidogrel is effective in emergency corona interventional therapy for non-ST segment elevation myocardial infarction,which can degrade the risk of emergency corona interventional therapy.

Objective To investigate the effect of tetramethylpyrazine (TMP) combined with cisplatin(DDP) on the expression of Mac2-binding protein(Mac2-BP) and vascular endothelial growth factor (VEGF) in mice with lung cancer. Methods C57 BL/6 mice were subcutaneously inoculated with Lewis lung adenocarcinoma cells , and Lewis lung adenocarcinoma mouse xenograft model was established .Forty mice were randomly divided into four groups:normal saline group(NS group,0.9%NaCl,0.2 ml), TMP group (TMP 100 mg/kg,0.2 ml), DDP group (DDP 2 mg/kg,0.2 ml), TMP plus DDP group (doses as above,0.2 ml totally) with 10 mice in each group.After 2 drug intervention,following 14 days of inoculation , the tumor diameter was measured every two days to calculate the tumor volume .The mice were sacrificed after 14 days of continuous medication , and the subcutaneous tumors were weighed after stripping to calculate the inhibitory rate.The expressions of Mac2-BP and VEGF was detected by Western blot and immunhistochemistry .Results Compared with NS group, the tumor growth rate of TMP group , DDP group and TMP+DDP group was slowed down , and the tumor growth rate in the TMP+DDP group was decreased most significantly .The inhibitory rate of TMP group , DDP group and TMP+DDP group was 25.57%, 45.24% and 66.5%,respectively.Kim, s formula was used to evaluate the synergy of the combined treatment .The q values for TMP +DDP group was 0.85

Objective To study the mechanism of chemotherapy resistance caused by interleukin-6 (IL-6) in ovarian cancer cells and its related signal pathways. Methods Ovarian cancer cell lines A2780(IL-6 receptor positive, while non-IL-6-expressing and cisplatin/paclitaxel-responsive) and SKOV3 cell lines( overexpressing of IL-6 receptor and IL-6 and cisplatin/paclitaxel-resistant) were suitable models for this study. The effect of exogenous (a short period of treatment with recombination IL-6) and endogenous IL-6(by transfecting with plasmid encoding for sense IL-6 ) in A2780 cells or deleting of endogenous IL-6expression in SKOV3 cells (by transfecting with plasmid encoding for antisense IL-6) on the sensitivity to cisplatin and paclitaxel was investigated. Meanwhile, the mechanism of chemotherapy resistance caused by IL-6 in ovarian cancer cells and its related signal pathways were also analyzed. Results We found that both exogenous and endogenous IL-6 induce cisplatin and paclitaxel resistance in non-IL-6-expressing A2780 cells (the resistance multiple to cisplatin and paclitaxel was: exogenous, 6. 25 and 7.31; endogenous, 7. 13 -8. 34 and 7. 61 - 10. 70), while deleting of endogenous IL-6 expression in IL-6-overexpressing SKOV3 cells promotes its sensitivity to anticancer drugs ( the resistance multiple to cisplatin and paclitaxel was 0. 15 and 0. 10, 0. 10 and 0. 08). IL-6 significantly up-regulated the expression levels of mRNA and protein of drug resistance-associated genes, MDR1 and GST-π, and apoptosis-inhibiting genes, bcl-2, bcl-xL and XIAP in a dose-dependent manner in A2780 cells. In accordance with this finding, the mRNA and protein levels of MDR1 and GST-π enhanced in sense IL-6-transfected A2780 cells, and reduced in antisense IL-6-transfected SKOV3 cells compared with the corresponding parental and control vector-transfected cells, which had no difference. It was found that PD98059 [ mitogen-activated protein kinase-extracellular signalregulated kinase (MEK) inhibitor ] and wortmannin [ phosphatidylinositol 3-kinase (PI3K) inhibitor ]significantly antagonized IL-6-induced phosphorylation of extracellular signal-regulated kinase ( ERK ) and protein kinase B (Akt), respectively, and both of them blocked IL-6-induced cisplatin and paclitaxel resistance and the inhibitory effects of PD98059 and wortmannin were dependent on its concentration.Conclusions These data suggest that IL-6-induced chemoresistance may be associated with increase of both drug resistance-associated genes ( MDR1 and GST-π) and apoptosis-inhibiting genes ( bcl-2, bcl-xL and XIAP), and activation of MEK/ERK and PL3K/Akt. Therefore, modulation of IL-6 expression or its related signaling pathway may be a promising strategy of treatment for drug-resistant ovarian cancer.

Objective: To study if there is an aryl-hydrocarbon receptor (AHR) expression in patients of pulmonary arterial hypertension associated with congenital heart disease (CHD-PAH) and to explore if the amount of AHR expression related to pulmonary vascular remodeling.
Methods:A total of 32 CHD-PAH patients diagnosed by echocardiography and right heart catheterization for surgical repair were enrolled, and the lung tissue biopsy was performed during the operation. The pulmonaryAHR was detected by immunolfuorescence assay, the ratios of vessel wall area/total area (WA/TA) and vessel wall thickness/vessel external diameter (WD/TD) of small pulmonary arteries were calculated with the imaging software, the mRNA expression of AHR, hypoxia-inducible factor-1α (HIF-1α), aryl-hydrocarbon receptor nuclear translocator (ARNT) and vascular endothelial growth factor (VEGF) were examined by RT-PCR. In addition, blood level of AHR was measured by ELISA.
Results: There was AHR expression in pulmonary tissue in all 32 patients. And AHR mRNA expressions were positively related to mPAP (r=0.809,P<0.001), WA/TA (r=0.723,P<0.001), WD/TD (r=0.746,P<0.001); and positively related to mRNA expressions of HIF-1α (r=0.889,P<0.001), ARNT (r=0.738,P<0.001), VEGF (r=0.822,P<0.001). Pulmonary tissue VEGF mRNA expressions were positively related to mPAP (r=0.739,P<0.001), WD/TD (r=0.702,P<0.001) and WA/TA (r=0.657,P<0.001). Blood levels of AHR were positively related to mPAP (r=0.754,P<0.001), WD/TD (r=0.754, P<0.001) and WA/TA (r=0.739,P<0.001).
Conclusion: AHR might be involved in pulmonary vascular remodeling in CHD-PAHpatients.

Objective To investigate the inhibition mechanism of tetramethylpyrazine combined with cisplatin on angiogenesis in Lewis lung cancer mice and to observe the mechanism of Arresten on angiogenesis in lung cancer. Methods The model of Lewis lung adenocarcinoma mouse xenograft was established in this work, and 40 mice were randomly divided into 4 groups: 0.9% sodium chloride solution group(NS group), tetramethylpyrazine group(TMP group), cisplatin group(DDP group), tetramethylpyrazine plus cisplatin group(TMP + DDP group), 10 mice in each group.Mice in NS group were given 0.2 mL of 0.9% sodium chloride solution, mice in DDP group were given 0.2 mL of 2 mg.kg-1 of cisplatin, mice in TMP group were given 0.2 mL of 100 mg.kg-1 of tetramethylpyrazine, mice in TMP+DDP group were given 2 mg.kg-1 of cisplatin and 100 mg.kg-1 of tetramethylpyrazine, each 0.1 mL .Tumor size was measured every day to calculate the tumor volume.The mice were sacrificed to stripp the subcutaneous tumor after continuous medication. The expressions of Arresten, integrin α1β1 and VEGF were determinated by immunhistochemistry and Western blotting. Results The tumor growth of NS group was the fastest and TMP+DDP group was the slowest. Compared with NS group, the expression of Arresten in the other three groups was increased( P<0.01) , and the TMP+DDP group exhibited the highest expression;at the same time, integrin α1β1 , VEGF in the other three groups was decreased(P<0.01), and the TMP+DDP group exhibited the lowest expression.The expression of integrinα1β1 and VEGF was negatively related to Arresten, and the expression of integrin α1β1 was positively correlated with VEGF. Conclusion TMP can inhibited the growth of Lewis lung carcinoma and angiogenesis. Moreover, in combination with cisplatin, TMP can also improved the effect of chemotherapy and then the survival state of mice. The mechanism of action, which TMP suppress tumor angiogenesis may be through improving Arresten and inhibiting integrin α1β1 and VEGF. And the action mechanism of Arresten may be implemented by inhibiting the expression of VEGF by incorporation with integrinα1β1 or by itself to inhibit the expression of VEGF.

Objective To compare the efficacy of native vessel percutaneous coronary intervention (NV-PCI) and optimal drug therapy (ODT) in patients with recurrent angina after coronary artery bypass grafting (CABG). Methods The clinical data of 142 recurrent angina pectoris after CABG patients who had underwent coronary angiography were retrospectively analyzed. Among the patients, 70 cases were treated with NV-PCI (NV-PCI group), and 72 cases were treated with ODT (ODT group). The incidence of major adverse coronary events (MACE) and left ventricular ejection fraction (LVEF) were compared between 2 groups. Results All patients were followed up for at least 1 years. There were no statistical differences in the number of bypass vessels and number of occluded vessels between ODT group and NV-PCI group: (2.5 ± 0.7) branches/case vs. (2.4 ± 0.9) branches/case and (1.4 ± 0.9) branches/case vs. (1.3 ± 0.7) branches/case, P>0.05. The incidence of MACE in NV-PCI group was significantly lower than that in ODT group: 12.9％ (9/70) vs. 22.2％ (16/72), and the LVEF was significantly higher than that in ODT group:(63.5 ± 14.0)％vs. (57.1 ± 9.0)％, and there were statistical differences (P<0.05). Conclusions Compared with the ODT, the NV-PCI has lower incidence of MACE and higher LVEF in patients with recurrent angina pectoris after CABG.

Objective To compare the prognosis of vascular in situ and bridge vessel percutaneous coronary intervention ( PCI) therapy strategies in patients with recurrent angina after coronary artery bypass grafting ( CABG) . Methods A total of one hundred and two patients with recurrent angina after CABG from January 2008 to January 2016 were involved in this study and were divided into two groups according to interventional therapy strategy:74 patients in the vascular in situ PCI group ( in situ group,74 cases) and 28 patients for bridge vessel PCI group ( bridge vessel group,28 cases) . The patients have been followed up for (33. 6± 10. 2) months. The major adverse cardiovascular events ( MACE) of the two groups were recorded, including non?fatal acute myocardial infarction ( AMI) ,target vessel revascularization ( TVR) and cardiac death, and multivariate logistic regression analysis was used to analyze the related factors of MACE. Results Compared with the bridge vessel group,the non?MACE survival rate,non?AMI survival rate and non?TVR survival rate of the in situ group were significantly increased ( ( 71. 6% ( 53/74 ) vs. 57. 1% ( 16/28 ) , 93. 2% ( 69/74 ) vs. 82. 1% (23/28),81. 1% (60/74) vs. 67. 9% (19/28) ),the differences were statistically significant (χ2=8. 141,4. 219,5. 436, P<0. 05) . Multivariable logistic regression analysis showed that age of bridge ( OR=1. 023,95%CI 1. 005-1. 026,P=0. 019) ,diabetes mellitus ( OR=2. 386,95%CI 1. 425-3. 991,P=0. 003) and bridge vessel PCI (OR=1. 884,95%CI 1. 093-3. 220,P=0. 025) were factors that affect the clinical prognosis in patients with recurrent angina pectoris after CABG. Conclusion The clinical prognosis of the in situ PCI is better than bridge vascular PCI in patients with recurrent angina after CABG,while the age of bridge, diabetes mellitus, vascular interventional treatment are factors for the effect of interventional therapy patients prognosis. The clinical prognosis is much better in native vessel PCI than that of bridge vessel PCI in patients with recurrent angina after CABG. The age of bridge,diabetes mellitus and bridge vessel PCI are the factors that affect the clinical prognosis in the patients.

BACKGROUND: Coronary artery disease (CAD) is the commonest cause of heart failure (HF), whereas pulmonary hypertension (PH) has not been established or reported in this patient population. Therefore, we assessed the prevalence, risk factors, and survival in CAD-associated HF (CAD-HF) complicated with PH. METHODS: Symptomatic CAD-HF patients were continuously enrolled in this prospective, multicenter registry study. Echocardiography, coronary arteriography, left and right heart catheterization (RHC), and other baseline clinical data were recorded. Patients were followed up and their survival was recorded. RESULTS: One hundred and eighty-two CAD-HF patients were enrolled, including 142 with HF with a preserved ejection fraction (heart failure with preserved ejection fraction [HFpEF]; left ventricular ejection fraction [LVEF] ≥50%) and 40 with a reduced ejection fraction (heart failure with reduced ejection fraction [HFrEF]; LVEF < 50%). PH was diagnosed with RHC in 77.5% of patients. Patients with PH showed worse hemodynamic parameters and higher mortality. HFrEF-PH patients had worse survival than HFpEF-PH patients. CAD-HF patients with an enlarged left ventricular end-diastolic diameter and reduced hemoglobin were at higher risk of PH. Nitrate treatment reduced the risk of PH. Elevated creatinine and mean pulmonary arterial pressure (mPAP), diastolic pressure gradient (DPG) ≥7 mmHg, and previous myocardial infarction (MI) entailed a higher risk of mortality in CAD-HF patients with PH. CONCLUSIONS: PH is common in CAD-HF and worsens the hemodynamics and survival in these patients. Left ventricle enlargement and anemia increase the risk of PH in CAD-HF. Patients may benefit from nitrate medications. Renal impairment, elevated mPAP, DPG ≥7 mmHg, and previous MI are strong predictors of mortality in CAD-HF-PH patients. TRIAL REGISTRATION ClinicalTrials.gov, NCT02164526.
Coronary Artery Disease/epidemiology* ; Creatinine ; Heart Failure/complications* ; Humans ; Hypertension, Pulmonary/complications* ; Nitrates ; Prevalence ; Prognosis ; Prospective Studies ; Registries ; Risk Factors ; Stroke Volume ; Ventricular Function, Left