Objective:To explore and analyze the predictive value of EuroSCORE Ⅱ and SYNTAX Ⅱ scores for clinical outcomes in patients undergoing coronary artery bypass grafting (CABG) surgery.Methods:A total of 500 coronary artery disease (CAD) patients who underwent CABG in Shanxi Cardiovascular Hospital from April 2014 to July 2023 were selected as the study subjects, all patients were given EuroSCORE Ⅱand SYNTAX Ⅱ scores to evaluate the predictive value of EuroSCOREⅡfor perioperative mortality and SYNTAX Ⅱ for 4-year mortality. Univariate and multivariate Logistic analysis were employed to analyze the independent risk factors for perioperative and 4-year mortality.Results:There were 3 deaths during the perioperative period, with a mortality rate of 0.60%, the predicted mortality rate of EuroSCOREⅡwas 1.71%; there were 21 deaths at 4 years after surgery, with a mortality rate of 4.23% and the predicted mortality rate of SYNTAX Ⅱwas 9.02%. Logistic regression analysis showed that left ventricular ejection fraction (LVEF) was the only independent protective factor for perioperative mortality, and advanced age was the only independent risk factor for 4-year postoperative mortality in patients ( P<0.05). The analysis of the working characteristic curve of the subjects found that the area under the receiver operating characteristic curve ( ROC) of EuroSCORE Ⅱ for perioperative mortality was 0.782, and the area under ROC curve of SYNTAX Ⅱfor postoperative 4-year mortality was 0.743. Conclusion:Both EuroSCORE Ⅱand SYNTAX Ⅱhave certain predictive value for perioperative mortality and postoperative 4-year mortality in patients undergoing CABG, respectively, but the predicted mortality rate is relatively higher.

Omentin-1 is one of the newly discovered Secretory protein,which is mainly synthesized and secreted by vascular stromal cells in visceral adipose tissue.Some related researches have shown that omentin-1 has effects of prevention and mitigation on pathological myocardial hypertrophy.With further explorations and clinical applications of omentin-1,it will provide new strategies and methods for the prevention and treatment of human pathological myocardial hypertrophy and heart failure.

Objective To observe the effects of granulocyte colony stimulating factor (G-CSF) on electrophysiological properties of post-infarct ventricles.Methods Sixty-seven survival Wistar rats were divided into 4 groups:Sham group,Control group,MI early G-CSF group (E-G) and MI delay G-CSF group (D-G) after ligation of the left coronary artery as myocardial infarction model.Monophasic action potential(MAP) was recorded by absorption electrode in ex vivo perfused rat hearts.Effective refractive period(ERP),sinus cardiac length (SCL),action potential amplitude (APA),maximal depolariged (Vmax),ventricular fibrillation threshold(VFF) and ventricular fibrillation duration(VFD) were measured.Results The electrophysiological parameters (SCL,VFT,VFD,APA,ERP/MAP90,dispersion of ERP and MAP90) of the E-G group were improved significantly (all P ＜ 0.05) at day 7 post MI.Improvement in SCL,dispersion of ERP and MAP 90 were found in the D-G group as well at day 7 post MI (all P ＜ 0.05).Substained improvement in electrophysiological parameters were found in the E-G group at 3 months after MI (P ＜0.05).Besides SCL,APA,Vmax and dispersion of MAP90,all other parameters in the D-G group were similar to that of the control group with no statistical significance and even had a tendency of deterioration in ERP and MAP90 3 months after MI.Conclusion G-CSF intervention could improve electrophysiological properties of ischemic ventricles.Early G-CSF intervention showed better outcomes compared to delay G-CSF intervention on electrical remodeling ischemia myocardiumwhich may have effect on reducing the development of ventricular arrhythmia.

In recent years,we have progressed in the treatment of coronary heart disease by a large margin,which improved the prognostic condition of coronary heart disease patients,conspicuously.Whereas,we have still harbored discordant reservations about what fuels in the theraputic stragety of the left main and/or three vessel disease which causes acute myocardial infarction and the sudden cardiac death,for the time being,internationally.EuroSCORE and SYNTAX Score are both widely accepted in probing in the theraputic stragetic credits,internationally.Hence,we are about to review the twin credits system on the optional directive meaning of the strategy of myocardial revasscularization in the left main and/or three vessel patients.

Objective To investigate the expression and biological function of miRNA-449 a in lung cancer . Methods A case-control study was conducted in 58 patients diagnosed with lung cancer ( carcinoma and adeno-carcinoma) and normal tissue closely adjacent to tumor.MiRNA-449a simulation was designed and synthesized, was dissolved into two different concentrations as 10 and 20 mg/mL.The expression of miRNA-449a in lung cancer tissues and matched normal tissues were detected by Real time PCR .The expression of luciferase gene was detected by chemiluminescence technique.MiRNA-449a mimics on cell apoptosis was evaluated by MTT assay . Results The mean tissues expression levels of miRNA-449 a in squamous carcinoma group and adenocarcinoma group were 1.48 ±1.63 and 1.52 ±1.54 respectively, and were significantly lower than in control group (2.74 ± 1.55 ) ( P<0.01 ) .The average intensity of fluorescent protein in 10 mg/mL group and 20 mg/mL group were 2 115 ±168 and 1 352 ±159 respectively , and were significantly lower than that in control group ( 4 975 ±115 ) ( P<0.01 ) .Conclusions MiRNA-449 a was down-regulated expression in lung cancer and induced apoptosis .

Objective Cervical heterotopic heart transplantation model was established in different inbred strains of mice with modified cuff technique. Inbred male Balb/c mice and C57BL/6 mice were selected as donors and recipients, respectively. Mice were randomly assigned into four groups: control group (the donor hearts were perfused through coronary artery with 200 μl, 0℃～4℃ St. Thomas Ⅱ solution during 2 to 3 min, then they were immersed in it for 15 min), CsA group ( the donor hearts were perfused with the same method as for the control's and intraperitoneal injection of CsA 5 mg· g-1 · d -1 was given after surgery ), H2-B1 transfection group (the donor hearts were perfused through coronary artery with 200 μl, 0℃ -4℃ St. Thomas Ⅱ solution contained with 30 μg H2-Bl plasmid vectors during 2 to 3 min, then they were immersed in it for 15 min ), and H2-B1 + CsA group ( the donor hearts were perfused with St. Thomas Ⅱ solution contained H2-Bl gene plasmid and intraperitoneal injection of CsA was given after surgery as mentioned above. ). At 1,3 and 7 days after transplantation, three allografts were harvested at each time points in all of the groups, respectively, for pathological examination and analysis of CD40 expression with immunohistochemistry assays. The expression of Th1/Th2 cytokines were also determined with flow cytometry. The survival time of rest allografts were observed. Results Histological features for rejection were observed more apparent in the grafts of control group than those in other groups, especially those in H2-Bl + CsA group. The expression of CD40 in H2-Bl + CsA group and CsA group was lower significantly than that of the control group ( P ＜0.01 ), so was the expression of CD40 in the H2-Bl group as compare with that of the control group (P ＜0.05). No significant difference between H2-Bl group and CsA group (P ＞0.05 ) at 7 days was observed. The expression of IL-2, TNF-α (Th1 cytokines) in control group was much higher than that in other groups, and the expression of IL-4 ( Th2 cytokine) in control group was much lower ( P ＜0.05 ). The level of IL-4 in CsA group increased significantly at 3 days ( P ＜ 0.05 ), with a peak level at 7 days after transplantation (P＜0.01). The survival time of grafts was significantly prolonged in CsA group (P＜0.01), H2-Bl group (P＜0.05) and H2-Bl+CsA group(P＜0.01). Conclusion Treating the donor hearts with H2-Bl plasmid vectors at the time of transplantation may suppress rejection in the heart allografts and prolong the survival time through some presumed mechanisms such as preventing upregulation of CD40 expression, relucing the production of IL-2 and TNF-α, increasing the production of IL-4, and as a result, inducing immune tolerance, as well as improving the function of transplanted heart grafts.

Objective To investigate the effects of Blastocyst MHC gene transfection to coronary on the survival time of mouse heart grafts and the mechanism. Methods Inbred male Balb/c mice and C57BL/6 mice were selected as donors and recipients respectively, to construct mouse cervical heart transplantation models. In the control group, the donor hearts were perfused using the 0～4 ℃ St. ThomasⅡ solution; in the cyclosporine A (CsA) group, the donor hearts were perfused as same as the control's and received intraperitoneal injection of CsA (5 rng·g-1·d-1) after surgery; in the transfection group, the donor hearts were perfused using St. Thomas Ⅱ solution with Blastocyst MHC gene plasmid; in the combined treatment group, the donor hearts were perfused using St. Thomas Ⅱ solution with Blastocyst MHC gene plasmid and received intraperitoneal injection of CsA (5 mg·g-1·d-1) after surgery. The survival time of transplanted heart allografts were observed, and their histopathological changes and the degrees of coronary intimal hyperplasia were estimated.Blastocyst MHC gene mRNA expression levels were detected by real-time fluorescence quantitative RT-PCR. Flow cytometry was applied in assessment of the levels of CD4+ CD25+ regulatory T cells (Treg) and CD3+ CD8+ T cells. Results The survival time in the CsA group, transfection group and combined treatment group was significantly longer than in the control group (P＜0.05) and that in the combined treatment group was the longest, up to (20. 50 ± 5. 61) days. On the postoperative day 1 and 3, Blastocyst MHC gene mRNA expression level in the transfection group was significantly higher than that in the control group (P＜0.05). On the postoperative day 7, the degrees of rejection and coronary intimal hyperplasia in the combined treatment group were the lightest. On the postoperative day 7 the number of Tregs in the CsA group and the combined treatment group was significantly increased as compared with that in the control group (P＜0.05), but that of CD3 + CD8+ T cells in the CsA group and the combined treatment group was less than that in the control group (P＜0.05). Conclusion Blastocyst MHC gene transfection in mouse transplanted cardiac allograft can extend its survival time through upregulation of Treg and downregulation of CD3 + CD8 + T cells in the mice. The combination of Blastocyst MHC gene and CsA may exert the synergic effects.

BACKGROUND:Great saphenous vein is the most common vascular material in coronary artery bypass grafting, however, the graft neointimal hyperplasia and subsequent atherosclerosis result in angiostegnosis, which affect the long-term efficacy. OBJECTIVE: To analyze the pathophysiology and mechanism of the angiostenosis, additionally, to construct smooth muscle cell specific SM22a promoter and SMHC enhancer. METHODS: The database of PubMed, HighWire and CNKI were retrieved with key words of "SM22α promoter, SMHC enhancer, stenosis, Pi3k and RNAi/RNA interference". The language was confined to English and Chinese. The literatures correlated with angiostenosis, VSMC-specific SM22α promoter and enhancer were selected. The reviews and overlapped researches were excluded. In vascular smooth muscle cell proliferation and apoptosis of graft neointimal hyperplasia, as well as the extent of graft thrombosis were considered as evaluation index. RESULTS AND CONCLUSION: More than 8 730 literatures were searched by the computer. According to inclusion and exclusion criteria, the SM22α promoter and angiostenosis were analyzed. The neointimal hyperplasia and thrombosis had a strong impact on prospective efficacy after coronary artery bypass grafting. The PI3K-Akt-mTOR pathway was a crucial signal passage which regulated cell proliferation and migration. RNA interference targeting Pik3cb can efficiently suppress the neointimal hyperplasia through down regulating the PI3K-Akt-mTOR pathway. The shRNA eukaryon expression plasmid vectors targeting rat Pik3cb were constructed using VSMC-specific SM22α promoter. On the one hand, it can suppress the neointimal hyperplasia, and on the other, it can prevent the occurrence of thrombosis.SM22a is a specific gene in vascular smooth muscle cell. The studies that applied VSMC-specific SM22α promoter/enhancer to vascular grafting provide a new strategy to prevent angiostenosis and thrombosis.