Abstract:Aim To study the effect of TNNI3K gene on differentiation of mouse embryonic stem cells into cardiomyocytes. Methods Firstly, we identified the omnipotency of mESC by the morphological characteristics and cellular immunofluorescence, alkaline phosphatase test (ALP) and HE staining. In addition, Embryonic body, cultured by hanging drop method, differentiated spontaneously into beating cardiomyocytes, which were identified by cellular immunofluorescence and transmission electron microscopy (TEM). Furthermore, hTNNI3K gene and siRNA, carried by Lentivirus, infected mESC more than 10 days, respectively, and spontaneously differentiated into mature cardiomyocytes, the differences of myocardial marker proteins expression levels were ananlyzed by flow cytometry (FCM), cellular immunofluorescence, Western blot. Results The membrane proteins of mESC, SSEA-1 and Oct-4, were presented green fluorescence, and ALP test presented blue-purple as well as HE staining with karyoplasmic ratio ＞＞1. What’s more, it was cTnⅠ, cTnT, MLC2 and α-actinin that were clearly visible by cellular immunofluorescence, as well as the unique structure of the muscle fibers by TEM. Furthermore, the cTnT⁺ positive cells rate of TNNI3K-overexpression group was remarkably higher than that in control group, likely the expression of cTnⅠ, MLC2, GATA4, et al. Interestingly, the contraction protein MHC6 expressed earlier than other groups. The rate of cTnT⁺ positive cells in the siRNA group was significantly lower than that of the control group, the same as the expression of other cardiac specific proteins. Conclusions TNNI3K gene might enhance the synthesis of cardiomyocytes and promote the differentiation of mESC into cardiomyocytes.

Abstract:Aim To investigate the mechanism of interleukin-35 (IL-35) in atherosclerosis, we observed the influence of IL-35 in atherosclerosis progression and the serum level variation of its related inflammatory factors, interleukin-10 (IL-10), transforming growth factor β (TGF-β) and IL-17, by establishing the animal models of atherosclerosis in ApoE－/－ mice. Methods 24 ApoE－/－ male healthy mice (8 weeks old) were randomly divided into three groups:control group, atherosclerosis group and IL-35 treatment group (every mouse received intraperitoneal injection of IL-35 (1.2 mg/kg, qd) after providing basic food for a week). Control group were provided basic food, the other two groups were provided fatty food to establish the animal models of atherosclerosis. The blood specimen and aorta vascular tissues were collected after 16 weeks. Hematoxylin-eosin staining was used to observe the atherosclerotic plaque formation, and intima-media thickness was investigated. Expression of IL-10, TGF-β and IL-17 in aortic arteries was detected by immunohistochemical staining. Enzyme-linked immunosorbent assay ( ELISA) method was used to detect the expression level of IL-10, TGF-β and IL-17 in mice serum. Results Compared with the control group, atherosclerotic plaque in atherosclerosis group was obviously formed, and the intima-media was obviously thickened (P ＜0.01), the expression of IL-10 in aortic arteries were significantly increased(P＜0.05), while no changes were found in the expression of TGF-β in aortic arteries(P＞0.05), and the serum levels of IL-10 and TGF-β were significantly decreased (P＜0.05), the expression of IL-17 in aortic arteries and the serum levels were significantly increased(P＜0.05). Compared with the atherosclerosis group, atherosclerotic plaque in IL-35 treatment group were improved, and the intima-media was obviously thinned (P＜0.01), the expression of IL-10 and TGF-β and the serum levels were significantly increased(P＜0.05), while the expression of IL-17 and the serum levels were significantly decreased(P＜0.05). Conclusion IL-35 may retard the pathogenesis of atherosclerosis by down-regulating the levels of inflammatory chemokines IL-17, up-regulating the levels of anti-inflammatory chemokines IL-10 and TGF-β.

Abstract:Aim To investigate and compare the effects of aminolevulinic acid (ALA)-mediated sonodynamic therapy (SDT) on macrophages and foam cells. Methods The THP-1 cells were differentiated into macrophages by adding phorbol-12-myristate-13-acetate, and then the macrophages were differentiated into foam cells by adding oxidized low density lipoprotein. The two kinds of cells were used to study. The protoporphyrin Ⅸ fluorescence intensity were observed after the cells incubated with ALA; The two kinds of cells were divided into control and SDT groups respectively, the following indicators were detected:reactive oxygen, mitochondrial membrane potential, cell apoptosis and the enzyme activity of caspase-9,3. Results Red PpⅨ fluorescence were observed in both macrophages and foam cells after incubation with ALA for three hours. The fluorescence of foam cells was stronger, but there was no statistical difference(P＞0.05); The reactive oxygen of macrophages and foam cells increased 1.84 (P＜0.01) and 1.44 (P＜0.001) times respectively after SDT; Cells with low mitochondrial membrane potential increased 1.96(P＜0.001) and 1.55(P＜0.001) times respectively; The apoptosis rate increased 1.36(P＜0.001) and 2.78 (P＜0.001) times respectively; The enzyme activity of caspase-9 increased 1.34(P＜0.05) and 2.59(P＜0.001) times; And the enzyme activity of caspase-3 increased 2.97(P＜0.01) and 4.88(P＜0.001) times respectively. Conclusion ALA-mediated SDT had apoptotic effects on THP-1 macrophages and foam cells via generation reactive oxygen and damaging mitochondrial, activating caspase apoptosis pathway. It is more effective to foam cells. ALA-mediated SDT may be a potential treatment to attenuate progression of atherosclerotic plaque.

Abstract:Aim To study the effect of angelica on miR-122 in myocardial tissue of spontaneously hypertensive rats (SHR) and its bioinformatics analysis. Methods All the spontaneously hypertensive rats were divided into angelica group, model group, captopril group and angelica captopril group, the same-age Wistar rats as normal control group, then the systolic blood pressure of the tails of all rats in different groups were measured before and after treatments. After 4 weeks, myocardial tissue of the rats were extracted to test miRNA expression profiling. Results Angelica can reduce blood pressure levels in SHR. 13 miRNAs were found up-regulated and 16 miRNAs down-regulated in angelica group, and 15 miRNAs were found up-regulated and 13 miRNAs down-regulated in captopril group and 4 miRNAs were found up-regulated and 21 miRNAs down-regulated in angelica captopril group. We made a analysis of biological process of miR-122, which was up-regulated in all of the three groups, and an amino acid transport gene Slc7a1 was found. By miRNA target precdiction, 8 miRNAs were found targeted by Slc7a1 in angelica group and 11 miRNAs were found targeted by Slc7a1 in captopril group and 11 miRNAs were found targeted by Slc7a1 in captopril group. Conclusions Angelica can regulate the expression of miR-122, with the mechanism that angelica influenced endothelial function by the target gene Slc7a1 of miR-122 and resulted in regulation of blood pressure, which established a foundation of further research.

Abstract:Aim To investigate the effect of Sestrin2 inhibition on apoptosis of human umbilical vein endothelial cells induced by oxidized low density lipoprotein (ox-LDL). Methods The cell injury model was induced by ox-LDL. Western blot was used to detect protein expression of Sestrin2 in human umbilical vein endothelial cells treated with different concentrations of ox-LDL at different time. Protein expression of Sestrin2 was observed by Western blot after transfection with Sestrin2 siRNA. Human umbilical vein endothelial cells were transfected with Sestrin2 siRNA, then treated with ox-LDL, cell apoptosis was detected by flow cytometry, Caspase-3 expression and JNK pathway were observed by Western blot. Results Sestrin2 expression was significantly induced after treatment at different concentrations (0,0 and 100 mg/L) of ox-LDL for 24 h. Moreover, human umbilical vein endothelial cells were incubated with 50 mg/L ox-LDL for various periods of time ranging from 0 to 48 h. The results showed a significant increase of Sestrin2 at protein levels in 24 h and 48 h, and it was the highest level in 24 h. Transfection with Sestrin2 siRNA significantly inhibited Sestrin2 expresssion. ox-LDL significantly induced cell apoptosis, transfection with Sestrin2 siRNA increased the effect. Expression of p-JNK and p-c-Jun was induced by ox-LDL, and this effect could be inhibited by SP600125. Conclusions Ox-LDL induces Sestrin2 expression through JNK/c-Jun pathway, inhibition of Sestrin2 expression significantly increases human umbilical vein endothelial cells apoptosis induced by ox-LDL.

Abstract:Aim To construct the mouse macrophage foam model by using oxidized low density lipoprotein(ox-LDL)； To investigate the effect of allopurinol on lipid accumulation in macrophage foam process and its mechanism. Methods Mouse macrophage cell line RAW264.7 was cultured in vitro, and foam model was constructed by using ox-LDL or Dil-ox-LDL incubating macrophage cells. Macrophage cells were treated with different concentrations of allopurinol, and MTT method was used to screen the suitable experimental concentration. Macrophage cells were treated with suitable concentration of allopurinol. After Dil-ox-LDL incubation, the lipid accumulation in RAW264.7 cells was observed under confocal fluorescence microscopy. The change of total cholesterol in the cells was detected by enzymatic end point method.Semi-quantitative, fluorescence quantitative RT-PCR and Western blot were used to detect the expressions of liver X receptor α(LXRα), ATP-binding cassette transporter A1(ABCA1) mRNA and protein in cells. Results Compared with the ox-LDL induced foam model group, the lipid accumulation and total cholesterol content were significantly decreased in RAW264.7 cells of the allopurinol group. Allopurinol could cause the high expressions of LXRα, ABCA1 mRNA and protein. Conclusion Allopurinol can restrain mouse macrophage foam process induced by ox-LDL, and regulate intracellular cholesterol content through the up-regulation of LXRα-ABCA1 pathway.

Abstract:Aim With the application of two-dimensional electrophoresis and mass spectrometry to study the effect of tanshinoneⅡA on ox-LDL-induced RAW264.7 mouse macrophage-derived foam cells proteome and explore the molecular mechanism of lipid and anti-atherosclerotic effect of tanshinoneⅡA. Methods The isolated purified human serum LDL, oxidized with CuSO₄ to give ox-LDL, co-incubated with RAW264.7 cells, the formation of foam cells containing tanshinoneⅡA 20 mg/L to continue for 24 hours was used as the tanshinoneⅡA group; and the control group excluding tanshinoneⅡA solution was incubated for 24 hours; cells were disrupted by ultrasonic and 4℃ 12000 g centrifugal 30 min, to get supernatant for protein quantitation; protein of the control group and the tanshinone ⅡA group was loaded with the same amount and two-dimensional electrophoresis (IEF and SDS-PAGE); after the completion of electrophoresis, they were stained with silver nitrate to get proteome map with different samples. Through Labscan difference proteomic analysis software, select the protein with expression difference of more than 2-fold. After gel digestion and mass spectrometry analysis, peptide mass fingerprinting was obtained, by Mascot database searching, combined with the 2-D map of protein molecular weight and isoelectric point information protein identification was realized. Results In TanshinonⅡA treated group calreticulin, vimentin, peroxidase-2, CuZn-SOD, zipper protein, stabilin-1, hematopoietic cell specific protein were up-regulated, while GTP protein, ATP synthesis, mimitin, IL-5, HSP70, translationally controlled tumor protein, chloride ion channel protein were down-regulated. Conclusions TanshinonⅡA improved the lipid regulation of foam cells by decreasing the expression of GTP protein and HSP70 and increasing the expression of CRT. TanshinonⅡA regulated the ability of endocytosis by increasing the expression of stabilin-1 and decreasing the expression of ATP synthesis. It also stimulated the metabolism of lipid and lipoprotein by improving the expression of leucine zipper protein and vimentin. Meanwhile, tanshinonⅡA eliminated ROS and lipid peroxidation by increasing the expressions of peroxidase-2 and CuZn-SOD. It also had the effects of anti-inflammation and anti-apoptosis by reducing the expressions of mimitin and IL-5. TanshinonⅡA played a role of anti-tumor by subsiding the expressions of CLIC1 and TCTP. In conclusion, tanshinonⅡA may have function of lipid regulation and anti-atherosclerosis, and can be used to treat cardiovascular diseases in clinic.

Abstract:Aim To explore the effect of liver X receptor-β(LXRβ) on chronic heart failure after myocardial infarction(MI) in mice. Methods The MI model was established by ligation of left anterior descending coronary artery in wild type(WT) mice and LXRβ gene knock-out(LXRβ－/－) mice. Third day after MI, cleaved caspase-3 was detected by Western blot, apoptosis of cardiac muscle cells was evaluated by terminal dUTP nick end labling(TUNEL) staining, and expressions of proinflammatory cytokines tumor necrosis factor α and interleukin-6 were detected by quantitative real-time polymerase chain reaction(qRT-PCR). Fourth week after MI, left ventricular function was assessed with ultrasonic echocardiography, myocardial infarct size was evaluated by triphenyl tetrazolium chloride(TTC) staining, myocardial fibrosis was observed by using Masson trichrome staining and α-smooth muscle actin(α-SMA) staining, and matrix metalloproteinase-9 and type Ⅰ collagen were detected by qRT-PCR to further assess myocardial fibrosis. Results Compared with WT mice, third day after MI, LXRβ－/－ mice exhibited more myocardial cell apoptosis and inflammation in the infarct area； Fourth week after MI, LXRβ－/－ mice showed a significant increase in infarct size, reduced ejection fraction and aggravated left ventricular dilation and enhanced myocardial fibrosis. Conclusions LXRβ gene knock-out aggravates the pathological damage and left ventricular remodeling after MI. As a targeted drug node, LXRβ may contribute to the treatment of MI.

Abstract:Aim To observe the change of Apelin-13 in the myocardium of spontaneously hypertensive rats(SHR), and study its relationship with myocardial hypertrophy and cardiac function. Methods 4 weeks and 20 weeks of male SHR and WKY rats of clean level were selected and divided into 4 groups according to weeks and species, with 8 rats in each group. Noninvasive tail arterial blood pressure and heart mass index were separately measured; echocardiography and hemodynamic system assess were used to ventricular remodeling and cardiac function; HE staining was used to evaluate myocardial cells and arrangement; expression level of Apelin-13 and APJ in the myocardium was detected by Western blot. Results ①The expression of Apelin-13 and APJ in the myocardium of SHR was lower (P＜0.05),and 20 weeks old SHR group was more obvious than 4 weeks old SHR group (P＜0.05). ②With increasing age in SHR, the level of SBP, left ventricular end-diastolic pressure (LVEDP), heart weight/body weight (HW/BW), left ventricular weight/body weight (LVW/BW), interventricular septal thickness at diastole (IVSD) and left ventricular posterior wall thickness at end diastole (LVWPd) increased significantly (P＜0.05), and the level of left ventricular end-diastolic diameter (LVEDd), ejection fraction (EF), fractional shortening (FS) and maximal rate of the decrease of the ventricular pressure(－dp/dt_max) decreased obviously (P＜0.05); cardiomyocytes hypertrophy and myocardial arranged disorder. And compared with 4 weeks old SHR group, the above indexes changed more obviously in 20 weeks old SHR group. ③ The level of Apelin-13 in the myocardium was negatively correlated with IVSD, HW/BW, LVW/BW, LVEDd and LVEDP (P＜0.05), and positively correlated with EF, FS and －dp/dt_max(P＜0.05). Conclusions The expression of Apelin-13 in the myocardium of SHR is lower, a positive correlation with myocardial hypertrophy but a negative correlation with cardiac function, suggests it may be one of influencing factors of hypertensive left ventricular myocardial hypertrophy and cardiac function.

Abstract:Aim To evaluate the relationship between the concentration of plasma retinol-binding protein 4 (RBP4) and subclinical atherosclerosis (subAs) in newly diagnosed type 2 diabetes mellitus (T2DM) patients. Methods 217 newly diagnosed T2DM patients were selected. Plasma RBP4 concentration, fasting and postprandial blood glucose, glycosylated hemoglobin A1 (HbA1c), blood lipid, fasting insulin (FINS) and common carotid artery intima-media thickness (IMT), common iliac artery IMT, femoral artery IMT were measured. The occurrence of subAs in patients was analyzed. Results The average age, FINS and plasma RBP4 concentration in T2DM patients with subAs were significantly higher than T2DM patients with non-subAs (all P＜0.05). The patients were divided into three groups based on the concentrations of RBP4. With the increase of RBP4 concentration, the common carotid artery IMT, common iliac artery IMT, femoral artery IMT were increased, and the common carotid artery IMT in high concentration RBP4 group was higher than that in the other two groups (P＜0.05). With the increase of RBP4 concentration, the prevalence of subAs was gradually increased, and the prevalence of subAs in high concentration RBP4 group was significantly higher than that in the other two groups (P＜0.05). Correlation analysis showed that the RBP4 concentration of newly diagnosed T2DM patients was positively correlated with common carotid artery IMT, common iliac artery IMT, body mass index, systolic blood pressure, blood glucose and FINS. Multiple stepwise Logistic regression analysis showed that the incidence of subAs in newly diagnosed T2DM patients was significantly correlated with the levels of plasma RBP4, age, and low density lipoprotein cholesterol. Conclusion Plasma RBP4 level is positively correlated with subAs, and plasma RBP4 elevation may be one of the independent risk factors of subAs in newly diagnosed T2DM patients.

Abstract:Aim To evaluate the myocardial level perfusion and clinical outcomes at 6 months of the acute myocardial infarction patients after thrombus aspiration combined with tirofiban and verapamil injection via aspiration catheter compared with thrombus aspiration alone. Methods A total of 281 consecutive patients with acute ST elevation myocardial infarction(STEMI) , who underwent primary percutaneous coronary intervention (PCI) within 24 hours of onset, were assigned to two groups:Group A, intracoronary administration(IC) of a fixed dose of verapamil (200 μg) plus tirofiban (10 μg/kg) after thrombus aspiration and group B, IC administration of heparinized saline 5 mL after thrombus aspiration (n=141 and n=140, respectively). The drugs were selectively injected into the infarct-related artery (IRA) via a thrombus aspiration catheter. The primary end-point was post-procedural corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC). The proportion of complete (>50%) ST-segment resolution (STR), the TIMI myocardial perfusion grade (TMPG) 2-3 ratio following PCI, the TIMI flow grade, the incidence of major adverse cardiac events (MACE), the left ventricular ejection fraction (LVEF), the left ventricular end-diastolic diameter (LVEDd) after 6 months of follow-up were observed as the secondary end-points. Results There were no significant differences in the baseline clinical and angiographic characteristics between the two groups. Compared with group B, group A had a lower CTFC (21±6 vs 25±8, P<0.001), a higher proportion of complete STR (66.7% vs 53.6%, P=0.025), an enhanced TMPG 2-3 ratio (65.2% vs 52.1%, P<0.001). There was no statistically significant difference in the final TIMI grade-3 flow between the two groups (91.5 vs 89.3%, P=0.531). The LVEF at 6 months in group A was higher than group B (50±8% vs 46±9%, P<0.001),and the LVEDd in group A was lower than group B (47.6±8.3% vs 52.6±7.7%, P<0.001). However, the incidence of MACE had no statistically difference between the two groups(2.1% vs 3.6%, P=0.712). Conclusions The selective IC administration of a fixed dose of verapamil (200 μg) plus tirofiban via a thrombus aspiration catheter advanced into the IRA after thrombus aspiration is a safe and superior treatment method compared with thrombus aspiration alone in patients with STEMI undergoing primary PCI. This novel therapeutic strategy improves the myocardial level perfusion, in addition to improving heart function. Furthermore, it may improve the postoperative clinical prognosis following PCI.

Abstract:Aim To investigate the image representation of ultrasonography and CT angiography (CTA) for carotid atherosclerosis (CAS) plaque in patients with ischemic cerebral stroke (ICS).Methods Carotid ultrasonography and CTA data were retrospectively analyzed in 575 patients with ICS from June 2013 to June 2015. The results of the two inspection methods were compared. ICS CAS plaque related risk factors were analyzed. Single factor and multi-factor analysis were applied for the related risk factors. Results The results of carotid ultrasonography and CTA were almost identical, and Kappa value was 0.867. Single factor analysis showed that diabetes, hyperlipidemia and age were the risk factors of CAS plaque in patients with ICS (χ²＝46.000, 15.018, 52.613, all P＜0.05). Multi-factor Logistic regression analysis showed that hyperlipidemia was an independent risk factor of CAS in patients with ICS. Conclusions Carotid ultrasonography is of high accuracy, and it is almost identical with CTA results to the CAS plaque screening. Hyperlipidemia is a major risk factor for the formation of CAS plaque. In the daily clinical work, patients with hyperlipidemia should be treated with lipid-lowering therapy and diet control, and then to avoid the occurrence of CAS.

Abstract:Aim To investigate the effect of H-type hypertension on prognosis of patients with coronary heart disease. Methods From August 2011 to June 3,5 patients with coronary heart disease diagnosed by coronary angiography in our hospital were included in this study. According to whether there were hypertension and hyperhomocysteinemia (HHcy), the patients were divided into H-type hypertension group, hypertension group, HHcy group and control group. All patients were followed up. The clinical data and prognosis of different groups were compared. Results The survival time in H-type hypertension group was significantly lower than that in control group (P＜0.05). Compared with the control group, there was no significant difference in survival time of hypertension group and HHcy group (P＞0.05). After adjusting for various factors such as age, sex, smoking, diabetes, body mass index, blood lipid, creatinine, uric acid, coronary artery lesions, Gensini score and left ventricular ejection fraction, multivariate Cox regression analysis showed that H-type hypertension was an independent risk factor for major adverse cardiac and cerebral event (MACCE) (P＝0.000). After adjusting for other factors, compared with the control group, MACCE risk increased significantly in H-type hypertension group (HR 5.3,5%CI 2.728-9.213), hypertension group (HR 2.9,5%CI 1.226-4.892) and HHcy group (HR 1.8,5%CI 0.910-4.214). MACCE risk was greater in H-type hypertension group. Conclusions Hypertension and high homocysteine have synergistic effects on the poor prognosis of patients with coronary heart disease. We should pay more attention to the screening and management of H-type hypertension in patients with coronary heart disease.

Abstract:Aim To investigate the correlation between insulin resistance and atherosclerosis in non-diabetic continuous ambulatory peritoneal dialysis (CAPD) patients. Methods Sixty-four non-diabetic CAPD adult patients were enrolled in this study. The clinical data including insulin resistance index (HOMA-IR) of 63 patients on CAPD was analyzed. The bilateral common carotid artery intima-media thickness (IMT) and carotid artery atheromatous plaque were measured by high resolution two-dimensional ultrasonic diagnostic apparatus. Patients were divided into two groups:non-atherosclerosis group (IMT＜1.0 mm) and atherosclerosis group (IMT≥1.0 mm or atheromatous plaque). Results Compared with the patients in non-atherosclerosis group, the level of plasma albumin in the patients in atherosclerosis group was lower (P＜0.01), but the levels of 2h PBG, HOMA-IR, hs-CRP, TG and LDLC were significantly higher (P＜0.05).The prevalence of insulin resistance was 53.49% in atherosclerosis group, but only 4.76% in non-atherosclerosis group (P＜0.01). Linear correlation analysis showed that atherosclerosis was correlated with age, 2h PBG, HOMA-IR, hs-CRP, LDLC and TG in non-diabetic CAPD patients (r＝0.5,0.3,0.0,0.5,0.351 and 0.458, all P＜0.05). Binary Logistic regression showed that age, 2h PBG, HOMA-IR, hs-CRP were independent risk factors of atherosclerosis. Conclusions HOMA-IR is positively correlated with atherosclerosis and may be a predictor of carotid atherosclerosis in non-diabetic peritoneal dialysis patients.

Abstract:Aim To observe the level of the serum cystatin C and β2-microglobulin of acute cerebral infarction patients and its relationship with different subtypes by the Trial of Org10172 in Acute Stroke Treatment (TOAST). Methods The investment contains 115 acute cerebral infarction patients and 50 controls ,and the patients were classified into five subtypes according to TOAST creteria . Recorded the serum Cyst-C and β2-MG level and analyzed the difference between the two groups and their TOAST subtypes. Results The serum Cyst-C and β2-MG of the patients was significantly higher than the controls(P ＜ 0.05). Logistic linear regression analysis showed that serum level of Cyst-C had significant correlation(P ＜ 0.05). The serum Cyst-C of the subtypes was significantly higher compared to the controls,and the level of Cyst-C in the CE was the highest (P ＜ 0.05). There was no difference among each subtypes of the serumβ2-MG. Logistic linear regression analysis showed that serum level of Cyst-C had significant correlation with CE (OR=8.98;95% CI 1.051-8.677 ). Conclusion The changes in the levels of serum Cyst-C, beta 2-MG may be risk factor of cerebral infarction. The serum Cyst-C varied with different subtypes of cerebral infarction,specially elevating in the subtype of CE,which indicates that the serum Cyst-C is possibly connected with etiology of cerebral infarction.

Abstract:Aim To explore the post-discharge death of patients with acute ST-segment elevation myocardial infarction(STEMI) after emergency percutaneous coronary intervention(PCI) and the risk factors affecting post-discharge death. Methods 413 patients with STEMI who underwent PCI were collected to investigate clinical data and follow-up results. The follow-up endpoint was all-cause death after discharge. The deaths of patients were recorded after discharged from the hospital, and the related factors affecting post-discharge death were analyzed. Results The average follow-up time was 26.38±14.21 months. There were 27 patients died and 43 patients lost to follow up(10.4%) during the follow-up period. COX proportional hazards regression model showed that age≥60 years(HR＝8.927, P＝0.037) and Killip class＞Ⅰ(HR＝2.546, P＝0.034) were associated with post-discharge death after PCI in STEMI patients. The cumulative mortalities of 1-year, 2-year, 3-year and 4-year in all follow-up patients were 4.9%, 7.3%, 7.9% and 10.1% respectively. The cumulative mortalities of 1-year, 2-year, 3-year and 4-year in age≥60 years group were significantly higher than those in age＜60 years group(7.7% vs 0.7%, 11.6% vs 0.7%, 12.7% vs 0.7%, 16.0% vs 0.7%, all P＜0.001).The cumulative mortalities of 1-year, 2-year, 3-year and 4-year in Killip class＞Ⅰ group were significantly higher than those in Killip class Ⅰ group(12.7% vs 2.5%, 19.8% vs 3.5%, 19.8% vs 4.4%, 26.5% vs 5.5%, all P＜0.001). Conclusions The post-discharge mortality rate of patients with STEMI after PCI is still higher. Age≥60 years and Killip class＞Ⅰ are independent risk factors of post-discharge death after PCI in STEMI patients.

Abstract:Aim To investigate the clinical incidence rate of cerebral microbleed (CMB) in patients with acute ischemic stroke (AIS) after intervention of antithrombotic therapy; To analyze the possible risk factors and imaging characteristics of CMB. Methods On the basis of clinical evaluation after admission, all AIS patients were administered mono-antiplatelet therapy or dual-antiplatelet therapy. At the end of treatment, CMB situation was evaluated by magnetic susceptibility weighted imaging. The differences of clinical data were compared between CMB group and non CMB group. Results A total of 240 patients with AIS was included in this study, and 70 cases (29.17%) were complicated with CMB among the patients. In the CMB group, microbleed lesions were located in basal ganglia region (48 cases, 68.57%), cortical-subcortical region (41 cases, 58.57%), thalamencephalon (26 cases, 37.14%), brainstem (24 cases, 34.29%), and parencephalon (16 cases, 22.86%). The size of microbleed lesions ranged from 0 to 108 μm, average of 14.02±0.32 μm. There were significant difference in the age, drinking history, hypertension history, history of cerebral hemorrhage, systolic blood pressure and diastolic blood pressure of CMB group compared with non CMB group (P＜0.05). Conclusions Patients with AIS are prone to concurrent CMB after intervention of antithrombotic therapy, and clinicians should pay special attention to this.

Abstract:Aim To study the morbidity rate of metabolic syndrome (MS) in patients with type 2 diabetes and the effects of accumulation of MS components on blood lipid profile. Methods According to the recommendation of National Lipid Association, components of MS and blood lipid profile were observed and analyzed in 3750 patients with type 2 diabetes.Results Morbidity rate of MS in type 2 diabetes in our study was 63%, and there are 1268 men (54%) and 1087 women (46%), respectively. Dyslipidemia was included in the most common combinations of MS. Morbidity rate of dyslipidemia in type 2 diabetes in our study was 58%, and there are 1322 men (60%) and 862 women (40%), respectively. With the accumulation of MS components, the levels of total cholesterol, triglyceride, low density lipoprotein cholesterol (LDLC) increased significantly, but the level of high density lipoprotein cholesterol (HDLC) decreased gradually. Conclusions We should pay more attention not only to blood glucose, but also to lipid metabolism disorder in type 2 diabetes complicated with MS. By doing so, the cardiovascular risk of patients with type 2 diabetes will be decreased.

Abstract:As we know, atorvastatin has been widely used to treat hyperlipidaemia and cardiovascular diseases. Atorvastatin also has anti-inflammatory effect on inhibiting the expression of pro-inflammatory cytokines, such as interleukin-1β, interleukin-6 and tumor necrosis factor-α, etc. However, the underlying mechanisms of anti-inflammatory effect of atorvastatin are still largely unknown. In this review, we summarize the progress of Toll-like receptors, inflammasome, microRNAs, small GTPase and peroxisome proliferator-activated receptors on the anti-inflammatory effect of atorvastatin, in order to provide new evidence for further understanding of the anti-inflammatory mechanisms of atorvastatin.

Abstract:MicroRNA-146a is a member of the microRNAs. It regulates immune response, inflammation, tumor, cell proliferation, differentiation and apoptosis. In addition, It plays an important role in the process of pathophysiology of cardiovascular disease. It will be a new therapeutic target of atherosclerosis by using microRNA-146a to suppress the inflammation of atherosclerosis.

Abstract:Atherosclerosis is recognized as a chronic inflammatory disease of the artery wall, in which monocytes/macrophages plays a key role in its development. The migration ability of monocytes/macrophages is damaged in atherosclerotic plaque, and retained in plaque. This increases plaque instability and accelerates the progression of atherosclerotic lesions. Recent studies show that neural guidance factor netrin-1, secreted by macrophages in atherosclerotic plaque, can inhibit macrophage migration out of plaque and promote the progress of atherosclerosis, through binding to receptors on the surface of macrophages. However, in the early stage of atherosclerosis, netrin-1 expressed in vascular endothelial cells is found to play a protective role in atherosclerosis.