Abstract:Aim To investigate the relationships between intercellular adhesion molecule-1 （ICAM-1）, vascular cell adhesion molecule-1 （VCAM-1）, and intraplaque angiogenesis. Methods Twenty-five New Zealand white rabbits underwent balloon-induced abdominal aortic wall injury and were fed with a diet of 1% cholesterol to establish a rabbit model of atherosclerosis. In week 4, 6, 8, 10 and 12 after balloon injury every 5 rabbits were euthanasia respectively. Tissue samples were taken from the abdominal aorta. Some segments were embedded in paraffin and cut into 5 μm thick sections for staining with H&E and reacted with platelet-endothelial cell adhesion molecule-1 （PECAM-1, i.e. CD31）, rat anti-rabbit macrophage antibody-11 （RAM-11）, ICAM-1, and VCAM-1. Results From week 4 to week 12, the expression of ICAM-1 and VCAM-1 increased with the development of atherosclerotic plaque in the abdominal aorta of rabbits.

Abstract:Aim High lipoprotein （a） ［（Lp（a）］ level had been identified as an independent risk factor for coronary and peripheral blood disease. In this study, we investigatd the effect of Lp（a） on endothelial progenitor cells （EPC） homing to the sites of hindlimb ischemia tissues and its potential mechanisms. Methods After treatment with PBS or Lp（a） for 12 h, EPC were transplanted into the hindlimb ischemia mouse model by a tail intravenous injection. The homing and vasculogenesis of EPC were determined. On the other hand, EPC adhesion ability and related gene expression were detected in vitro. Results Lp（a） inhibited homing of EPC to the sites of ischemic tissues and weakened fuction of EPC vasculogenesis. Further, Lp（a） impaired EPC adhesion ability and down-regulated expression of P-selectin glycoprotein ligand-1 （PSGL-1） as well as CXCR4 in EPC in vitro. Conclusion Lp （a） inhibited EPC homing to the sites of hindlimb ischemic tissues possibly by lowering adhesion ability of EPC and PSGL-1, CXCR4 expression in EPC.

Abstract:Aim To explore the changes of aortic morphology and expression of miRNA-195 in aorta of spontaneously hypertensive rats （SHR）, and the effect of benazepril on them. Methods 8-week-old male SHRs were randomly divided into SHR benazepril treatment group （SB group, benazepril 10 mg/（kg·d）, n8） and SHR control group （SC group, n8）, and Wistar rats of the same age served as control were also randomly divided into benazepril treatment group （WB group, benazepril 10 mg/（kg·d）, n8） and control group （WC group, n8）. After 8 weeks treatment, tail arterial blood pressures of rats were measured, aortic morphology were detected by hemotoxylin and eosin staining, and expression level of mi RNA-195 in aorta of rats were detected by qRT-PCR, and expression level of TGF-β1, Smad3, COL-Ⅰ and COL-Ⅲ proteins were detected by Western blot. Results After 8 weeks of medication, the tail arterial systolic blood pressure and diatolic blood pressure of rats in SB group was lower than that in SC group （P< 0.01）, but was higher than that in WB group （P< 0.01）. The expression of miRNA-195 in aorta of rats in SB group was higher than that in SC group, WB group and WC group （P< 0.05 or P<0.01）. The expression levels of TGF-β1 and Smad3 in aorta of rats in SB group were lower those that in SC group （P< 0.05）, but higher than those in WB group （P< 0.01）, and the expression of COL-Ⅰ and COL-Ⅲ protein showed a similar change （P< 0.05 or P< 0.01）. Aortic morphology of rats in SB group was improved compared with SC group, but did not reach the level of that in WC group. Conclusions Treatment with Benazepril can ameliorate the aortic morphology of SHR, and miRNA-195 may play a role in this process, by inhibiting TGF-β1/Smad3 signaling pathway.

Abstract:Aim To observe the effect of apolipoprotein A Ⅰ （ApoA Ⅰ） on the expression of inflammatory cytokines and explore the role of tristetraprolin （TTP）-translational modification in the ApoA Ⅰ inhibition macrophage-derived foam cells expression of inflammatory cytokines. Methods THP-1 macrophage-derived foam cells were treated with ApoA Ⅰ and/or lipopolysaccharide（LPS）. Enzyme linked immunosorbent assay was used to determine levels of interleukin-1β （IL-1β） in cell lysates. Real-time polymerase chain reaction was used to determine mRNA and degradation rate of IL-1β. Western blot was used to determine protein levels of TTP and p-TTP. Results ApoA Ⅰ significantly inhibited the levels of LPS-induced macrophage-derived foam cells inflammatory cytokines, and influenced the expression of TTP and TTP dephosphorylation. Conclusion ApoA Ⅰ inhibiting the expression of inflammatory cytokines in macrophage-derived foam cells may be involved in the dephosphorylation of TTP, which can bind and target ARE-containing mRNA for rapid degradation.

Abstract:Aim To explore the effects and mechanisms of testosterone on the migratory capacity of bone marrow-derived endothelial progenitor cells （BM-EPC）. Methods BM-EPC were cultured and identified from 6-week-old orchiectomized BALB/C male mice. The adherent cells were collected and divided into eight groups randomly, and cocultured with 0, 1, 10, 100 nmol/L testosterone or corresponding concentration of testosterone and androgen receptors antagonists flutamide. BM-EPC' migration towards stroma cell-derived factor-1α （SDF-1α） was assessed by the method of transwell chamber with or without treatment of chemokine receptor 4 （CXCR4） inhibitor AMD3100, and the CXCR4 expression in BM-EPC was detected by reverse transcription polymerase chain reaction （RT-PCR） and Western blot. BM-EPC'migration was assessed by the method of transwell. Results Compared with control group, the migration towards SDF-1α of BM-EPC was increased by testosterone in a dose-dependent manner （group A: 61.80±9.31 group B: 83.20±6.53 group C: 107.00±12.85 group D: 134.80±8.64 P＜0.05）. The CXCR4 mRNA expression of BM-EPC was increased by testosterone in a dose-dependent manner compared with control group （group A: 0.065±0.005 group B: 0.114±0.002 group C: 0.149±0.019 group D: 0.209±0.013 P＜0.05）. The CXCR4 protein expression of BM-EPC was increased by testosterone in a dose-dependent manner compared with control group （group A: 0.23±0.06 group B: 0.40±0.02 group C: 0.62±0.04 group D: 0.77±0.05 P＜0.05）. However, these effects were blocked by flutamide. Different concentrations of testosterone on the role of BM-EPC migration were blocked by AMD3100. Conclusion Testosterone enhances the migratory capacity of BM-EPC by up-regulating the CXCR4 expression via androgen receptors pathway.

Abstract:Aim To examine whether L-type calcium channel （LCC） of human umbilical arterial smooth muscle cells （HUASMC） was influenced by endothelin-1（ET-1）, and whether the possible influence was interfered with by quercetin which has been shown to provide protection against cardiovascular diseases. Methods Primary HUASMC at the third passage culture were identified by immunocytochemistry and randomly divided into following groups:①control group: cultured only with vehicle for 24 h. ② Quercetin alone group: cultured with 80 μmol/L quercetin for 24 h. ③Model group: cultured with 10 nmol/L ET-1 for 24 h. ④U0126 plus ET-1 group: pretreated with 10 μmol/L U0126 for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. ⑤Quercetin pretreatment group: pretreated with quercetin in concentrations of 20 μmol/L, 40 μmol/L and 80 μmol/L respectively for 1 h, then coincubated with 10 nmol/L ET-1 for another 24 h. ⑥ET-1+Que+U0126 group: pretreated with 80 μmol/L quercetin and 10 μmol/L U0126 together for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. ⑦ET-1+nifedipine group: pretreated with 10 μmol/L nifedipine for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. Expression of α_1C, a LCC major subunit , was assayed by RT-PCR and Western blot analysis. The LCC currents（ICaL） were detected by technique of whole-cell patch-clamp. Results α_1C expression , in both mRNA and protein level, as well as ICaL density of model group were significantly down-regulated compared with that of control group or quercetin alone group（P<0.05）, and the repressing effect of ET-1 on LCC was partly reversed by pretreating with U0126 or quercetin（P<0.05）. No significant difference between control group and quercetin alone group was detected. Conclusion Downregulation of α_1C expression and ICaL density in HUASMC by ET-1 partly via ERK parthway was antagonized by quercetin, which could be an important mechanism contributing to the protective effect of quercetin on cardiovascular system.

Abstract:Aim To investigate the effects and possible mechanism of metformin （Met） on anoxia/reoxygenation （A/R） injury in cultured human umbilical vein endothelial cells （HUVECs）. Methods HUVECs were cultured and anoxia /reoxygenation model was set up, then randomly divided into 5 groups:the control group, A/R group, A/R+Met（0.1 mmol/L） group, A/R +Met（0.5 mmol/L） group, A/R+Met（1.0 mmol/L） group. The apoptosis rate of HUVECs was detected by flow cytometry. The mRNA expression of nuclear factor kappa B/P65（NF-κB/P65） was quantified by real-time PCR （RT-PCR） and the supernatant concentrations of intercellular adhesion molecule（ICAM-1） and tumor necrosis factor-α（TNF-α） were detected by enzyme linked immunosorbent assay （ELISA）. Results Compared with control group, apoptosis rate of A/R group was increased（P<0.05）, the mRNA expression of NF-κB/P65 was increased significantly in A/R group, the concentrations of ICAM-1 and TNF-α were improved （P<0.05）. However, compared with A/R group, cell apoptosis rate was decreased in groups treated by metformin（P<0.05）. The mRNA expression of NF-κB/P65 was decreased significantly and the concentrations of ICAM-1 and TNF-α were reduced in metformin pretreatment groups（P<0.05）.

Abstract:Aim To investigate the effects of rosuvastatin on cardiac expression of adiponectin and its receptors in high-fat-fed rats. Methods Male Wistar rats （n＝48） were randomly divided into three groups: control group （NC）, high fat fed group （HF）, high fat fed＋rosuvastatin group （HF＋RS）. After 20 weeks, serum concentrations of triglyceride （TG）, total cholesterol （TC）, low density lipoprotein cholesterin （LDLC）, high density lipoprotein cholesterol （HDLC） and blood glucose （BG） were tested by automatic biochemical analyzer, serum level of adiponectin was measured by ELISA, the expression of adiponectin and its receptors in the myocardium was determined by RT-qPCR and Western blot. Results Compared with NC group, HF group showed increased serum TG, TC, LDLC, BG and adiponectin （P＜0.01）, and decreased serum HDLC （P＜0.01）. Compared with HF group, HF＋RS group showed decreased serum TG, TC, LDLC and adiponectin （P＜0.05）, increased serum HDLC （P＜0.01）, and with no obvious difference in serum BG （P＞0.05）. Compared with NC group, myocardial adiponectin expression were higher （P＜0.01）, myocardial adiponectin receptors expression were lower （P＜0.05） in HF group. Compared with HF group, myocardial adiponectin expression were downregulated （P＜0.05）, myocardial adiponectin receptor 1 expression were upregulated in HF＋RS group （P＜0.05）, while there was no obvious difference in myocardial adiponectin receptor 2 expression between the two groups （P＞0.05）. Conclusions There were elevation of serum adiponectin level and myocardial adiponectin expression, and reduction of myocardial adiponectin receptors expression in the process of feeding rats with high fat food. Rosuvastatin treatment could partly reverse these effects.

Abstract:Aim To evaluate the characteristics of coronary artery lesion in unstable angina （UA） patients with metabolic syndrome （MS） by intravascular ultrasound（IVUS）. Methods According to being complicated with MS or not, 106 patients with UA were reviewed and divided into MS group（n51） and non-MS group （n55）. The levels of body mass index（BMI）, systolic blood pressure （SBP）, diastolic blood pressure （DBP）, fasting plasma glucose （FPG）, 2h postprandial blood glucose（2hPBG）, total cholesterol （TC）, high density lipoprotein （HDL）, low density lipoprotein（LDL）, triglyceride（TG） were observed. The external elastic membrane（EEM） cross section area, lumens area, plaque area, plaque burden, remodeling index （RI） of coronary arteries and the plaque composition were measured by IVUS in two groups. Results BMI, SBP, DBP, FPG, 2hPBG and TG in MS group were significantly higher than those in non-MS group （P<0.05）. HDL was lower than that in non-MS group （P<0.05）. The plaque area and remolding index in MS group were larger than those in non-MS group（P<0.05）. Compared with non-MS group,there were more necrotic core and less dense calcium in the atheroma plaque of MS group（P<0.05）. Multiple regression analysis showed that FPG, SBP and BMI remained as predisposing risk factors for plaque area levels（P<0.001）. Conclusions From our observasion we concluded that in unstable angina patients with MS, the remolding index, plaque area and the amount of necrotic core material are greater in the culprit vessel. Therefore，the plaque of culprit vessel is more vulnerable.

Abstract:Aim To determine whether small, dense low density lipoprotein cholesterol （sdLDLC） affects common carotid artery intima-media thickness （CCA-IMT） or not. Methods 130 patients who had dyslipidemia, diabetes mellitus, hypertension, or smokers participated in this experiment. SdLDLC was collected from automatic analyzer, and CCA-IMT analysis datas were obtained from high-resolution B-mode ultrasound. Results The sdLDLC in CCA-IMT thickening group was significantly higher than that in CCA-IMT normal group （43.97 ± 11.35 mg/dL vs 26.01 ± 7.62 mg/dL, P＜0.001）. The positive association of CCA-IMT with sdLDLC was significant （r0.857, P＜0001）. Conclusions This result indicates that sdLDLC was the best marker of CCA-IMT and suggests that quantitative measurement of sdLDLC provides useful information for the risk assessment of CCA-IMT.

Abstract:Aim Heme oxygenase 1 （HO-1） is a rate-limiting enzyme in the degradation of heme and has potent anti-oxidant and anti-injury effects. The HO-1 gene promoter has different （GT）n repeats （STR） and single nucleotide polymorphisms （SNP） associated with its expression. In this study, we aimed to assess the association between combination of STR and SNP in the HO-1 gene promoter and the susceptibility for coronary heart disease. Methods 171 patients with coronary heart disease and 70 control subjects with sex and age matching were collected Capillary electrophoresis and Sanger sequencing were used for genotyping. Classification tree was performed to distinguish patients from controls. Multiple factors regression was employed to detect the association between genotyping and disease susceptibility, and multifactor dimensionality reduction method was used to identify best factor interacting with STR-SNP haplotype. Results The classification tree distinguished patients with coronary heart disease from controls with 71% of correct prediction （P<0.001）. STR-SNP haplotype was an independent risk factor for coronary heart disease （OR: 1.890, 95%CI: 1.162～3.076, P0.010）, and interacted with smoking to increase risk （OR: 6.994, 95%CI: 3.428～14.272, P0.001）. Conclusion STR and SNP functional polymorphisms in HO-1 promoter could be a marker for screening susceptibility individual of coronary artery disease.

Abstract:Aim To detect the serum levels of hepatocyte growth factor （HGF） and transforming growth factor beta one （TGF-β1） in cerebral atherosclerosis（CAs） patients, explore the relationship between CAs degree and the extent of HGF, TGF-β1, hope to provide the basis for the intervention of exogenous HGF. Methods 71 CAs patients and 33 normal control ones were enrolled, using the double antibody sandwich enzyme linked immunosorbent assay（ELISA） to detect the serum level of HGF, TGF-β1. Results The patients’ serum levels of HGF in CAs group were significantly lower than the control group （P<0.05）. Levels of serum HGF was different compared with each other in CAs groups （P<0.05）, HGF levels in the CAs groups gradually increased with the CAs degree. The patients’ serum levels of TGF-β1 in CAs group were significantly higher than the control group （P<0.001）. Levels of serum TGF-β1 was different compared with each other in CAs groups （P<0.005）, TGF-β1 levels in the CAs groups gradually decreased with the CAs degree. Conclusion There has been a dynamically reciprocal balanced relationship between HGF and TGF-β1, considering viability existing in the administration of exogenous HGF treatment for ischemic cerebrovascular disease caused by CAs in the future.

Abstract:Aim To explore whether the heart rate and heart rate variability relation to heart failure and prognosis. Methods The 245 chronic heart failure patients admitted in General Hospital of Ningxia Medical University between October 2010 and June 2012 were enrolled in this study. Mean heart rate at rest was categorized into predefined groups: A group （50～70 beats/min）, B group （71～90 beats/min）, and C group （＞90 beats/min）. After one year follow-up, the clinical data of 230 patients was collected. 97 patients among them performed a holter monitoring. Based on functional classifications, they were divided into class Ⅰ, Ⅱ, Ⅲ, Ⅳ group and 26 healthy one as comparison. Heart rate variability indexs including standard deviation of all normal RR interval （SDNN）, standard deviation of the 5 minute average RR interval （SDANN）, the percentage of intervals＞50 ms different from preceding interval （PNN50）, square root of the mean of the squares of successive RR interval differences （RMSSD） were collected. Results With increased heart rate, ejection fraction decreased significantly and readmission and mortality rised up at the end of follow-up.

Abstract:Aim To assess the efficiency of rotational atherectomy （RA） with drug-eluting stents （DES） for heavily calcified lesions. Methods By retrospective analysis of 31 cases of severe calcified coronary atherectomy with interventional treatment of patients, 13 patients were carried out under the guidance of intravascular ultrasound （IVUS）, and we analyzed the clinical characteristics, immediate success rate of percutaneous coronary intervention （PCI）, and cardiac events of hospitalization and long-term follow-up results. Results The mean age of 31 patients was 71.81±10.70 years,and 22 patients were male, 9 patients were female. Their coronary artery were confirmed as severely calcified coronary by angiography, including single-vessel disease in 2 cases （6.5%）, double vessel disease in 7 cases （22.6%）, three lesions in 15 cases （48.4%）, left main （LM）＋three lesions in 1 case （3.2%）, LM disease in 6 cases （19.4%）. Rotational atherectomy target vessel in LM-left anterior descending artery （LAD） was 2 cases （6.5%）, LAD was 22 cases （70.9%）, left circumflex artery （LCX） was 2 cases （6.5%）, LAD＋LCX was 1 case （3.2%）, right coronary artery （RCA） was 4 cases （12.9%）. 1 case （3.2%） needed intra-aortic balloon pump （IABP） intraoperation, 6 cases （19.4%） were presented with coronary dissection and 2 cases （6.5%） were with slow flow, but all of them were successfully implemented with rotational atherectomy and stent implantation. Serum troponin T, serum creatine kinase-MB, and serum creatinine had no significant difference. 13 cases were carried out by IVUS, and the minimum lumen diameter, the smallest diameter stenosis rate, the effective area of ？？the lumen had significantly statistical difference pre- and post-operative, respectively（2.0±0.3 mm vs 3.6±0.8 mm, 74.5%±6.8% vs 20.3%±12.5%, 4.0±1.4 mm² vs 10.7±5.5 mm², P＝0.000）. With an average follow-up 10.4±6.4 months, no angina, acute myocardial infarction, sudden cardiac death, target vessel revascularization occurred. Conclusions The combination of rotational atherectomy with stents may selectively ablate calcific plaque and may increase the success rate of the PCI.

Abstract:Aim To evaluate the independent risk factors for restenosis in patients treatment of coronary stenting. Methods One hundred and seventy one patients who underwent the coronary stent implantation with a follow-up of angiography from July 2009 to November 2011 were included in this retrospective study. Among the 171 subjects, 48 patients with 56 target diagnosed of restenosis according to the angiography were defined as case group, and 123 patients with 133 target vessels without restenosis were deemed as control group. The logistic regression model was applied to evaluate the independent risk factors for restenosis in patients treatment of coronary stenting. Results Univariate analysis showed that Univariate analysis showed that stenosis prior PCI ＞90% （χ²4.71，P0.03）, diameter of the stent ≤3 mm （χ²27.92，P0.00）, length of the leision＞15 mm （χ²4.67，P0.03）, residual stenosis ＞5%（χ²10.05，P0.00）, smoking （χ²4.78，P0.03）, diabetes （χ²4.72，P0.03）, irregular anticoagulation（χ²6.70，P0.01） were associated with restenosis in patients treated with coronary stenting. Logistic regression demonstrated that diameter of the stent ≤3 mm （OR4.34, 95%CI:2.01～8.38，P0.02）, residual stenosis ＞5% （OR2.2, 95%CI: 1.56～4.88，P0.03） and irregular anticoagulation （OR1.88, 95%CI:1.21～3.68，P0.04） were the independent risk factors for restenosis. And the proportional hazards model showed patients with diameter of the stent ≤3 mm had the higher risk for restenosis than that with ＞3 mm （HR3.53, 95%CI:2.08～5.99, P0.00） . Conclusion Patients treated with smoler diameter stent, serious residual stenosis and irregular anticoagulation had the higher risk to develop restenosis after coronary stenting and this kind of patients should be taken seriously.

Abstract:Aim To study the influence of abnormal glucose tolerance on oxidative stress and endothelial function and heart rate variability in patients with coronary heart disease （CHD） and the intervention effect of acarbose. Methods 60 patients with glucose tolerance abnormal CHD were chosen as group A, and 30 patients with documented stable coronary artery disease and normal glucose tolerance as group B, and fasting blood glucose （FBG）, 2 hours postprandial blood glucose （2hPBG）, total cholesterol （TC）, triglyceride （TG）, high density lipoprotein cholesterol （HDLC）, low density lipoprotein cholesterol （LDLC）, malondialdehyde （MDA） and erythrocyte superoxide dismutase （SOD）, nitric oxide （NO）, endothelin-1 （ET-1） were measured. 24 hours dynamic electrocardiogram （ecg） was used to monitor heart rate variability, and the above indicators were compared. The abnormal glucose tolerance patients with coronary heart disease were randomly divided into control group （30 cases） and treatment group （30 cases）, the control group was given routine therapy for coronary heart disease, the treatment group was given routine therapy for CHD combined with acarbose 50 mg tid, and we observed them for 6 months. We reviewed the test items after 6 months. We compared the above indexes of the two groups before and after treatment, and analyzed the correlation of the above indicators. Results MAD, ET-1 level in group A is significantly increased compared with group B patients. SOD and NO levels in group A is decreased compared with group B patients （P＜0.05）. Heart rate variability （HRV） indexes, SDNN, SDNN5, SDANN of group A are significantly reduced compared with the B group （P＜0.05）, TRIA, PNN50, rMSSD of group A has no statistically significant difference from group B. After carbose treatment for six months, MAD, ET-1 level of treatment group after treatment declined obviously compared with before treatment and the control group after the treatment. SDNN, SDNN5, SDANN of treatment group after treatment significantly increased compared with before treatment and the control group after treatment （P＜0.05）, TRIA, PNN50, rMSSD of treatment group after treatment has no obvious difference compared with before treatment. No obvious difference was found between the indicators before and after treatment in the control group. Changes in the value of HRV indexes before and after treatment and values of MDA, SOD and NO change before and after treatment were positively correlated （correlation coefficient respectively: r＝0.512, r＝0.368, r＝0.420, P＜0.05）. Conclusions Merger of abnormal glucose tolerance in patients with coronary heart disease has more severe vascular endothelial injury and dysfunction of the autonomic nervous function, and oxidative stress participates in the process. After acarbose's treatment， and oxidative stress relieve, endothelial function and autonomic nervous function improve significantly. Acarbose has a therapeutic effect on vascular endothelial function and autonomic nerve function damage in patients with coronary heart disease and abnormal glucose tolerance.

Abstract:Aim To investigate the effects of oxidized LDL （ox-LDL） on peripheral blood level of regulatory T cells （Tregs） in patients with acute coronary syndrome （ACS）. Methods 18 patients with acute myocardial infarction （AMI）, 27 patients with unstable angina （UA）, 23 patients with stable angina （SA） and 30 healthy subjects （NC） were recruited. The plasma levels of ox-LDL and IL-10 were measured by ELISA, and the percentage of Tregs in peripheral blood were detected by flow cytometry. Peripheral blood mononuclear cells （PBMC） were prepared by Ficoll density gradient, then were incubated with ox-LDL for 48 h for analysis of flow cytometry. Results The frequencies of Tregs and level of IL-10 were significant lower in AMI and UA patients than those in the SA and NC groups, while the level of ox-LDL was elevated markedly in patients with AMI and UA compared with SA and NC group. In addition, the levels of plasma ox-LDL were negatively correlated with the levels of Tregs and IL-10. Moreover, the peripheral blood level of Tregs was obviously decreased after incubation with ox-LDL for 48 h. Conclusion ox-LDL could down-regulate the peripheral blood level of Tregs in patients with ACS, thereby promoting the progression of ACS.

Abstract:Aim To evaluate the efficacy and safety of the treatment in coronary in-stent restenosis with the cutting balloon angioplasty （CBA） and the plain old balloon angioplasty （POBA）. Methods Cochrane Library Controlled Clinical Trials Database （CCTR）, Pubmed, Embase, Wanfang Database, China Journal Full-text Database （CNKI）, Chinese Biomedical Literature Database （CBM）, VIP Database （VIP） were retrieved. The randomized controlled trial （RCT） materials of the treatment in coronary in-stent restenosis with the CBA and the POBA was collected, 7 RCTs was withdrawed, including 960 patients （493 patients in the CBA group and 467 patients in the POBA）, the RevMan 5.0 software was used in the meta analysis. Results （1）The immediate elastic retraction of the CBA group was lower than the POBA group, there was difference between two groups （MD: －0.52, 95%CI: －0.76～－0.29, P＜0.0001） （2）The elastic retraction rate of the CBA group was lower than the POBA group, there was difference between two groups （MD: －13.83, 95%CI: －16.17～－11.49, P＜0.00001） （3）The stenosis degree of coronary diameter after balloon dilatation in the POBA group was higher than the CBA group, there was difference between two groups （MD: －12.99, 95%CI: －18.09～－7.88, P＜0.00001） （4）The late loss of blood vessel diameter in the CBA group was lower than the POBA group, there was difference between two groups （MD: －13.83, 95%CI: －0.50～－0.28, P＜0.00001） （5）The instent restenosis rate after 6-months-followup in the POBA group was higher than the CBA group, there was difference between two groups （MD: 0.44, 95%CI: 0.44, 10.24, 0.80, P＜0.00001）. Conclusion CBA was more safe and effective in treatment of the coronary in-stent restenosis.

Abstract:Apelin/APJ system, a new G-protein-coupled receptors （GPCR） system, is wide distributed in human and animal tissues. Apelin/APJ system could affect many mammalian biological characteristics, including the neuroendocrine system, cardiovascular system and so on. Angiogenesis is described as the sprouting of new capillaries from existing microvessels. Its process is dependent on the proliferation, migration, and capillary-like tube formation of vascular endothelial cells, which plays a critical role in physiological and pathological conditions. Here, we reviewed the function of Apelin in the angiogenesis.

Abstract:Lipoprotein lipase （LPL） plays a central role in lipid metabolism by hydrolyzing triglyceride rich lipoproteins, chylomicrons （CM）, low density lipoproteins （LDL） and very low density lipoproteins （VLDL）, and releasing free fatty acids. Recent studies have shown that LPL is regulated by multiple factors during its synthesis and transport, as well as have influenced on atherogenesis, but the mechanism is unclear. Therefore, we focus on the regulation of LPL's synthesis and transport, its physiological function, and the mechanism of its proatherogenic effect. So as to provide novel therapeutic targets for treating atherosclerosis-related diseases.

Abstract:Coronary artery ectasia （CAE） is defined as a localized or diffused non-obstructive lesion of the epicardial coronary arteries with a luminal dilation exceeding 1.5 fold of the diameter of the normal adjacent arterial segment. The underlying etiology is variable and includes atherosclerosis, degenerative, congenital, inflammatory, infectious, toxic, and traumatic causes. The severity of the changes in the media correlates positively with the diameter of ectasia. The exact mechanism of its development is unknown, therefore this review is necessitated.