Abstract:AimTo investigate the effects of hydrogen sulfide (H₂S) on oxidized low density lipoprotein (ox-LDL) induced expression of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in endothelial cells.MethodsHuman umbilical vein endothelial cells (HUVEC) were cultured and treated with ox-LDL (50 mg/L) in the absence or presence of NaHS for 24 h.The mRNA expression and protein content of TF and TFPI in HUVEC were determined by RT-PCR and ELISA, respectively.ResultsTreatment with ox-LDL for 24 h caused an increased TF mRNA and protein expression by 8 and 7 times, respectively (p<0.01), and a decreased TFPI mRNA and protein expression by 73% and 65%, respectively (p<0.01).However, pretreatment of HUVEC with different concentrations (25, 50, 100 and 200 μmol/L) of NaHS (the donor of H₂S)　for 1 h before ox-LDL stimulation resulted in a marked inhibition of ox-LDL-induced TF mRNA and protein expression by 12%, 31%, 63%, 80% and 13%, 30%, 62%, 77%, respectively (p<0.05), and an increase of ox-LDL-induced inhibition in TFPI mRNA and protein expression by 0.6, 1.2, 2.0, 2.6 times and 0.3, 0.7, 1.1, 1.6 times, respectively (p<0.05).ConclusionH₂S can inhibit ox-LDL-induced TF expression and increases ox-LDL-inhibited TFPI expression in endothelial cells.

Abstract:AimTo study the proinflammatory cytokines production and apoptosis of macrophages upon Mycoplasma pneumoniae (M.pneumoniae) lipid-associated membrane proteins (LAMP) stimulation, and evaluate the molecular mechanism of M.pneumoniae to cause atherosclerosis.MethodsThe cultured human macrophages were incubated with various concentrations of M.pneumoniae LAMP preparations.The proinflammatory cytokines TNF-α, IL-1β and IL-6 production were detected by ELISA and cell apoptosis by flow cytometry.At the same time, the activation of NF-κB and the effects of pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, on M.pneumoniae LAMP-induced macrophages apoptosis were analyzed by Western blot.ResultsM.pneumoniae LAMP could induce high level of TNF-α, IL-1β and IL-6 production and macrophages apoptosis.These effects were highly associated with NF-κB activation of macrophages.PDTC could significantly inhibit the activation of NF-κB and partially reduce M.pneumoniae LAMP-induced macrophages secretion and apoptosis.ConclusionsM.pneumoniae LAMP can induce proinflammatory cytokines secretion and macrophages apoptosis by activating NF-κB, and it may be an important etiological factor for atherosclerosis.

Abstract:AimTo study the influence of angiotensinⅡ（AngⅡ） and angiotensin(1-7)(Ang(1-7))on expression of ATP-binding cassette transporter A1（ABCA1）and cholesterol efflux in THP-1 macrophages.MethodsTHP-1 monocytes were stimulated and differentiated into macrophages.They were divided into blank control, AngⅡ group, Ang(1-7) group, concentration of Ang(1-7) + AngⅡ group, and Ang(1-7) + AngⅡ+A-779 group.The expression of ABCA1 mRNA and protein were measured by RT-PCR and Western blot, cholesterol effluent was measured by liquid scintillator.ResultsCompared with the control group, AngⅡ decreased ABCA1 in both protein (0.473±0.029 vs 0.652±0.031,p<0.05) and mRNA(0.471±0.036 vs 0.857±0.053,p<0.05) and inhibited the cholesterol efflux(8.937±0.353 vs 13.942±0.478,p<0.05).However, Ang(1-7) opposed the reduction of ABCA1(0.722±0.045 vs 0.652±0.031,p<0.05) and ABCA1 mRNA(0.949±0.087 vs 0.857±0.053,p<0.05） induced by AngⅡ, and promoted the cholesterol efflux(15.477±0.882 vs 13.942±0.478,p<0.05), which appeared dose-dependent.When incubated with A-799, an inhibitor of Ang(1-7), the effects of Ang(1-7) on promoting the expression of ABCA1, ABCA1 mRNA and the cholesterol efflux were significantly attenuated(0.515±0.048 vs 0.473±0.029,0.472±0.063 vs 0.471 ±0.036,9.309±0.333 vs 8.937±0.353,p>0.05).ConclusionThe effects of AngⅡ on the atherosclerosis may be correlated to the down-regulation of ABCA1.Ang（1-7）concentration-dependently attenuated the reduction of ABCA1 induced by AngⅡ in THP-1 derived macrophages through its specfic receptor Mas,and increased the cholesterol effluent.

Abstract:AimTo investigate whether aerobic exercise could decrease plasma homocysteine (Hcy) level and reduce atherosclerosis accelerated by hyperhomocysteinemia (HHcy) in ApoE-/- mice.MethodsSix-week-old female ApoE-/- mice were assigned to three groups: control group, HHcy group and HHcy＋exercise group.HHcy animal model was made by feeding a high Hcy chow.After 1 week of acclimatization, HHcy＋exercise group was trained in a motorized rodent treadmill for 8 weeks (slope: 0°, speed: 15 m/min, 60 min/d, 5 d/wk).Plasma Hcy level and lipid levels were determined enzymatically by auto-biochemistry analysis system.Aortic roots were isolated for immunohistochemistry to compare the plaques’ areas.ResultsPlasma Hcy levels in HHcy group were higher than control group, furthermore, the Hcy levels significantly decreased in HHcy＋exercise group compared with HHcy group.There were not significant differences in body weight, daily drinking amount, plasma total cholesterol, LDLC, HDLC and triglyceride concentrations in the three groups.Compared with control group, atherosclerotic plaque area and plaque burden were increased in HHcy group.However, the plaque area and plaque burden in HHcy＋exercise group were decreased when co-mpared with HHcy group.ConclusionAerobic exercise decreases plasma Hcy levels and reduces the development of atherosclerosis in HHcy ApoE-/- mice, which does not depend on the decrease of cholesterol levels.

Abstract:AimTo investigate the effect of hydrogen sulfide on cardiac remodeling in rats, after the two-kidneys-one-clip (2K1C) model built.Methods 34 male Sprague-Dawley (SD) rats were randomly divided into four groups: control group, sham-operated group, 2K1C model group and hydrogen sulfide (H₂S) group.Systolic blood pressure (SBP), the left ventricle weight/body weight (LVW/BW), the heart weight/body weight (HW/BW) and the left ventricle weight/heart weight (LVW/HW) were measured to assess cardiac remodeling.The diameter, the cross-sectional area of the myocardial cells were evaluated by HE stain.Collagen deposition were detected by Masson stain.Angiotensin Ⅱ receptor-1 (AT1) expression in the myocardial cells were assessed by immunohistochemistry.ResultsCompared with the control group, SBP increased persistently in 2K1C group and LVW/BW, HW/BW, LVW/HW increased accordingly. While in the H₂S group, SBP elevated transiently and tended to decrease afterward.LVW/BW, HW/BW, LVW/HW decreased in H₂S group compared with 2K1C group.HE stain showed significantly milder myocardial injury in H₂S group than that in 2K1C group.Masson stain showed less collagen deposition in H₂S group than that in 2K1C group.The expression of AT1 receptor was up-regulated in the 2K1C group, which can be reversed by treatment with H₂S.ConclusionH₂S can attenuate cardiac remodeling in 2K1C rats by down-regulating AT1 expression.

Abstract:AimTo investigate the intermittent hypoxia and high-fat diet promoting the formation of atherosclerosis through increasing expression of lipoprotein-associated phospholipase A₂ (Lp-PLA₂) and oxidized low density lipoprotein (ox-LDL).MethodsUsing randomized controlled study, prospective animal and factorial experiment, the animal models were established by intermittent hypoxia and high-fat diet.24 New-Zealand white rabbits (4 months old) were divided into the following 4 groups: control group, intermittent hypoxia group(IH), high-fat-feeding group(HFD) and intermittent hypoxia & high-fat-feeding group (IH+HFD).Each group had 6 rabbits.Rabbits in IH group and IH+HFD group were placed in a cabin which nitrogen and air were periodically infused every 5 minutes for 8 h/day.The lowest level of oxygen concentration was at 8%.The highest level of oxygen concentration was at 21%.The HFD group and IH+HFD group were fed with fat-rich-stoyer.The intervention experiment lasted for 12 weeks.Blood samples for measurements of Lp-PLA₂ and ox-LDL were collected at 0 w, 4 w, 8 w and 12 w.The formation of atherosclerosis in the aortic arch and abdominal aorta was observed.ResultThe Lp-PLA₂ level of IH group, HFD group and IH+HFD group at 8th and 12th week was higher than control group and at 4th week, the difference has statistic significance (p<0.05).The Lp-PLA₂ level of IH+HFD group at 4th, 8th and 12th week was higher than control group, IH group and HFD group(p<0.05).The two factors of IH and HFD had significant synergistic effects on the Lp-PLA₂ at 4th, 8th and 12th week（p=0.000,p=0.001,p=0.000）.The ox-LDL level of IH group, HFD group and IH+HFD group at 4th, 8th and 12th week was higher than control group(p<0.05).It was higher at 4th week than at 8th and 12th week (p<0.05).The ox-LDL level of IH+HFD group at 4th, 8th and 12th week was higher than control group, IH group and HFD group(p<0.05).The two factors of IH and HFD had significant synergistic effects on the ox-LDL at 4th week（p=0.000）, however they had no significant synergistic effects at 8th and 12th week（p=0.104 and p=0.166）.The formation of atherosclerosis was observed by oil red "O" staining in abdominal aortic and by HE staining in aortic arch and abdominal aorta under IH and HFD intervention.ConclusionThe intermittent hypoxia and high-fat diet can promote the formation of atherosclerosis through increasing expression of Lp-PLA₂ and ox-LDL.

Abstract:AimTo investigate the effect and underlying mechanisms of Caffeic acid phenethyl ester(CAPE) on inflammatory cytokines secretion in oxidized low density lipoprotein (ox-LDL)-stimulated THP-1 macrophages.MethodsThe THP-1 macrophages were preincubated with CAPE at different concentrations for 2 h, and then treated with ox-LDL(40 mg/L) for 24 h.The secret levels of TNF-α, IL-6 and MCP-1 in cells were determined by ELISA.After treated with 40 mg/L of ox-LDL for the indicated times, the expression of COX-2 in THP-1 macrophages was measured by Western blot.Subsequently, THP-1 cells were pretreated with indicated concentrations of CAPE, and then incubated with or without 40 mg/L of ox-LDL for 1 h.The expressions of COX-2, IκB-α and nuclear NF-κB were measured by Western blot.ResultsCAPE suppresses the ox-LDL-induced up-regulation of TNF-α, IL-6 and MCP-1 in THP-1 macrophages.The expression of COX-2 was markedly increased by ox-LDL, which, however, could be significantly attenuated by CAPE.CAPE suppresses ox-LDL induced IκB-α degradation and NF-κB nuclear translocation in THP-1 macrophages.ConclusionCAPE suppresses inflammatory cytokines secretion in ox-LDL treated THP-1 macrophages through inhibition of NF-κB activation and COX-2 expression.

Abstract:AimTo explore the correlation between serum γ-glutamyl transferase (γ-GT) and blood pressure.Methods1480 subjects were enrolled in the cross-sectional study, and standard questionnaire was used to collect information on smoking, alcohol intake and medication.Fasting blood was drawn to test γ-GT, serum glucose, liver and renal function, and body weight, body height and blood pressure were measured.Results1480 subjects included 886 male and 594 female with age range from 20 to 84 years old.By Pearson correlation analyses, γ-GT was positively correlated with systolic blood pressure, diastolic blood pressure, total cholesterol, serum glucose, low density lipoprotein cholesterol, serum uric acid, serum creatinine and body mass index, and negatively correlated with high density lipoprotein cholesterol.Compared with the lowest quartile, the highest quartile had significantly higher level of systolic blood pressure, diastolic blood pressure, total cholesterol, serum glucose, alanine aminotransferase and aspartate aminotransferase.After adjustment of sex, age, body mass index, current smoking, current alcohol intake, Logistic regression analysis indicated that there was a 74% higher risk of hypertension when compared the highest quartile with the lowest quartile (OR=1.74, 95% CI was 1.13～2.68, p=0.01).Conclusionγ-GT was positively correlated with blood pressure and can predict hypertension in Chinese.

Abstract:AimTo evaluate the plasma epoxyeicosatrienoic acids（EET） levels in patients with coronary heart disease，in order to investigate the relationship between EET and high sensitivity C-reactive protein（hs-CRP） and blood lipoprotein.MethodsPlasma samples of peripheral venous blood of 30 patients and 30 controls were drawn.Enzyme-linked immunosorbent assay(ELISA) was used to measure the plasma EET levels.hs-CRP, total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDLC), and low density lipoprotein-cholesterol (LDLC) levels were measured with a Hirachi 7170A analyzer.ResultsThe levels of EET (60.01±35.06 μg/L) were significantly lower in patients with coronary heart disease compared with those in control group (88.07±33.60 μg/L,p<0.05),and the EET levels were inversely correlated with hs-CRP（r=－0.286, p=0.027）.ConclusionsThe levels of EET were significantly lower in patients with coronary heart disease, and the levels of EET were inversely correlated with hs-CRP.It is suggested that the decrease of plasma EET might be involved in the atherosclerosis inflammatory process.

Abstract:AimTo investigate whether systemic or local (culprit artery) plasma alpha-defensin 1-3 (DEFA1-3) levels are associated with stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI).MethodsSystemic or local blood samples were obtained from 122 consecutive male subjects including no CAD (n=31) controls, stable CAD (n=44) and STEMI (n=47).Plasma DEFA1-3 levels were measured by ready-to-use solid-phase enzyme-linked immunosorbent assay (ELISA) based on the sandwich principle.ResultsSystemic DEFA1-3 in STEMI were increased compared with no CAD (p<0.05) and stable CAD (p<0.05), and systemic DEFA1-3 in stable CAD were higher than in no CAD (p<0.05).However, local and systemic levels of DEFA1-3 did not differ (p>0.05).Receiver operating characteristic (ROC) analysis revealed that the best cutoff value for systemic DEFA1-3 levels discriminating STEMI from no CAD and stable CAD was 136.3 μg/L with a sensitivity of 77.2%, a specificity of 66.7% and an area under the curve (AUC) of 0.717 (95%CI: 0.624 to 0.811, p=0.000).ConclusionSTEMI was associated with increased DEFA1-3 in systemic circulation.Future studies should be directed to their prognostic values for myocardial infarction.

Abstract:AimTo investigate the isolation and culture of endothelial progenitor cells from peripheral blood in patients with coronary heart diseases, and to determine cell shape, amount and clusters.And to study the correlation of endothelial progenitor cells (EPC) number and the stenosis degree in coronary artery.MethodsMononuclear cells were isolated from peripheral blood of patients with coronary heart diseases (n＝57) and control (n＝30).The isolated cells were cultured.And the correlation of EPC number and the stenosis degree of coronary artery was studied in patients with coronary heart disease.ResultsThe number of EPC was significantly reduced in patients with coronary artery disease (CAD) compared with control subjects (23.1±1.8 vs 56.7±2.4).In addition, the number of cell clusters was also impaired in patients with CHD (14.7±2.5 vs 24.2±1.7).EPC number and function were decreased with the degree and extent of coronary artery stenosis.ConclusionsThe number of cell clusters, proliferative capacity of EPC was significantly reduced in patients with CHD compared with control subjects.The number of EPC have negative correlation with the degree and extent of coronary artery stenosis.

Abstract:AimTo explore the correlation between the clinical ischemic events and the character of carotid atherosclerotic plaque detected by computed tomography angiography (CTA). Methods100 patients with carotid atherosclerosis were divided into ischemic event group (n＝48) and non-ischemic event group (n＝52).The character of carotid atherosclerotic plaque was detected by 64 slices computed tomography (CT).Results103 plaques were detected in ischemic event group, of which, the incidences of fatty plaque, calcified plaque and mixed plaque were 35.4%, 30.1% and 34.5% respectively.78 plaques were detected in non-ischemic event group, of which, the incidences of fatty plaque, calcified plaque and mixed plaque were 21.8%, 51.3% and 26.9% respectively (p＜0.05).The proportion of mixed plaques, composed mainly by fatty plaque, was 64.1% and 23.8% respectively in ischemic event group and non-ischemic event group (p＜0.01).The incidences of ulcerated plaques was significantly higher in ischemic event group (n＝8) than that in non-ischemic event group (n＝2)(p＜0.05).ConclusionsCharacteristics of carotid atherosclerotic plaque can be accurately assessed by 64 slices CT.Patients with fatty plaques and mixed plaques composed mainly by fatty plaque are more likely to be symptomatic, compared to those with either calcified plaque.

Abstract:AimTo assess the efficacy and safety of sequential therapy with atorvastatin (80 mg atorvastatin pretreatment within 24 hours before percutaneous coronary intervention (PCI) and following 40 mg atorvastatin for one month after PCI) in patients undergoing elective PCI.Methods328 patients undergoing elective PCI were grouped into atorvastatin sequential therapy (ST group, n=127) or routine therapy (RT group, n=201).The primary endpoint was peri-procedural myocardial infarction (defined as a CK-MB elevation >3 times upper limit of normal levels (ULN)) and the second endpoint was 30-day major adverse cardiac event (MACE, a composite end point, including all-cause death, MI, target-lesion revascularization), respectively.Glutamic pyruvic transaminase (GPT) elevation ≥3 times ULN as a safety endpoint was also addressed.ResultsNo patient had loss of follow-up.The incidence of peri-procedural myocardial infarction was 8.7% in the ST group and 17.9% in the RT group (odds ratio: 0.435, 95%confidence interval: 0.212 to 0.889, p=0.020).The incidence of 30-day MACE was 9.4% in the ST group and 18.4% in the RT group (odds ratio: 0.435, 95%confidence interval: 0.231 to 0.925, p=0.027).GPT elevation ≥3 times ULN occurred in 5 cases in the ST group and 1 case in the RT group (3.94% in the ST group vs 0.5% in the RT group, p=0.034).ConclusionAtorvastatin sequential therapy reduces peri-procedural myocardial infarction and 30-day MACE but may result in more elevated aminotrasferase ≥3 times ULN in patients undergoing elective PCI.

Abstract:AimTo evaluate the levels of plasma lipoprotein associated phospholipase A2 (Lp-LPA2) in patients with coronary heart disease(CHD) and provide effective biomarkers for early diagnosis of acute coronary syndrome (ACS).Methods230 subjects with angiographic inpatients were didvided into three groups: ACS group with 98 cases, Non-ACS group with 81 cases, and normal cornary artery group (NCA) as control with 51 cases.ACS group included unstable angina pectoris (UAP) subgroup with 61 patients and acute myocardial infarction (AMI) subgroup with 37 patients; Non-ACS group included stable angina pectoris (SAP) subgroup with 49 cases and chronic total occlusion (CTO) subgroup with 32 patients.Plasma concentrations of Lp-LPA2 in all individuals were measured using commercial kit by enzyme linked immunosorbent assay (ELISA).ResultsLp-LPA2 and hs-CRP levels were significantly higher in CHD patients including ACS and Non-ACS groups than in NCA group (p<0.001).ACS group showed very significantly higher Lp-LPA2 levels (p<0.001) and higher hs-CRP level(p<0.05) than Non-ACS group.Compared with NCA gro-up, subgroups including UAP, AMI, and CTO subgroup showed obvious increases in plasma Lp-LPA2 levels (p<0.001), and SAP subgroup showed no significant increase (p>0.05).Hs-CRP level was significantly higher in every subgroup (p<0.001).ConclusionsElevated Lp-LPA2 levels in CHD patients suggest the instability of atherosclerotic plaque and may be viewed as aneffective indicator for prediction of ACS.

Abstract:AimTo investigate the association between plasma lipids and presence of unstable carotid plaques in middle-aged and elderly people with carotid plaques.MethodsTwo hundred and seventy patients with carotid plaques detected by B-mode ultrasonography were enrolled in the study and divided into the unstable plaque group(n=130) and the control group(n=140).The plasma lipid levels were also determined in all subjects.ResultsAfter the adjustment of age, gender, hypertension, diabetes and smoking, the Logistic analysis revealed that the following lipid parameters are associated with unstable carotid plaque: Non-HDLC(OR=1.27,95%CI 1.02～1.58, p=0.032), TC/LDLC(OR=1.67,95%CI 1.17～2.38, p=0.005), apoB(OR=4.53, 95%CI 1.21～16.94, p=0.025) and apoB/apoA1(OR=17.85,95%CI 3.63～87.87, p<0.001) .Among them, apoA1 was the protective factor of unstable carotid plaque, while the others were risk factors.In addition, apoB/apoA1 was determined as the independent risk factor of the presence of unstable carotid plaque.ConclusionsThese results suggest that apoB/apoA1 can be used as an independent predictive index to assess the risk of unstable carotid plaque formation in middle-aged and elderly people.

Abstract:AimTo study the feasibility and short term efficacy of retrograde subintimal angioplasty via popliteal artery access for treatment of long occlusive disease of superficial femoral artery.Methods17 patients were performed with retrograde subintimal angioplasty and endovascular stent implantation via popliteal artery access for treatment of long occlusive disease of superficial femoral artery (SFA) and proximal popliteal arteries (PA).Procedural success rate and short-term clinical efficacy were summarized.The complications together with the therapy and preventions were also analyzed.ResultsThe success rate of popliteal artery puncture was 100%.All operations were finished successfully.The mean ankle brachial index increased from 0.43±0.23 to 0.89±0.26(p<0.01) at discharge and remained improved at 6 (0.86±0.25) and 12 months (0.81±0.23）（p<0.01）.Primary patency were 94.7%（16/17）, 76.5%（13/17）at 6 months and 12 months respectively.Secondary patency was 100% at 12 months.Three (17.6%) major complications occurred, including pseudoaneurysm of PA, bleeding at the femoral puncture site and acute embolism of distal limb artery.ConclusionFailed antegrade attempts to recanalize long occlusive disease of the SFA and proximal PA can be salvaged using a retrograde popliteal access for subintimal angioplasty and endovascular stent implantation, with a low complication rate.

Abstract:AimTo observe the effects of hydration on renal function and the incidence of contrast-induced nephropathy in patients undergoing coronary angiography.MethodsThe low osmolar and nonionic contrast media (iohexol) was used in all patients.A total of 216 patients, who would undergo coronary angiograph or percutaneous coronary interventional theraphy were enrolled into the study.They were randomly divided into two groups: the hydration group(n=112) and the control group (n=104).The treated group received hydration theraphy as well as general intravenous fluid infusion.The control group only received general intravenous fluid infusion.The levels of serum creatinine (Scr) and urine β2-microglobulin (β2MG) were measured before angiography and 48 hours, one week after coronary angiograpy.The incidence of contrast-induced nephropathy (CIN) was observed in the two groups.ResultsThe levels of Scr and β2MG were both elevated in the two groups, especially in the control group.The levels began to decrease after one week.The incidence of CIN was 4% in hydration group, 17% in control group.ConclusionThe strengthened hydration therapy can reduce the renal damage and effectively prevent from contrast-induced nephropathy.

Abstract:AimTo evaluate the efficacy and safty of thrombus aspiration without additional ballooning or stenting to treat patients with ST-elevation myocardial infarction.MethodsWe report the angiographic and clinical outcome of a series of selected ST-elevation myocardial infarction patients undergoing mechanical reperfusion by thrombus aspiration with or without additional ballooning or stenting.Thoracalgia and elevated ST segment resolution rate 2 hours after intervention, peak values of creatine kinase (CK) and creatine kinase-MB (CK-MB), left ventricular ejection fraction (LVEF) in 5-7 days, stenting and secondary outcomes 1 month after intervention were compared.ResultsThe rate of stenting in group A is significantly lower than group B; other index were not significantly different from these two groups.ConclusionIn selected patients with ST-elevation myocardial infarction undergoing mechanical reperfusion, thrombus aspiration without additional ballooning or stenting may be successfully performed.

Abstract:AimTo investigate the relationship between serum homocysteine (Hcy) levels and stroke severity and subclassification in patients with acute cerebral infarction (ACI).MethodsThe serum Hcy levels in 423 patients with acute cerebral infarction were measured by enzyme-linked immunosorbent assay (ELISA), and they were grouped according to Chinese ischemic stroke subclassification (CISS) subclassification and National Institutes of Health Stroke Scale (NIHSS).The patients between all the subclassification and 179 healthy controls were compared.ResultsThe serum Hcy levels in ACI group were significantly higher than those in control group (18.07±10.23 μmol/L vs 7.40±3.48 μmol/L); The serum Hcy levels in light, medium, heavy stroke group were 16.76±6.37 μmol/L, 20.41±6.01 μmol/L, 24.48±6.29 μmol/L, and the difference of groups were statistically significant.No futher significant difference was found among different subclassification.ConclusionsThe serum Hcy levels increased in acute cerebral infarction, which is closely related with the occurrence of cerebral infarction, and can be used to be a indicator to determine the severity of ACI.No further significant difference was found among different subclassification.

Abstract:AimTo observe the effect of atorvastatin on serum adiponectin and blood vessel endothelium function in patients with hyperlipemia combined with stable angina pectoris and asymptomatic coronary artery disease.Method150 cases with hyperlipemia combined with stable angina pectoris and asymptomatic coronary artery disease were randomly divided into three groups.Control group was given conventional treatment of coronary heart disease; observation group Ⅰ was treated with additional atorvastatin 20 mg/d; observation group Ⅱ received additional atorvastatin 40 mg/d.The treatment duration was 12 weeks.Fasting venous blood was collected to detect serum levels of adiponectin, serum amyloid A，nitric oxide and endothelin-1.The changes of nitric oxide and endothelin-1 were used as indirect indexes for blood vessel endothelium function.ResultsAfter treatment, serum levels of adiponectin and nitric oxide were increased, but endothelin-1 and serum amyloid A were decreased in observation group Ⅰ and Ⅱ(all p<0.05)， with significantly greater changes of each index in observation group Ⅱ than those in group Ⅰ.Serum adiponectin correlated significantly with nitric oxide, and was inversely related to endothelin-1 and serum amyloid A.ConclusionAtorvastatin improves blood vessel endothelium function via reduction of serum adiponectin level.This agent may play an important role in the prevention of atherosclerosis.

Abstract:CXC ligand 16 (CXCL16) as a member of the chemokines family can act as the adhesion molecule，Chemokines and scavenger receptor.It promotes the adhesion of activated T lymphocytes to endothelial cell and the proliferation of smooth muscle cell.Besides，it facilitates the aggregation of antigen presenting cells(APC) to the inflammation location and increases uptake of ox-LDL by macrophage which then convert to foam cells.It also takes part in the occurrence and development of atherosclerosis，angiostenosis and inflammation.In conclusion，CXCL16 and its receptor are related to the occurrence， severity and prognosis of the circulation system disease，such as atherosclerosis，coronary disease，stroke.And it may act as a predictor of the occurrence of clinical diseases.

Abstract:Percutaneous coronary intervention has revolutionized coronary revasculari- zation therapy, restenosis is a major challenge and has been described as the Achilles heel of the procedure. The drug-eluting balloon (DEB) represents an excellent therapeutic concept, its efficacy and safety in the treatment of stent restenosis has been confirmed.However, this technique carries a number of unanswered questions and is being further evaluated in different clinical settings.

Abstract:The mitochondrion is a vital component in cellular energy metabolism and intracellular signaling processes and they are involved in a myriad of complex signaling cascades regulating cell survival vs death.Mitochondrial dysfunction and the resulting oxidative stress are central in the process of I/R injury.Alleviating the mitochondrial dysfunction will contribute to mitigating the severity or progression of the myocardial injury.Recently, advances in mitochondrial biology have led to selective targeting of drugs designed to modulate or manipulate mitochondrial function.This review will provide an overview of the potential role for targeting mitochondria with potential drugs that lead to protect against cell injury.