Abstract:Aim To observe the effects of erythropoietin （EPO） on neonatal rat cardiac fibrosis phenotypic switched into myofibroblasts induced by angiotensin Ⅱ （ AngⅡ ） and the association with possible signaling pathway （tran sforming growth factor-beta1（TGF-β₁）-TGF-β-activated kinase-1（TAK₁）-mitogen-activated protein kinase（p38MAPK））. Methods Cardiac fibroblasts were isolated from new-born Sprague-Dawley rats, and the cells were used to establish the model of fibrosis by Ang Ⅱ（10^-6 mol/L） in vitro. Then they were treated with EPO（20 kU/L），at the same time，they were treated with or without the p38MAPK inhibitor SB203580（15 μmol/L）. Immunohistochemistry was used to detect the intracellular protein expression of α-smooth muscle actin（α-SMA）. The mRNA levels of TGF-β₁ and p38MAPK was analyzed by quantitative real-time PCR. The protein expression of α-SMA，TGF-β₁, TAK₁, and p38MAPK and the phosphorylation of TAK₁ and p38MAPK were analyzed by Western blot. Results 20 kU/L of EPO can effectively inhibit AngⅡ-induced cardiac phenotypic switched into myofibroblasts, reduce the intracellular protein expression of α-smooth muscle actin （α-SMA）, and also can significantly suppress AngⅡ-induced upregulation of TGF-β₁, TAK₁, and p38MAPK expression and phosphrylation of TAK₁ and p38MAPK. The effects can be strengthened by SB203580. Conclusion EPO can effectively inhibit AngⅡ-induced cardiac phenotypic switched into myofibroblasts, reduce myocardial fibrosis, and can reduce the related signaling molecules mRNA and protein expression. Preliminary consideration of the EPO can inhibit myocardial fibrosis, reduce the process of ventricular remodeling through TGFβ₁-TAK₁-p38MAPK.

Abstract:Aim To study the effects of doeosahexecnoic acid （DHA） on hypoxic pulmonary vasoconstriction （HPV） and its mechanism. Methods Pulmonary arteries were cut by 2 to 3 mm for vascular rings. Following the vascular constriction induced by acute hypoxia, DHA was administrated and the relaxing forces were measured without endothelia. Using the whole cell patch-clamp technique in freshly isolated pulmonary artery smooth muscle cells, the effects of DHA on total K^＋ currents, the large conductance Ca^2＋-activated K^＋ （BK_Ca） and voltage gated K^＋ currents were recorded. Results DHA relaxed vascular ring tone without endothelia （P<0.05）. DHA could significantly activate total K^＋ currents in pulmonary artery smooth muscle cells （P<0.01）. It also greatly enhanced BK_Ca currents （P<0.05） and at a testing potential of ＋60 mV, 125.21%±5.62%of BK_Ca currents were increased. In contrast, DHA inhibited K^＋ currents and at a testing potential of ＋60 mV, 63.21%±7.32% of K^＋ currents were decreased. Conclusion DHA can activate BK_Ca channels and relax the vascular constriction induced by acute hypoxia.

Abstract:Aim To investigate the effects of angiotensin （1-7） ［Ang（1-7）］ on the expression of lipids and reverse cholesterol transport related factors: ATP binding cassette transporter A1 （ABCA1）, peroxisome proliferator-activated receptor γ （PPARγ）, liver X receptor α （LXRα） and retinoid X receptor α （RXRα） in rats. Methods 40 healthy SD male rats were randomly divided into normal control group, high-fat diet group, Ang（1-7） group and Ang（1-7）＋A779 group. Ang（1-7） was continuably given by osmotic pump and jugular vein cannulation, after 28 d, total cholesterol （TC）, triglyceride （TG）, low density lipoprotein cholesterol （LDLC） and high density lipoprotein cholesterol （HDLC） in rat plasma were detected, gene expression of ABCA1, PPARγ, LXRα and RXRα in the aortic tissues of rats were measured by quantitative real-time polymerase chain reaction （qRT-PCR） and Western blot. Results Compared with the normal control group, TC, TG, LDLC of high-fat diet group were increased （P<0.05）, HDLC of high-fat diet group were lower （P<0.05） compared with high-fat diet group, TC, TG, LDLC of Ang（1-7） group were lower （P<0.05）, HDLC of Ang（1-7） group were increased （P<0.05） compared with Ang（1-7） group, TC, TG, LDLC of Ang（1-7）＋A779 group were increased （P<0.05）, HDLC of Ang（1-7）＋A779 group were lower （P<0.05）. Compared with the normal control group, ABCA1, PPARγ, LXRα, RXRα mRNA and protein levels of high-fat diet group were lower （P<0.05） compared with high-fat diet group, ABCA1, PPARγ, LXRα, RXRα mRNA and protein levels of Ang（1-7） group were increased （P<0.05） compared with Ang（1-7） group, ABCA1, PPARγ, LXRα, RXRα mRNA and protein levels of Ang（1-7）＋A779 group were lower （P<0.05）. Conclusion Ang（1-7） reduced the lipid levels in rat plasma, raised the gene expression of ABCA1, PPARγ, LXRα and RXRα in the aortic tissues of rats, cured the hyperlipidemia.

Abstract:Aim To explore whether hydrogen sulfide （H₂S） protects H9c2 cells against doxorubicin-induced injury by modulating p38 mitogen-activated protein kinase（MAPK） pathway. Methods H9c2 cells were treated with doxorubicin（DOX） to establish the model of cardiac cell injury In order to explore the protective effect of H₂S, cells were pretreated with 400 μmol/L NaHS （a donor of H₂S）for 30 min before exposure to DOX. The expression level of p38MAPK protein was tested by Western blot Cell viability was measured by cell counter kit-8 （CCK-8） Morphological changes of apoptotic cells were detected by Hoechst 33258 staining Intracellular level of reactive oxygen species （ROS） was measured by DCFH-DA staining and photofluorography. Results At range of 15 to 60 min, DOX at 5 μmol/L time-dependently upregulated expression level of phosphorylated（p） p38MAPK. Pretreatment with 400 μmol/L NaHS for 30 min before exposure of H9c2 cells to DOX not only obviously inhibited upregulation of p-p38MAPK expression induced by DOX, but also significantly blocked DOX-induced cardiomyocyte injuries, as evidenced by an increase in cell viability, decreases in amount of apoptotic cells and intracellular ROS generation. Similar to the cardioprotective effect of NaHS, pretreatment with SB203580 （an inhibitor of p38MAPK） for 60 min also protected H9c2 cardiac cells against DOX-induced injury. Conclusion p38MAPK pathway participates in DOX-induced cardiomyocyte damage H₂S may protect cardiomyocyte against DOX-induced injury by inhibiting p38MAPK pathway.

Abstract:Aim To investigate the effect and mechanism of probucol on macrophages reverse cholesterol transport in vivo, we quantitated the ³H-contents in feces of mice after 48 hours intraperitoneally injected macrophages, which were labeled with ³H cholesterol. And the gene and protein expression of SR-BⅠ,CYP7α,ABCG5 in liver and ABCG5 in intestine were evaluated. Methods 32 male C57BL/6 mice were randomly divided into four groups and treated with either vehicle or different dosage （0.1%, 0.5%, 1.0% W/W） of probucol respectively for 4 weeks, Then In vivo ³H-cholesterol-labeled and cholesterol-loaded macrophages were injected intraperitoneally into the mice. The appearance of ³H-tracer in feces as free cholesterol or bile acids were monitored 48 hours later. RNA and membrane protein of the liver and intestine were extracted and the gene and protein expression of SR-BⅠ,CYP7α,ABCG5 in liver and ABCG5 in intestine were quantified with RT-PCR and Western-blot respectively. Results The fecal total ³H-cholesterol levels were dose-dependently and significantly higher than those in control group, but there were no significant difference between 0.5% and 1.0% probucol groups. The mRNA expression of liver CYP7A1 were dose-dependently up-regulated in mice treated with probucol compared with those in the control group The mRNA expression and the protein expression of liver and intestine ABCG5 dose-dependently increased also in mice treated with probucol. No significant difference exists between 0.5% and 1.0% probucol groups. The SR-BⅠ mRNA and protein levels of the liver in mice treated with probucol did not change significantly compared with control mice. Conclusions Probucol dose-dependently promoted macrophages RCT in vivo in mice. The possible mechanism was that probucol up regulated the expression of liver CYP7A1 and ABCG5 in liver and intestine.

Abstract:Aim To investigate the effect of the caveolin-1 on the expression of interleukin-10（IL-10） and interleukin-6（IL-6） in rabbit carotid artery anastomotic stoma. Methods 32 New Zealand white rabbits were randomly divided into sham operation group, operation group, empty vector group and caveolin-1 transfected group. The rest specimens were taken for HE staining at 7 d and 28 d, which were used to observe the proliferation of intima, and the ratio of intima/media area was measured by Image-Pro Plus 6.0 software;Real time PCR was used to detect the mRNA, and immunohistochemistry was used to assay the expression of protein. Results Anti-inflammatory cytokine IL-10 and pro-inflammatory cytokine IL-6 were increased by carotid artery end-to-end-intestinal anastomosis. Local transfected caveolin-1 plasmid can increase the expression of caveolin-1 mRNA in rabbit carotid artery anastomotic stoma. Compared with other groups, the mRNA and protein of IL-10 were increased in caveolin-1 transfected group. However, IL-6, a potent pro-inflammatory cytokine, was decreased in caveolin-1 transfected group. Conclusion Caveolin-1 promotes anti-inflammatory factor in the balance between the pro- and anti-inflammatory cytokines in rabbit carotid artery anastomotic stoma.

Abstract:Aim To evaluate the effect of trimetazidine on myocardial stunning by pressure-volume loops in rats and its probable mechanism. Methods Thirty SD rats were randomly divided into 3 groups equally,control group and myocardial stunning group （physiological saline 2 mL）, trimetazidine group （trimetazidine tablet 3 mg/kg）. All rats, except for those in control group, were subjected to 20 minutes of left anterior descending artery occlusion and 120 minutes reperfusion, while in control group only threading without ligation. Hemodynamic variables （as heart rate, left ventricular end-diastolic pressure, left ventricular end-systolic pressure and so on） were dynamicly observed by the pressure-volume loops and PowerLab system and software offline were applicated to analyse. Myocardial tissue ATP content, ATPase activity and phosphate fructokinase （PFK） activity were detected after reperfusion for 120 min, and myocardial mitochondria ultrastructure was tested using the electron microscope by stereology method. Results Compared with myocardial stunning group, in trimetazidine group, end-diastolic pressure（EDP）, end-systolic volume （ESV） and preload recruited stroke work （PRSW） were significantly reduced （P<0.01）, end-diastolic pressure-volume （EDPVR） were also decreased （P<0.05）. End-diastolic volume （EDV） and end-systolic pressure-volume （ESPVR） were obviously increased by pressure volume ring analysis. ATP content and ATPase activity elevated （Ca²⁺-Mg²⁺ATPase and Na⁺-K⁺ATPase, P<0.05） PFK activity added（P<0.01） and myocardial mitochondria ultrastructure significantly ameliorated abnormal changes （P<0.01）. Conclusions Trimetazidine attenuates myocardial stunning by the energy metabolism, and pressure volume ring can evaluate cardiac function accurately and sensitively.

Abstract:Aim To observe the effect of glucagon-like peptide-1 receptor agonist exenatide on the expression of NADPH oxidase subunits and oxidative stress damage in the aorta of type 1 diabetic rats. Methods Thirty male Sprague-Dawley（SD） rats were randomly divided into normal control group（n7） and model group（n23）. Type 1 diabetic model was established by intraperitoneal injection of streptozotocin. Nineteen diabetic rats induced successfully were randomly divided into diabetic group （n10）, and diabetic group treated with exenatide （n9）. Rats in diabetic group treated with exenatide were injected subcutaneously with exenatide in dose of 5 μg/kg twice daily. Rats in normal control group and diabetic group were given equivalent volume of normal saline by subcutaneous injection. All rats were sacrificed after exenatide treatment for eight weeks. The mRNA expression of aortal p22phox and NOX4 were detected by real-time fluorescence quantitative PCR. The protein expression of aortal transforming growth factor-beta （TGF-β1） was detected by immunohistochemical staining. Specimen sections were stained with hematoxylin and eosin for histological examination. Results The mRNA expression of aortal p22phox and NOX4 and the protein expression of aortal TGF-β1 were significantly increased in diabetic group than those in normal control group（P<0.05）. The mRNA expression of aortal p22phox and NOX4 and the protein expression of aortal TGF-β1 were decreased in diabetic group treated with exenatide than those in diabetic group（P<0.05）. Compared with rats in normal control group, rats in diabetic group had the obviously thickened intima and tunica elastica, unsmooth intima, endothelial cell protrusion, the irregular shape of endothelial cells, and the smooth muscle cells arranged in disorder in the aorta. The intima was locally thickened and unsmooth, endothelial cells and smooth muscle cells were arranged in order, and the unica elastica was lightly thickened in the aorta in diabetic group treated with exenatide compared with diabetic group. Conclusions Exenatide can down-regulate the mRNA expression of p22phox and NOX4 and the protein expression of TGF-β1 in the aorta of type1 diabetic rats, which can relieve the aortal damage by oxidative stress, thus play a protective role on the blood vessel of diabetic rats.

Abstract:Aim To evaluate the relation between non-high density lipoprotein cholesterol （non-HDLC）/HDLC and early carotid plaque in type 2 diabetes patients. Methods 1021 type 2 diabetes patients without history of cardiovascular disease were retrospectively analyzed. Carotid plaque and plaque area were measured by B ultrasound. The general data, duration of diabetes, glycosylated hemoglobin, low density lipoprotein cholesterol （LDLC）, HDLC, non-HDLC and the lipid ratios were compared in the group with carotid plaques and without plaques. The relation between serum lipid parameters and carotid artery plaque was analysed. The prediction power of the lipid parameters on carotid artery plaque were analysed by receiver operating characteristic curve （ ROC ）. In the group with carotid plaques, the correlation of the lipid parameters and plaque area were anayzed. Results The male ratio, age, duration of diabetes, systolic blood pressure, non-HDLC levels, non-HDL/HDLC, total cholesterol（TC）/HDLC and LDLC/HDLC were significantly higher in the group with paques than the group without plaques. However, the HDLC level was significantly lower in the group with plaques than the group without plaques. The difference of the above was statistically significant （P<0.05）. Logistc regression analysis showed that non-HDLC levels, non-HDLC/HDLC, TC/HDLC and LDLC/HDLC were independent risk factors for carotid plaque （P<0.05）. There were no correlation between LDLC levels and carotid plaques after adjustment for confounding factors. The area under ROC curve of non-HDLC/HDLC and other lipid parameters were compared: non-HDLC/HDLC was higher than that of LDLC/HDLC, TC/HDLC, but the difference was close to statistical significance （P0.052 and 0.058）. Non-HDLC/HDLC was significantly higher than that of HDLC and LDLC （P<0.001）. In the group with plaques, multiple regression analysis showed non-HDLC/HDLC and LDLC/HDLC were the independent impact factors （P<0.05） for plaque area. Non-HDLC and TC/HDLC were in no correlation with plaque area after adjusting for confoundings. Conclusion Non-HDLC/HDLC is a useful lipid parameter to assess the risk of early carotid plaque and plaque area in type 2 diabetes.

Abstract:Aim To investigate the association of the level of adiponectin （ANP）and its gene SNP+276 polymorphism with the patients with type 2 diabetes mellitus and those people complicated with carotid intima media thickness（IMT） in Yanbian district . Methods Only depth-endogamy were selected in this study. All participants come from Yanbian,Jilin province after excluding coronary heart disease, liver and kidney disease, malignant tumors and immune system diseases. The subjects were divided into normal control group and T2DM group. T2DM group consisted of the Han nationality and the Korean nationality, and T2DM group was also divided into carotid atherosclerosis group （including GG genotype group, GT genotype group and TT genotype group） and group without carotid atherosclerosis. The genotype was confirmed by using Taqman probe. Results There was significant difference in the distribution of adiponectin gene SNP+276T/G polymorphism between the normal control group and T2DM group. In the T2DM group,there was no significant difference in the distribution of adiponectin gene SNP+276 T/G polymorphism between the Han and Korea nationality. There was no significant difference in the distribution of adiponectin gene SNP+276 T/G polymorphism between the T2DM patients with and without carotid atherosclerosis. There was significant difference in the level of adiponectin between the T2DM patients with and without carotid atherosclerosis. Among T2DM carotid atherosclerosis group, there was significant difference in the age, course of disease, carotid IMT and the level of adiponectin between the GG genotype group and TT genotype group. Conclusion Adiponectin gene SNP+276 T/G is correlated with type 2 diabetes mellitus in Yanbian district. There in no correlation between adiponectin gene SNP+276 T/G and T2DM patients with carotid IMT in Yanbian district. The level of adiponectin is correlated with type 2 diabetes mellitus and carotid IMT. Adiponectin is a protective factor for type 2 diabetes mellitus and carotid IMT. G allelomorphic gene maybe is a risk factor for type 2 diabetes mellitus and carotid IMT.

Abstract:Aim To investigate the effect and significance of programmed cell death 4 （PDCD4） abnormal expression of CD4＋T lymphocytes in patients with unstable angina pectoris during perioperative period of percutaneous coronary intervention （PCI）. Methods A total of 62 unstable angina patients were enrolled. Of the 62 patients, 33 patients undergoing PCI were involved as PCI group, the other 29 patients without PCI were set as control group. Peripheral blood was extracted before and after coronary angiography or PCI. Circulating CD4＋T cells were obtained by magnetic cell sorting system （MACS） at baseline and 18 h～24 h post-PCI. Real-time fluorescent quantitative polymerase chain reaction （RFQ-PCR）, Western blot analysis, enzyme-linked immunosorbent assay （ELISA） were used to evaluate the levels of PDCD4 mRNA in CD4＋T lymphocyte, the expression of PDCD4 protein and also the serum level of tumor necrosis factor-α （TNF-α）. Results Compared to the control group, the post-operative expression of PDCD4 mRNA and protein dramatically increased in the PCI group （P<0.05）. Compared to the pre-operation, the serum level of TNF-α was increased in 18 h～24 h post-operation in the PCI group （16.11±1.45 ng/L vs 7.60±0.75 ng/L P<0.05）. As to the level of TNF-α in the control group, no significant change was found （P>0.05）. Conclusions The expression of PDCD4 was increased in patients with unstable angina pectoris undergoing percutaneous coronary intervention, which contributed to the intensive inflammation response in the myocardial level after PCI.

Abstract:Aim To evaluate the relationship between diabetic retinopathy （DR） and subclinical coronary atherosclerosis （CAs） on coronary 64-slice multidetector computed tomography angiography （MDCT） in individuals with type 2 diabetes mellitus. Methods From July 2007 to December 2009, 114 and 124 type 2 diabetic patients with and without CAs were enrolled. They received fundus photochromy, coronary 64-slice multidetector computed tomography angiography, physical examination, and measurement of fasting plasma glucose（FPG）, glycosylated haemoglobin （HbA1c）, plasma lipid profile, estimated glomerular filtration rate （eGFR） and urinary albumin excretion rate（UAER）. Then the analysis of the relationship among the detection and measurement outcomes were conducted. Results Diabetic patients with CAs had a higher prevalence of DR than those without CAs （67.5% vs 33.1%, P<0.001）. After adjustment for the traditional risk factors for cardiovascular disease, CAs was independently associated with DR （OR5.0, 95%CI 2.6～9.8）. There was significant difference in the prevalence of CAs by the number of CAs vessels among patients without DR （NDR）, those with pre-proliferative retinopathy （pre-PDR） and those with proliferative retinopathy （PDR） （P<0.01）. The prevalences for CAs, the prevalences of CAs ≥3 vessels involved by plaque, and proportions of vessels with significant coronary plaque and of involved vessels in all detected coronary arteries were significantly increased with the presence and severity of DR （NDR vs Pre-PDR, Pre-PDR vs PDR, P<0.01 for each）. Conclusions The severity and extent of CAs were significantly increased with the incidence and progression of DR, and much of CAs and DR could be still multifactoral with common pathway.

Abstract:Aim To investigate the effect of different obese type on arterial stiffness in essential hypertension. Methods The basic information was collected in a total of 776 essential hypertensive patients. According to body mass index （BMI） and waist circumference （WC） level, all patients were divided into four groups, namely, normal BMI and normal waist circumference group （Ⅰgroup, n194）, normal BMI and elevated waist circumference group （Ⅱgroup, n195）, excessive BMI and normal waist circumference group （Ⅲ group, n196）, excessive BMI and elevated waist circumference group （Ⅳgroup, n191）. Brachial ankle pulse wave velocity （BaPWV） and ankle-brachial blood pressure index （ABI） were observed in all patients. Arterial stiffness index （AI） was calculated using the blood lipid of all hypertension patients. Results BaPWV （2120±263 mm/s） and AI （3.35±0.87） in Ⅳ group were significantly higher than Ⅰgroup （P<0.01）, Ⅱgroup and Ⅲ group （P<0.05）. ABI （0.72±0.15） in Ⅳ group were significantly lower than Ⅰgroup （P<0.01）, Ⅱgroup and Ⅲ group （P<0.05）. There were no statistical differences between Ⅱgroup and Ⅲ group in ABI and AI （P>0.05）. Results of 2×2 factorial analysis showed that there was a distinctive and synergistic effect between excessive BMI and elevated waist circumference on arterial stiffness. Conclusion Arterial elasticity function was aggravatedly damaged in essential hypertension in patients with abdominal obesity. Excessive BMI and elevated waist circumference had interaction and synergistic effect on the damage of arterial elasticity function.

Abstract:Aim To investigate the preliminary scanning significance of artery stenosis with intracranial internal carotid artery’s plaque calcium score using conventional brain unenhanced computed tomography （CT）. Methods By retrospectively analyzing brain and neck CT artery imaging （including conventional brain unenhanced CT, CTA） of 110 cases, the intracranial internal carotid artery’s calcification were classified into 4 grades. Of them, there are 26 cases which can be successfully classified into 3/4 grade by Agatston Calcium Score and receive CT artery imaging analysis of vascular and artery （AVA） software. AVA software was used to analyse the calcification segment artery’s stenosis degree and its North American Symptomatic Carotid Endarterectomy Trial criteria （NASCET） classification. Results In the 26 cases, there are 18 cases of mild grade with Agatston Calcium Score 2.69±1.01, 5 cases of moderate grade with Agatston Calcium Score 5.25±0.88, 3 cases of high grade with Agatston Calcium Score 6.80±0.30. The difference between high, moderate grade and mild grade has statistic significance （P<0.05）. The difference between high and moderate grade has no statistic significance （P>0.05）. There were positively significant correlation between stenosis degree and calcification’s Agatston Calcium Score（r0.938，P<0.05）. Conclusions Conventional brain unenhanced CT intracranial internal carotid artery’s Plaque Calcium Score can be used to scan artery stenosis, and the one with Agatston Calcium Score over 5.25±0.88 is suggested to proceed CTA examination.

Abstract:Aim To observe the influence of aspirin combined with atorvastatin on arterial stiffness in the hypertensive patients with complicating diabetes and early renal damage. Methods The hypertensive patients with complicating diabetes and early renal damage （n＝80） were randomly divided into the aspirin group （treated with 100 mg/d bayaspirin） and combination group （treated with 100 mg/d bayaspirin and 20 mg/d atorvastatin）. The levels of blood lipids, urinary albumin, β₂-microglobulin （β₂-MG）, urinary albumin excretion rate （UAER）, cardio-ankle vascular index （CAVI） and ankle-brachial index （ABI） were detected before the treatment and 20 weeks after the treatment respectively. Results （1）Blood lipids: the levels of total cholesterol （TC） and low density lipoprotein cholesterol （LDLC） in two groups were lower than those before the treatment （P<0.05 and P<0.01）. The TC level was lower in the combination group than that in the aspirin group （P<0.05） after 20 weeks. （2）Arterial stiffness: the indexes of CAVI （12.67±1.40 vs 11.20±0.87, 11.64±1.28 vs 9.58±1.04） increased and ABI （0.87±0.12 vs 0.98±0.11, 0.88±0.40 vs 1.06±0.10） in two groups were decreased significantly （all P<0.05） after the treatment. After 20 weeks the index changes of CAVI and ABI were more significant （all P<0.05）. （3）Urine microprotein: the difference in the levels of urinary albumin, β₂-MG and UAER was not statistically significant in the aspirin group, but decreased in the combination group with statistical significance after the treatment, and compared to the aspirin group after the treatment, the decrease of urine microprotein was statistically significant （13.30±2.87 mg/L vs 15.70±3.73 mg/L, 2.15±1.29 mg/L vs 3.13±0.38 mg/L, 20.02±7.62 μg/min vs 23.13±7.60 μg/min, all P<0.05）. （4）In multiple linear regression model, CAVI, ABI, UAER were all significantly associated with blood pressure and plasma glucose. Conclusion Aspirin combined with atorvastatin can decrease the urine microprotein and improve the arterial stiffness in hypertensive patients with complicating diabetes and early renal damage.

Abstract:Aim To evaluate the changes of the strain and the strain rate at carotid atherosclerotic plaque in cerebral infarction patients by velocity vector imaging （VVI）. Methods 188 carotid plaques in cerebral infarction patients and 154 carotid plaques in patients with no-cerebral infarction were selected. Every plaque was examined by Siemens Sequoia 512 with VVI work station. The maximum strain （Smax） and maximum strain rate （SRmax） at the shoulder, surface and base of plaque in short axis were measured. Results The Smax, SRmax at plaque shoulder were higher significantly than that at plaque surface and plaque base, and the SRmax at plaque surface was higher than that at plaque base in both groups. The SRmax at the soft plaque shoulder was higher than that at the hard plaque in both groups （P<0.05）. The SRmax at plaque shoulder and the soft plaque shoulder in the cerebral infarction group were higher than that in the no-cerebral infarction group （P<0.05）. Conclusion VVI technology can be mechanical characteristics of quantitative detection of carotid artery in cerebral infarction patients with different plaques, which provides a new method for clinical analysis of the stability of plaque.

Abstract:Aim To explore the significance of the change of CD4^＋CD25^＋ regulatory T cells （Treg） in patients with high-risk transient ischemic attack （TIA） in posterior circulation. Methods The frequencies of Treg were detected in 21 patients with high-risk TIA in posterior circulation, 19 patients with dizziness syndrome and 20 health adults by flow cytometer. Results The frequencies of Treg were found to be significantly lower in patients with high-risk TIA in posterior circulation （5.66%±1.91%） than those of dizziness syndrome （9.18%±2.26%） and health adults （9.21%±2.71%）. Conclusions The frequencies of Treg decrease in patients with high-risk TIA in posterior circulation. The decrease of Treg may lead to the breakdown of autoimmune tolerance and participate in the progression of atherosclerosis, which could be one of the pathogenesis of the high-risk TIA in posterior circulation.

Abstract:Traditionally, the tunica adventitia has been regarded as loose connective tissue, which was composed of fibroblasts, inflammatory cells, vasa vasorum, nerve endings and so on. It mainly functioned as supportive tissue and supplied nutrition to the vessel wall. Recently, accumulating data suggested that stem/progenitor cells were present in the adventitia. Under pathological conditions, resident stem/progenitor cells in the adventitia could differentiate into endothelial cells or smooth muscle cells, which were involved in atherosclerosis, vascular repair and remolding. This article briefly reviews the research status and advancement of stem/progenitors in adventitia.

Abstract:The mechanism of how diabetes causes vascular injury is still unclear. The recent researches indicate that high glucose can directly influence the proliferation, apoptosis and phenotype transformation of vascular endothelial cells and smooth muscle cell, promote vascular remodeling. Fluctuating high glucose is proved to have more obvious effect on vascular remodeling than persistent high glucose. Recent data indicate that the ATP binding cassette transporter G1 would play a key role in cholesterol reverse transportation and in atherosclerosis formation. This brief overview will focus on the recent research progress concerning effect of fluctuating high glucose on vascular remodeling and the possible role of the ATP binding cassette transporter G1.