Abstract:Aim To observe the effects of Xiongshao capsule on blood vessel collagens during the course of vascular remodeling in rabbits with atherosclerosis. Methods Atherosclerosis model was established by injuring rabbits' abdominal aorta endothelium by balloon dilation with high fatty diet for 6 weeks.80 rabbits were randomly allocated into 8 groups,including normal control group,endothelium-simply-injuried group,endothelium injuried with high fatty diet 3 days group,2 weeks group and 6 weeks group,6 weeks with Probucol group,small dose of Xiongshao capsule group and large dose of Xiongshao capsule group.Elastic fibres staining and picrosirius red staining methods combined with computer image analysator were applied to determine the pathomorphological indexes,collagen contents and OD values. Results 3 days post injury in model group,there was no thickening change in endarterium,no stenosis in lumens;2 weeks post injury,compensation dilation appeared in lumens;but to 6 weeks,the diameters of lumens diminished obviously(p<0.01,compared with that in 2 weeks),proliferation index heightened especially more in the groups using large dose of Xiongshao capsule and Probucol.As to collagens in blood vessels,accumulation was not obvious in intima 2 weeks post injury in model group,but in tunica media and externa,the contents of type Ⅰcollagens increased compared with the control group,while the contents of type Ⅲcollagens decreased.In the course,type Ⅰcollagens played important roles,so leading to collagens total amount increasing and to the peak.6 weeks post injury,the extent of typeⅠ collagens increasing were less than that of typeⅢ collagens decreasing,collagens total amount didn't increase obviously;but collagens in intima gradually accumulated to peak.In the groups using Probucol and Xiongshao capsules,the contents of collagens in intima decreased gradually,in the group using large dose of Xiongshao capsule,the contents decreased more than the model group without any drugs;total amount of collagens in tunica media and externa also decreased,especially in the group using large dose of Xiongshao capsule. Conclusions Intima hyperplasia and pathological vascular remodeling led to the loss of lumens in the course of atherosclerosis,collagens played key roles in pathological vascular remodeling.Large dose of Xiongshao capsule could improve pathological vascular remodeling and inhibit intima hyperplasia by regulating the contents of collagens in blood vessels during the course of atherosclerosis,thus prevent lumens stenosis.

Abstract:Aim To investigate the expression of tissue factor(TF) and its mechanism in endothelial cell induced by fluid shear stress in vivo. Methods Fifty-four male SD rats(weight 300±16 g) were randomly divided into nine groups(n=6,respectively). The time course of mRNA and protein expression of TF,nuclear factor stimulatory protein(Sp1) and early growth response-1(Egr-1) were examined on the model of loop ligature method of stenosis the left arteries carotis communis intima in the rat with the combination of in situ hybridization and immunohistochemistry methods,performed computer image analysis were used. Results The mRNA and potein of TF and Egr-1 and Sp1 were faintly expressed in intima of control group,after exposed to stenosis,the staining intensity was increased 30 minutes after wall shear stress.The mRNA and protein expresion of TF markedly increased compared with control group(p<0.05).The mRNA and protein expresion of Egr-1 and Sp1 increased(p<0.05).The change of Egr-1 was more significant than that of Sp1(p<0.05).The change trend of Egr-1 and Sp1 expresion were similar to that of TF.The mRNA and potein of TF peaked at 6 hour,the mRNA and potein of Egr-1 peaked at 3 hour,the mRNA and potein of Sp1 peaked at 1 hour,with significant differences from control group(p<0.05). Conclusion In carotid artery stenosis, the shear stress can up-regulate TF expression in the endothelium,and its mechanism is related to the activation of Sp1 and Egr-1.

Abstract:Aim To evaluate the effect of atorvastatin on proliferation and mRNA expression of endothelial lipase(EL) in cultured human umbilical vein endothelial cells(hUVEC). Methods Each group of cultured hUVEC was incubated with atorvastatin of 2,4,6,8 and 10 μmol/L for 2,4,8,12 and 24 h separately.The expression of EL mRNA in hUVEC was detected by quantitative competitive reverse transcription-polymerase chain reaction(RT-PCR).The proliferation of hUVEC was observed by AgNORs analytical method. Results Atorvastatin markedly restrained the expression of EL mRNA in hUVEC.The effect appeared dose dependence and time dependence.With the effect of atorvastatin,the quantity of AgNORs were decreased.The downtrend was evident along with the increased concentration and the prolonged time.There was positive correlativity between the expression of EL mRNA and the quantity of AgNORs(r=0.963,p<0.01). Conclusions Atorvastatin dose-dependently and time-dependently restrained the proliferation of hUVEC.As a result,the expression of EL mRNA was decreased too.There was a positive correlativity between them.

Abstract:Aim To investigate the effect of peroxisome proliferator-activated receptors α(PPARα)agonist fenofibrate on the immune maturation of monocyte-derived dendritic cell(DC) induced by oxidized low-density lipoprotein(ox-LDL). Methods Monocytes were purified(over 98%) using Anti-CD14 microbeads. After cultured with DC Cellgro medium containing recombinated human granulocytemacrophage colony stimulating factor(rhGM-CSF)(100 μg/L) and recombinated human interleukin-4(rhIL-4)(20 μg/L) for 5 days,monocytes were derived into immature DC.Human monocyte-derived DC were incubated with fenofibrate(100 μmol/L) for 24 hours,and subsequently stimulated with ox-LDL(50 mg/L)for another 48 hours. The immunophenotypic expressions(CD1a,CD40,CD86,and HLA-DR) were analyzed by FACS and endocytosis function by FITC-dextran,and the cytokines secretions of culture supernatants(IL-12,IL-10,TNF-α) were measured with enzyme-linked immunosorbent assay(ELISA). Results Fenofibrate reduced ox-LDL induced immunophenotypic expressions of DC(CD1a: 68.80%±5.89% vs 46.50%±11.39%,p<0.05;CD40: 72.97%±10.38% vs 56.76%±11.16%,p<0.05;CD86: 79.82%±22.07% vs 65.74%±9.94%,p<0.05;HLA-DR: 83.24%±6.60%vs 60.72%±11.85%,p<0.05).Ox-LDL inhibited the endocytosis of DC,which was partly prevented by fenofibrate(83.12%±3.10% vs 57.78%±23.28%,p<0.05);fenofibrate attenuated ox-LDL induced cytokine secretions of DC(IL-12: 106.7±20.7 ng/L vs 64.9±18.5 ng/L,p<0.05;TNFα: 50.3±9.9 ng/L vs 26.0±8.8 ng/L,p<0.05;IL-10: 66.1±2.6 ng/L vs 33.4±13.4 ng/L,p<0.05). Conclusion PPARαagonist fenofibrate partly inhibits ox-LDL induced immune maturation of DC,through which it may play an anti-atherosclerosis effect.

Abstract:Aim To observe the expression of angiotensin Ⅱ(AngⅡ) and plasminogen activator inhibitor-1(PAI-1) in rabbits atherosclerotic plaques,and to study the inhibiting efficiency of captopril and valsartan. Methods Male New Zealand white rabbits were randomly divided into four groups: cholesterol group,captopril group,valsartan group and control group.After feeding 10 weeks,plasma PAI-1 activity was evaluated by spectrphotometric assy,plasma AngⅡ level was measured with competitive radioimmunoassays.The expression of AngⅡ and PAI-1 in atherosclerotic plaques were observed by immunohistochenistry measure. Results In cholesterol group,plasma AngⅡ level and plasma PAI-1 activity were increased significantly compared with control group(p<0.01),and the percent of positive cells of AngⅡ and PAI-1 in atherosclerotic plaques were higher compared with control group(46.97%±14.32% vs 4.17%±1.01% and 48.5%±13.46% vs 1.33%±0.52% respectively,p<0.01).Captopril and valsartan significantly reduced plasma AngⅡ level and PAI-1 activity compared with cholesterol group(p<0.05).Also captopril and valsartan markedly decreased the percent of AngⅡ positive and PAI-1 positive cells in atherosclerotic plaques compared with cholesterol group(26.30%±5.00% vs 46.97%±14.32% and 20.37%±(8.23%) vs 48.50%±13.46%,p<0.05 in captopril group;27.83%±7.30% vs 46.97%±14.32% and 22.50%±(7.06%) vs 48.50%±13.46%,p<0.05 in valsartan group).The expression of PAI-1 were positively correlated with the expression of AngⅡ in atherosclerotic plaques(r=0.796,p<0.01). Conclusion The expression of AngⅡ and PAI-1 in atherosclerotic plaques were increased,there was significant correlation between the expression of PAI-1 and AngⅡ,both captopril and valsartan have the efficiency of inhibiting the expression of Ang Ⅱ and PAI-1 in plaques of rabbit atherosclerosis.

Abstract:Aim To observe the effect of vascular endothelial growth factor(VEGF) on the apoptosis and the expression of Fas mRNA and Bcl-2 mRNA in human umbilical vein endothelial cell(hUVEC). Methods hUVEC were randomly divided into three groups: control group,hydrogen peroxide group and hydrogen peroxide + VEGF group.After 12 hours,the apoptosis of hUVEC was determined by flow cytometry(FCM) and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL),the expression of Bcl-2 mRNA and Fas mRNA were examined by reverse transcription polymerase chain reaction(RT-PCR). Results Apoptosis number in hydrogen peroxide group was higher than that in control group(27.83±2.14 vs 2.50±1.05,p<0.01).However,in hydrogen peroxide+VEGF group,apoptosis number was lower than that in hydrogen peroxide group(13.00±2.10 vs 27.83±2.14,p<0.01).Apoptosis rate in hydrogen peroxide group was higher than that in control group (14.17%±0.45% vs 1.55%±0.87%,p<0.01) and in hydrogen peroxide+VEGF group(14.17%±0.45% vs 5.69%±0.38%,p<0.01).Compared with control group,hydrogen peroxide markedly increased Fas mRNA expression(94.50%±3.45% vs 21.17%±1.17%,p<0.01) and decreased Bcl-2 mRNA expression(23.17%±1.17% vs 85.17%±1.47%,p<0.01).Compared with hydrogen peroxide group,VEGF significantly decreased Fas mRNA expression((40.67%)±2.16% vs 94.50%±3.45%,p<0.01) and increased Bcl-2 mRNA expression(60.33%±1.75% vs 23.17%±1.17%,p<0.01). Conclusions VEGF can inhibit the apoptosis induced by hydrogen peroxide in HUVEC,which may correlated with upregulation Bcl-2 mRNA expression and inhibiting Fas mRNA expression.

Abstract:Aim To study the expression of aldose reductase(AR) in the carotids of the rats with restenosis in order to probe into the relationship between AR expression and intimal hyperplasia,and further explore the inhibition of atorvastatin on AR expression and intimal hyperplasia in the carotids with restenosis. Methods 24 healthy male SD rats were divided into the injuried group without treatment,the fake operation group and the atorvastatin group by chance.Each group had 8 rats.The right carotids were injuried by air-drying operation in the treatment group and the group with operation but without treatment.The left carotids were acted as the controls.The rats were killed after 7 days and 14 days respectively.Dying with HE to examine the intimal and the medial layers' proliferation.And the acreage of the intimal and the medial layers and their ratio were calculated as well.Then the expression of nuclear factor-κB(NF-κB) and AR were examined by immunohistochemical methods and FISH in situ hybridization. Results Seven days after the injury,the intimal hyperplasia could be seen obviously in the injuried sides of the carotids,by the end of 14 days,the intimal hyperplasia aggravated.While the carotids in the control sides were not.The acreage of the intimal layers,the ratio of the intimal and the medial layers in the atorvastatin group was obviously lower than that of the operation group without treatment.The difference was obvious when compared with each other(p<0.05 or p<(0.01)).The expression of AR and NF-κB in the injuried sides was obviously higher than that of the control sides.The expression of AR and NF-κB in the atorvastatin group was obviously lower than that of the untreatment group.Compared with each other,the difference was obvious(p<0.05 or p<0.01). Conclusion AR may be concerned with the neointima and the form of restenosis in the injuried carotids of the rats.Atorvastatin could obviously inhibit the neointima and the form of the restenosis.Atorvastatin might inhibit vascular smooth muscle cells(VSMC) proliferation through inhibiting AR and NF-κB expression.

Abstract:Aim To test the hypothesis that Pioglitazone decrease CD40L expression in hypercholesterolemia rabbit aorta. Methods 15 male healthy New Zealand rabbits were randomly divided into three groups: control group(n=5)was fed with normal diet for eight weeks;high cholesterol group was fed with high-cholesterol diet for eight weeks;Pioglitazone treatment group(n=5)was fed with high-cholesterol diet for eight weeks supplemented with Pioglitazone [3 mg/(kg·d)] from the fourth week of cholesterol diet.CD40L was detected by immunohistochemistry, lectin-like oxidized low density lipoprotein receptor-1(LOX-1) mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR). Results Aortic intimal hyperplasia and smooth muscle cells proliferation in rabbits fed with high-cholesterol diet were decreased.Pioglitazone could improve high density lipoprotein and decrease the expression of CD40L and LOX-1 mRNA in hypercholesterolemia rabbits aorta. Conclusions Pioglitazone can inhibit the upregulation of LOX-1 in hypercholesterolemia rabbits aorta and decrease CD40L expression.These observation provide novel insight into a potential novel antiinflammatory and antiatherosclerosis pathway of thiazolidinediones.

Abstract:Aim To study the changes of protein kinase B Akt/ glycogen synthase kinase-3β(GSK-3β) signal transduction pathway in hypertrophic myocardial tissue of rats induced by pressure overload. Methods Wistar rats,male,were divided into aortic banding group(AOB group)(n=19) and sham group(n=20) at random.After 4 weeks,the left vertricular hypertrophy models were built successfully,measured the hemodynamic datas and left ventricular weight index,then detected the protein expression of Akt,phospho-Akt,GSK3β and phospho-GSK3β in myocardiac tissue by Western Blot. Results Compared with controls,inter ventricular septum(1.60±0.10 mm vs 0.9±0.10 mm),left ventricle posterior wall(1.60±0.07 mm vs 1.00±0.07 mm) were significantly increased(p<0.01);left ventricular fractional shortening was also significantly increased(56.9%±3.4% vs 47.8%±2.1%,p<0.05);dp/dtmax was decreased significantly(3 508±310 mmHg/s vs 4 675±322 mmHg/s,p<0.05);the expression of phospho-Akt in hypertrophic myocardiac tissue was increased significantly(1.2±0.3 vs 0.9±0.3,p<0.05);the expression of phospho-GSK3β was decreased significantly(0.7±0.2 vs 0.9±0.2,p<0.05). Conclusions Akt/GSK3β signal transduction pathway took part in the pathophysiological process of myocardiac hypertrophy which caused by pressure overload.Particularly,the Akt expression had a positive change in the myocardiac hypertrophy,and GSK3β had a negative change,we hypothesized that GSK3β maybe has a inhibition function to myocardiac hypertrophy.

Abstract:Aim To investigate the effect of advanced glycation end products modified human serum albumin(AGE-HSA) on morphological changes of tight junction associated protein ZO-1 in endothelial cell and the mechanism in this pathological procedure. Methods Human umbilical vein endothelial cell(hUVEC)-derived cell line(ECV304) were incubated with AGE-HSA in different concentrations and timing. To visualize the morphological changes of tight junction protein ZO-1,the treated cell were incubated with mouse anti-ZO-1 primary antibody and then FITCanti-mouse IgG secondary antibody.The morphological changes of ZO-1 were observed with confocal microscope.The cell were pre-administrated with PD98059,a specific inhibitor of MEK1(ERK upstream kinase)or SB₂03580,a specific inhibitor of p38 MAP kinase,respectively,before exposed to AGE-HSA,then the cell were rinsed with DMEM for three times and exposed to AGE-HSA. The cell were transfected with dominant negative MEK1 or MEK6b(p38 upstream kinase) mutant adenoviruse,then exposed to AGE-HSA.And the cell were transfected with constitutively active MEK1 or MEK6b mutant adenoviruse. Results In normal control group,ZO-1 staining appeared as a continuous and smooth line along the regions of cell cell contact.Under the stimulation of AGE HSA,morphology of ZO-1 in endothelial cell were changed greatly in a concentration and time-dependent manner.The changes were partially blocked by PD98059 and SB₂03580.The transfection of dominant negative MEK1 and MEK6b mutant adenoviruse had the similar effects.The transfection of constitutively active MEK1 and MEK6b disrupted the structure of ZO-1. Conclusion AGE modified proteins can induce morphological changes of ZO-1 in endothelial cell.Activations of ERK and p38 MAP kinase pathways play an important role in this procedure.

Abstract:Aim To explore the effects of probucol on the plaques formation of aorta and soluble thrombomodulin in hypercholesterolemic rabbits. Methods 16 male New Zealand white rabbits were fed with 1% cholesterol, 7.5% protein,8% lard diet for 8 weeks,and then were randomly divided into two groups.Starch group(n=8): maintained cholesterol and starch(500 mg/kg everyday) diet for 6 weeks;probucol group(n=8): the same cholesterol diet supplemented with(500 mg/kg everyday) probucol for 6 weeks;and control group(n=8) was fed with normal diet for 14 weeks.The soluble thrombomodulin concentrations were detected by enzyme-link-immuno sorbent assay,and the histopathological changes of the aortas were detected at the end of the study. Results Compared with control group,rabbits fed with high cholesterol diet showed higher levels of serum total cholesterol,low-density lipoprotein cholesterol and high-density lipoprotein cholesterol,all of which were significantly reduced by probucol treatment.There were atherosclerotic lesions in aortas in starch group as compared with control group.The areas of the plaque(51.54%±8.32%) and the intima thickness(0.58±0.17 mm) of the aorta were ameliorated in probucol group as compared with starch group(84.81%±9.35%,1.62±0.18 mm,respectively).The base concentrations of soluble thrombomodulin in the three groups were very low. The levels of sTM were significantly increased after 10 weeks of high-cholesterol diet in starch group,and probucol significantly reduced the level of soluble thrombomodulin(3.25±0.52 μg/L) as compared with starch group(7.56±0.62 μg/L) at the end of the study.The concentration of soluble thrombomodulin was positively associated with the plaques areas of aorta(r=0.72,P=0.008). Conclusions Probucol decreased the plasma cholesterol and soluble thrombomodulin concentrations and protected the endothelial function,which may inhibit the formation of plaques of aortas in cholesterolemic rabbits.

Abstract:Aim To explore the effects of homocysteine(Hcy) on the expression of matrix metalloproteinase-2(MMP-2) in rat vascular smooth muscle cells(VSMC). Methods Cultured rat VSMC was incubated with different concentration of Hcy in vitro for 24,48 and 72 h.The expression of MMP-2 was determined by using the methods of gelatin zymography and western blotting. Results 0.05～1.0 mmol/L Hcy increased the expression of MMP-2 significantly.Incubated with the same concentration of Hcy the level of MMP-2 of 72 h was higher than that of 24 h and 48 h. Hcy >5.0 mmol/L reduced the expression of MMP-2.Incubated with the same concentration of Hcy(>5.0 mmol/L) the level of MMP-2 of 72 h was lower than that of 24 h and 48 h. Conclusions These datas suggested that Hcy can affect the expression of MMP-2 in VSMC.It may be one of factors in the pathogenesis of atherosclerosis induced by Hcy.

Abstract:Aim To study the effects of methyl 3β-hydroxy-5α,6α-epoxycholanate(MHEC) and T-0901317 on the expressions of nitric oxide synthase(NOS),proliferating cell nuclear antigen(PCNA) and plasminogen activator inhibitor-1(PAI1) in the artery wall. Methods Apolipoprotein E-deficient(ApoE~(-/-)) mice were fed with an atherogenic diet,two types of liver X receptor(LXR) agonists(T-0901317 and MHEC) were orally administered daily at dose of 10 mg/kg for 6 weeks.SP immunohistochemistry analysis was performed to detect the expressions of induced NOS(iNOS),endothelial NOS(eNOS),PCNA and PAI-1 in the aortic atherosclerotic lesions. Results The expression of iNOS in the aortic wall was decreased in MHEC group and T-0901317 group compared with control group(p<0.01);while the expression of eNOS in the endothelium was increased significantly(p<0.01).The expressions of PCNA and PAI-1 in each group didn't differ markedly(p<0.05). Conclusions MHEC and T-0901317 could induce the expression of eNOS in the endothelium,while the expression of iNOS in the aortic wall was partly inhibited.This suggests that LXR agonists may take its anti-atherosclerosis role by inhibiting the inflammation in the artery wall and protecting the endothelial function.

Abstract:Aim This study sought to evaluate the endogenous female sex hormones secretion abnormality in postmenopausal women with coronary artery disease(CAD)and its influence on nitric oxide synthesis. Methods We assessed the concentration of serum female hormones,estradiol(E₂)and progesterone(P)by using radioimmunoassay and determined serum NO(Nitrite/Nitrate) and the activity of NO synthetic enzyme(NOS)by colorimetry in 100 postmenopausal women with coronary artery disease and 100 healthy postmenopausal women who were enrolled in this study. Results Postmenopausal women with coronary artery disease had significantly lower E₂,higher P levels(121±32 pmol/L vs 156.2±30.6 pmol/L,5.67±1.6 nmol/L vs 3.14±1.1 nmol/L respectively)and lower E₂/P ratio(52.4±26.5 vs 127.9±37.8) than healthy postmenopausal women.The serum NO level and NOS activity were lower in women with CAD than in healthy women.The serum E₂ level and E₂/P ratio were positive correlative with NO level and NOS activity,whereas,the serum P level was passive relative with NO level and NOS activity. Conclusions Compared with healthy postmenopausal women,women with CAD have lower estrogen,higher progesterone levels and significantly lower E₂/P ratio.This endogenous female hormones imbalance do adverse effect on the vascular endothelial function.

Abstract:Aim Aim To explore the effects of two different doses of simvastatin (10 mg,20 mg/day) on vascular endothelial function of patients with coronary heart disease(CHD). Methods Totally 66 patients with CHD were included and randomly divided into: control group and simvatatin groups of different dose groups(10 mg/day,20 mg/day),22 patients in each group.The endothelial dependent flux modulated dilation(FMD) of brachial artery was measured by ultrasound technique before and after 8 weeks treatment.At the same time,we also examined the changes of the serum levels of lipids. Results After 8 weeks treatment,2 simvastatin groups(10 mg,20 mg) apparently reduced the serum level of TC(18.3%,29.3%,respectively) and the serum level of LDLC(25.3%,35.4%,respectively).The values of P between different dose groups comparison were all less than 0.05.The serum levels of lipids in control group did not significantly change after therapy.The values of FMD apparently increased in simvastatin groups(10 mg: 3.51%±4.03% vs 7.46%±5.90%;20 mg: 3.89%±3.97% vs(7.98%)±6.16%;p<0.01).But there was no statistic difference between them.The increase of FMD did not relate to the changes of TC and LDLC level in the serum.Although the value of FMD slightly increased in control group,it had no statistic significance.There was no significant change of vasodilation responding to nitroglycerin and brachial diameter in all groups after simvastatin therapy. Conclusion Different doses of simvastatin(10 mg,20 mg) can obviously improve the vascular endothelial function of patients with CHD in 8 weeks.But there is no significant changes between two different doses and it may not relate to lipid-lowering action.

Abstract:Aim To understand the paraoxonase(PON) activity in the patients with coronary heart disease,and the relationship between paraoxonase activity and coronary heart disease. Methods 106 cases having one or more than two branches narrow(≥50%), and 62 control group with no coronary artery narrow or narrow ≤50%,were diagnosed by coronary angiography.Blood paraoxonase(PON1) activity,superoxide dismutase(SOD) and malondialdehyde(MDA) levels were tested and analyzed by pheny acetate method and colorimetric method respectively in these two groups. Results Compared with the control group,PON1 activity and SOD were markedly decreased(p<0.05),MDA were increased in coronary heart disease(p<0.01);PON1 activity was positively associated with high density lipoprotein(HDL) cholesterol and SOD,was negatively associated with MDA.Compared with no coronary artery narrow or narrow ≤50%,the PON1 activity were markedly decreased(p<0.05),with the more severe lesion of coronary artery,the more lower PON1 activity. Conclusion PON1 activity were lower in the patients with coronary heart disease,lower PON1 activity was relative with the severe degree of coronary heart disease.

Abstract:Aim To investigate the association between paraoxonase 2 gene 311 Cys/Ser polymorphism and macrovascular disease in type 2 diabetes mellitus patients. Methods A case-control study of 272 subjects(including randomly selected 183 type 2 diabetes mellitus patients with or without macrovascular disease and 89 healthy controls) was performed.Genomic DNA was extracted from the subjects'peripheral blood leukocytes.The paraoxonase 2 gene 311 Cys/Ser polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism analysis with Ddel Ⅰ digestion. Results Paraoxonase 2 gene 311 Cys/Ser polymorphism was detected in population of Qingdao.The genetype distribution(CC, CS and SS) of paraoxonase 2 gene 311 Cys/Ser polymorphism showed significant differences between type 2 diabetes mellitus complicated with macrovascular disease group and the other two groups(type 2 diabetes mellitus group & healthy group),the former had significantly higher S allele frequency(p<0.05 or p<0.01).The ratio of diabetic macrovascular disease,if S allele existed,increased(2.932) times.Levels of serum lipids in different genotypes of paraoxonase 2 gene 311 Cys/Ser in cases showed no evident differences. Conclusions The paraoxonase 2 gene 311 Cys/Ser polymorphism is associated with type 2 diabetes mellitus complicated with macrovascular disease in Qingdao's population.S allele may be a risk factor for type 2 diabetes mellitus complicated with macrovascular disease.

Abstract:Aim To evaluate the effect of oral folic acid on endothelial function in elderly hypertensive patients. Methods Fourty-two elderly patients with mild essential hypertension were divided with randomized principle into two groups: folic acid administrative group(n=22) and control group(n=20).Flow-medicated dilatation(endothelium dependent) and nitroglycerin-induced dilatation(endothelium independent) using high-resolution ultrasound were measured before and 12 weeks after treatment. Results The difference of baseline diameter(D_0) in the two groups were not statistically significant before and after treatment.Flow-mediated dilatation of patients with folic acid administration group(11.59%±4.79%) was improved significantly compared with that of pretherapy(7.15%±3.20%) and control group(8.14%±3.01%)(p<0.05).Endothelium-independent dilation(19.73%±5.80%) also was improved significantly compared with that of pretherapy(16.69%±4.75%) and control group(17.55%±6.05%)(p<0.05). Conclusion Folic acid administration improves arterial endothelial function in elderly hypertensive patients.

Abstract:Aim To evaluate the risk factors,renal functions,and serum lipid levels of atherosclerotic renal artery stenosis(ARAS) patients,and analyze the correlation between them and the extent and severity of renal artery lesion. Methods Renal functions and serum lipids were measured in 70 patients with ARAS.They were analyzed and compared with those in 62 healthy controls. Results The morbilities of hypertension,coronary artery disease,chronic renal dysfunction and hyperlipoidemia were significantly increased compared with the controls(p<0.01).There were significant differences in blood urea nitrogen(BUN),serum creatinine(SCr),total cholesterol(TC),high density lipoprotein cholesterol(HDL),apolipoprotein A1(apo A1) in the ARAS patients compared with the controls(p<0.05 or p<0.01),BUN,SCr and TC have significant differences in the different extent and severity of ARAS patients(p<0.01). Conclusion Hypertension,coronary artery disease,chronic renal dysfunction and hyperlipoidemia are risk factors for ARAS.

Abstract:Aim To evaluate the related factors that affect thrombolysis in myocardial infarction(TIMI) flow after primary percutaneous coronary intervention(PCI) in patients with acute myocardial infarction(AMI). Methods Clinical and angiographic data of AMI patients treated by primary PCI were collected.Relative analysis was completed. Results 75 AMI patients treated by primary PCI were included in the study,60 patients had TIMI 3 flow(60/75,80%),and 15 patients had less than TIMI 3 flow(15/75,20%).Univariate analysis showed that the infarct related artery diameter,times of balloon dilation,stent number, stent diameter,times of stent dilation,history of diabetes mellitus,time from symptom onset to emergency room,catheterization room and flow reopened could affect TIMI flow obviously(p<0.05),multivariate analysis showed that the infarct related artery diameter,times of balloon dilation,history of diabetes mellitus,time from symptom onset to emergency room were independent factors which influenced TIMI flow after primary PCI(p<0.05). Conclusions The infarct related artery diameter,times of balloon and stent dilation,history of diabetes mellitus,time from symptom onset to flow reopened were independent factors which influenced TIMI flow after primary percutaneous coronary intervention in patients with acute myocardial infarction.

Abstract:Aim To explore the changes of the prevalence rate of blood pressure abnormality in Shanghai Bao-Steel Company-based population. Methods All medical records of the employees were analyzed,who underwent health examination biennially from 1995 to 2002.Systolic blood pressure(SBP) abnormality,diastolic blood pressure(DBP) abnormality and hypertension were diagnosed by SBP≥140 mmHg, DBP≥90 mmHg and SBP≥140 mmHg or DBP≥90 mmHg or administrated hypotensive drugs.SPSS 11.5 of statistical software was used for data analysis. Results During the study period,59 131 person-times received periodic medical check-up,of which 27.1% participants received four times check-up,and 26.6% three times,24.0% twice,respectively.The mean SBP increased from 115.7 mmHg to 123.6 mmHg,and the mean DBP increased from 76.8 mmHg to 83.0 mmHg.The standardization prevalence rates of SBP abnormality and DBP abnormality increased separately from 4.1% and 12.3% to 8.0% and 20.6%.The standardization prevalence rate of hypertension increased from(13.4%) to 23.6% from 1995 to 2000,then decreased to 20.1%.The standardization prevalence rates of SBP abnormality and DBP abnormality of the total increased with time.By the analysis of age and sex,it was found that the prevalence rate of SBP abnormality increased significantly with time in men younger than 60 years old and the prevalence rate of DBP abnormality increased significantly with time in men younger than 50 years old,but the prevalence rates of SBP abnormality and DBP abnormality were so only in women in 40～49 years old.No matter in the total or men or women younger than 60 years old,the prevalence rate of hypertension increased with time from 1995 to 2000,but decreased in 2001～2002.At the same time and the same age range the prevalence rate of blood pressure abnormality in men was higher than that in women.At the same time the prevalence rate of DBP abnormality was higher than that of SBP abnormality. Conclusion The prevalence rates of SBP abnormality and DBP abnormality were increasing in Bao-Steel Company employees,which occured mainly in the middle-age and young men.