Abstract:Aim To observe the effects of Chlamydia pneumoniae infection on migration of endothelial cells,to investigate the interventive effect of Berberine on Chlamydia pneumoniae induced-endothelial cell migration and to explore its possible mechanism. Methods Endothelial cells pretreated with Berberine at different concentration(0,100,150 and 200 mmol/L) were infected by Chlamydia pneumoniae AR-39 in vitro.At 24,48 and 72 h after Chlamydia pneumoniae infection,the wound healing assay and Transwell assay were performed to observe the effects of Berberine on migration of endothelial cells.The mRNA expression and enzymatic activity of PI3K were detected by RT-PCR and ELISA at the corresponding time point. Results Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K increased significantly at 24,48 and 72 h after Chlamydia pneumoniae infection in comparison with the control group(P<0.01).Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K decreased markedly after administration of the PI3K inhibitor of LY294002 compared with the Chlamydia pneumoniae infection group(P<0.01).Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K decreased markedly after administration of the middle-dose and high-dose Berberine compared with the Chlamydia pneumoniae infection group(P<0.01),and migration of endothelial cells was positively correlated with the mRNA expression(r1) and enzymatic activity of PI3K(r2)(r1=0.841,r2=0.832,P<0.01). Conclusions Chlamydia pneumoniae may induce endothelial cell migration via the activation of PI3K.Berberine can antagonize Chlamydia pneumoniae induced-endothelial cell migration possibly through down-regulating the PI3K mRNA expression and inhibiting the activation of PI3K.

Abstract:Aim To evaluate whether heat shock protein 60(HSP60) oral administration could induce antigen-specific CD4+CD25+ regulatory T cells and its effect on the formation of atherosclerotic plaque in hypercholesterolemic apolipoprotein(Apo) E-/-mice. Methods At 8 weeks of age,12 male Apo E-/-mice were divided into two groups that were orally administrated PBS plus HSP60 and only PBS separately for 5 days,and a high-cholesterol diet was started 5 days after the last treatment for 12 weeks,at which time pathological analysis of plaque was performed,percentage of CD4+CD25+ regulatory T cells in splenocytes were analyzed by FCAS,proliferation response of splenocytes to HSP60 was detected and cytokines in the superanant were determined by ELISA. Results Compared with control animals,oral tolerance to HSP60 resulted in a significant decrease in the size of atherosclerotic plaques,and had a significant increase in CD4+CD25+ regulatory T cells in spleen.Specifical proliferation response of CD4+CD25+ regulatory T cells in splenocytes to HSP60 was significantly suppressed and the level of TGF-β and IL-10 in the superanant increased while IFN-γ decreased significantly. Conclusion HSP60 oral tolerance can induce antigen-specific CD4+CD25+ regulatory T cells which in turn attenuates the progression of atherosclerotic plaque.This provides a new immunologic approach for the prevention of atherosclerosis.

Abstract:Aim To study the role of mutations of Mfn2 protein kinase A phosphorylation site in the proliferation of vascular smooth muscel cell(VSMC) and related signaling pathways. Methods Two novel mutations were constructed,Adv-Mfn2-αPKA and Adv-Mfn2-asnPKA,then VSMC were infected with them.The effect of mutations on the proliferation of VSMC was explored by WST-1 assay.The cell cycle was determined using flow cytometry.Western blotting were used to detect the expression of Mfn2 and p-ERK1/2. Results The expression of Mfn2 protein has no significant difference in Adv-Mfn2,Adv-Mfn2-alaPKA and Adv-Mfn2-asnPKA groups.Mfn2-alaPKA and Mfn2 both showed stronger inhibitory effect on VSMC proliferation(P<0.01).Most of the cells in these two groups were blocked in the stage of G0/G1(P<0.01),and the expression levels of p-ERK1/2 also decrease(P<0.01).Mfn2-alaPKA is superior to Mfn2 in attenuating the proliferation of VSMCs.The effect of Mfn2-asnPKA is similar to the control. Conclusion Mfn2-alaPKA has more stronger inhibitory effect on the proliferation of VSMC than Mfn2,while Mfn2-asnPKA has no effect.PKA phosphorylation site plays an important role in regulating the function of Mfn2 gene.

Abstract:Aim To investigate the effects of advanced glycation end-products(AGE) on endothelial nitric oxide synthase type 3(NOS-3) and whether estrogen may influence such effects,then to discover the underlying mechanisms. Methods Cultured human umbilical endothelial cells were administered with different concentrations of AGE and/or estrogen,then western blotting was applied to detect the variation of NOS-3 and Akt protein expression. Results After the administration of AGE(50,100 and 200 mg/L) for 4 h,endothelial cells exhibited lower protein expression of NOS-3 and Akt;after administration of estrogen(10-9,10-8 and 10-7 mol/L),endothelial cells presented higher protein expression of NOS-3 and Akt.Furthermore,with the pretreatment of estrogen(10-8mol/L),the inhibition on NOS-3 protein expression by AGE(100 mg/L) was remarkably ameliorated.As for protein kinase Akt,it demonstrated similar changes. Conclusions AGE could notably suppress the protein expression of NOS-3 in endothelial cells,while estrogen could effectively ameliorate this suppression.The protective effects of estrogen might relate to its positive regulation on the up-stream signaling protein kinase Akt.

Abstract:Aim To investigate whether atorvastatin can improve the endothelial function through activating peroxisome proliferator-activated receptor gamma in human umbilical vein endothelial cells. Methods Human umbilical vein endothelial cells were cultured in vitro.And the 2~4 generation were used.Experiment 1: ①control group;②lipopolysaccharide group(1.0 mg/L);③atorvastatin 1.0 group(atorvastatin 1.0 mmol/L);④lipopolysaccharide+atorvastatin 1.0 group(atorvastatin 1.0 mmol/L);⑤lipopolysaccharide+atorvastatin 5.0 group(atorvastatin 5.0 mmol/L).After human umbilical vein endothelial cells were incubated with different concentrations of atorvastatin and lipopolysaccharide for 24 hours,the expression of Peroxisome proliferator-activated receptor gamma of human umbilical vein endothelial cells were evaluated with reverse transcription-polymerase chain reaction.The content of nitric oxide,soluble intracellular adhesion molecule-1 in cell culture fluid were measured with Nitrate reductase and ELISA.Experiment 2: ①control group;②atorvastatin 5.0 group(atorvastatin 5.0 mmol/L);③GW9662 group(GW9662 0.2 mmol/L);④lipopolysaccharide+atorvastatin 5.0 group(atorvastatin 5.0 mmol/L);⑤GW9662+lipopolysaccharide+atorvastatin group 5.0 group(GW9662 0.2 mmol/L,atorvastatin 5.0 mmol/L).After human umbilical vein endothelial cells were incubated with atorvastatin,lipopolysaccharide and GW9662(the specific inhibitor of peroxisome proliferator-activated receptor gamma) for 24 hours,the expression of Peroxisome proliferator-activated receptor gammain human umbilical vein endothelial cells were evaluated with RT-PCR.The content of nitric oxide,soluble intracellular adhesion molecule-1 in cell culture fluid were determined with the way of Nitrate reductase and ELISA. Results The expression of Peroxisome proliferator-activated receptor gamma of human umbilical vein endothelial cells were upregulated by different concentrations of atorvastatin.The expression reinforced with the increased concentration of atoravastatin.Compared with control group,the contents of nitric oxide significantly increased and soluble intracellular adhesion molecule-1 decreased in cell culture fluid when Human umbilical vein endothelial cells were incubated with lipopolysaccharide+atorvastatin 1.0 mmol/L and lipopolysaccharide+atorvastatin 5.0 mmol/L.The effects reinforced with the increased concentration of atorvastatin.The effects of atorvastatin are partially inhibited by GW9662(the specific inhibitor of peroxisome proliferator-activated receptor gamma). Conclusion The endothelial function was improved by atorvastatin partially through activating Peroxisome proliferator-activated receptor gamma.

Abstract:Aim To eluciadate the genesis of atherosclerosis by investigating the level of angiotensinⅡ(AngⅡ),the expression of scavenger receptor class B type Ⅰ(SR-BⅠ),angiotensinⅡ receptors type 1(AT1),type 2(AT2) and the relationships among them. Methods Eighteen rats were randomly divided into two groups as control group and atherosclerosis group.Atherosclerosis group were given high cholesterol feeds,vitamin D3 and aorta balloon injury.At the end of 12 weeks,HE and Masson stain were used to detect the structure of aorta wall and atherosclerotic plaque.The concentration of AngⅡ was detected by the method of radio-immunity.The protein expression of SR-BⅠ,AT1 and AT2 were investigated by Western Blot and immunohistochemistry,while their mRNA expression were measured by real time reverse transcription polymerse chain reaction(RT-PCR).The correlation between variances were analyzed by linear regression analysis. Results In atherosclerosis group,some endothelial cells were lost and the intima thicked.The smooth muscle cell(SMC) proliferated and lined up in disorder.The smooth muscles in the media were atrophic slightly.The structures and arrangements of elastic fibers were in disorder and the fibrous tissues proliferated.There were some hyperplasy in the aortic wall and formed atherosclerotic plaques contained with hyperplastic fibers.All of these were observed by HE and Masson stain.The level of AngⅡ in atherosclerosis group was higher than that in control group(210.80±31.56 ng/L vs 121.26 ± 25.32 ng/L,P<0.01).Compared with control group,the protein expression of SR-BⅠ,AT1 and AT2 increased significantly in atherosclerosis group(0.83±0.19 vs 0.16±0.03,P<0.01;1.02±0.12 vs 0.48±0.11,P<0.01;0.97±0.24 vs 0.13±0.03,P<0.01),and expressed mainly in cell membrane and cytoplasma.The aorta mRNA expression of SR-BⅠ,AT1 and AT2 increased significantly in atherosclerosis group than that in control group(0.76±0.17 vs 0.16±0.04,P<0.01;0.83±0.20 vs 0.33±0.08,P<0.01;0.78±0.13 vs 0.12±0.03,P<0.01).The protein expression of SR-BⅠ was directly related to the level of AngⅡ and the expression of AT1(r=0.717,P<0.05 and r=0.711,P<0.05). Conclusion The expression of aortic SR-BⅠ,AT1 and AT2 increase significantly in atherosclerotic rats,furthermore the increased expression of SR-BⅠ is related to the elevation of AngⅡ and activation of AT1.

Abstract:Aim To observe changes of peroxisome proliferator activated receptor γ(PPARγ) mRNA,ATP-binding cassette transporter A1(ABCA1) mRNA and CD36 mRNA in foam cells which come from the peritoneal macrophage of apolipoprotein E knock out mice with giant knotweed rhizome,hawthorn and both of them,and discuss possible mechanism of anti-atherosclerosis on gene level. Methods ApolipoproteinE knock out mice peritoneal macrophage were incubated and divided into seven groups: blank group,polydatin group,extractive of hawthorn group,polydatin and extractive of hawthorn group,Lovastatin group,Rosiglitazone group and model group.Except for blank group,all other groups were added with oxidative low density lipoprotein and lipopolysaccharide.The course of incubation was 48 hours. Intracellular PPARγ mRNA,ABCA1 mRNA and CD36 mRNA of all groups were detected at 0 hour,24 hours and 48 hours respectively by method of RT-PCR. Results Compared with the blank group,above three indexes of the model group and all medicine groups increased obviously after they were induced for 24 or 48 hours(P<0.01).Compared with the model group,PPARγ mRNA of the polydatin and extractive of hawthorn group and the rosiglitazone group all increased obviously,ABCA1 mRNA of the polydatin group,the polydatin and extractive of hawthorn group and the rosiglitazone group all increased obviously(P<0.05 or P<0.01),and CD36 mRNA of all medicine groups had no obvious difference after they were treated for 24 hours(P>0.05).Compared with the model group,PPARγ mRNA and ABCA1 mRNA of all medicine groups increased obviously,CD36 mRNA of them decreased obviously after they were treated for 48 hours,moreover,the polydatin and extractive of hawthorn group was superior to the polydatin group,the extractive of hawthorn group and the lovastatin group(P<0.05 or P<0.01). Conclusions The compatibility of giant knotweed rhizome and hawthorn may have similar agitating effect on PPARγ with rosiglitazone.It can inhibit macrophages foaming and prevent formation of atherosclerosis through up-regulating PPARγ mRNA and ABCA1 mRNA,and down-regulating CD36 mRNA of apolipoprotein E knock out mice.

Abstract:Aim To evaluate the effect of rosuvastatin on myocardial inflammation and left ventricular disfunction after coronary microembolization(CME). Methods 48 male SD rats were randomized into control group,CME group,low-dose rosuvastatin group[0.5 mg/(kg·d)] and high-dose rosuvastatin group [3.0 mg/(kg·d)] averagely.Rosuvastatin was fed from pre-to post-CME for two weeks.Αt 3 days post-CME,the expression of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-10(IL-10) in myocardium was assayed by ELISΑ,immunostaining and pathological changes were detected by HE staining.Αt 28 day post-CME,collagen deposition was detected by Masson staining and cardiac function was assessed by echocardiography. Results The levels of TNF-αand IL-1β were lower,and IL-10 was higher in high-dose rosuvastatin group compared with CME group.High-dose but not low-dose rosuvastatin also reduced inflammatory cell infiltration and collagen deposition in farct zone,decreased LVEDD,LVESD and increased LVEF,LVFS. Conclusion In rats with CME,perioperative therapy with high-dose rosuvastatin prevents cardiac remodeling and dysfunction.This benefit may be partly derived from reducing myocardial inflammation.

Abstract:Aim To observe the effect of minocycline on atherosclerosis(As) after the treatment of atherosclerosis plaque-intervention with changes in the level of molecular pathology,evaluate drug effects on treatment of As and analyze its mechanism. Methods 5 as normal control group were randomly taken from 40 New Zealand rabbits. 35 rabbits were used as atherosclerotic animal model after balloon-induced arterial injury to the epithelium and use of high-fat diet for 3 months.In addition to death or illness of five rabbits during experiment,remaining 30 rabbits were randomly divided into 4 groups,namely,model group(8 rabbits,high fat diet for 1 month),reconverted normal diet group(7 rabbits,conventional feeding for 1 month),fluvastatin treatment group(7 rabbits,given fluvastatin 1 mg/(kg·d) intervention for 1 month);minocycline treatment group(8 rabbits,given minocycline with a dose on 3 mg/(kg·d)).The animals were sacrificed and the abdominal aorta in each group were cut,paraffin-embedded sections,Masson staining were used to observe the morphological changes of As plaque and inflammatory cells,expression levels of matrix metalloproteinases(MMP) were examined with the immuno-histochemistrical staining,using in situ hybridization-Tunel staining detection of apoptotic cells in As plaque of these animal. Results Histopathology artery wall by Masson staining showed no pathological changes in normal group,model control group and reconverted normal diet group showed the typical features of As lesions,and two groups with treatment of the minocycline and fluvastatin significantly reduce the pathological change,especially the former.In plaque of As of each group,macrophage(RAM-11) and expression levels of matrix metalloproteinase(MMP-3 and MMP-9)had positive correlation (P<0.001).But macrophage content in plaque and MMP expression level in the minocycline treatment and the fluvastatin treatment group were significantly lower compared with the model control group(P<0.05).And smooth muscle cells markedly increased in minocycline group. Conclusion Minocycline can relieve severity of As treatment of diseases and improve the stability of atherosclerotic plaque.

Abstract:Aim To study the effects of macrophage-derived lipoprotein lipase(LPL) on the lipid metabolism in inherited hypertriglyceridemia mice. Methods After lethal irradiation,8 female LPL-deficient(LPL-/-,LK) mice were divided into two groups and reconstituted by bone marrow transplantation(BMT)from male C57BL(LPL+/+,WT) and LK mice,respectively.Plasma levels of triglyceride,total cholesterol were surveyed,plasma lipoprotein profile was detected by fast protein liquid chromatography(FPLC),and LPL activities were assayed at week 4 post-BMT. Results It was demonstrated that plasma triglyceride(TG) and cholesterol(Chol) levels in BMT(WT→LPL-/-) mice were reduced by 83.2%(P<0.05,n=4) and 74.4%(P<0.05,n=4) compared with those in LPL-/-→LPL-/-mice,while similar reduction by 86.2% and 78.8% in TG and Chol before and after BMT were observed in WT→LPL-/-mice.Post-heparin plasma LPL activities were increased by 4.5-fold after BMT.There were no effects of BMT in LK→LK mice on TG,Chol and LPL activities. Conclusion Macrophage-derived LPL plays a significant role in the lipid metabolism,and improves lipoprotein disorder in inherited hypertriglyceridemia mice.

Abstract:Aim To investigate time course of nuclear factor-κB(NF-κB) activation after artery endothelium denudation and its relationship with local vascular cell adhesion molcular-1(VCAM-1) expression. Methods Deendothelialization injury of rat aorta was produced by ballooning(3 times) with PTCA catheter.Crucify 6 rats before and at every time points after procedure: 0 h,12 h,24 h,1 d,2 d,3 d,7 d and 14 d.NF-κB activation was measured by electrophoretic mobility shift assay(EMSA).Local VCAM-1 expression was measured by immunohistochemical Assay. Results Scanning electron microscopy showed that endothelium was completely denudated.Significant neointima proliferation was seen at 14 days after injury.NF-κB was activated at 12 h and culminated at 1 to 3 days after operation,and then decreased gradually.Its activation was higher at 14 days after operation than control,but there was no statistical significance.No local VCAM-1 expression could be detected immediately after denudation.At 7 days after operation,VCAM-1 was positive on the surface of endothelium and in the medium smooth muscle cells(SMC).At 14 days after operation,VCAM-1 was still positive on the surface of uncovered endothelium,while more abundant expression was seen in the bottom of neointima near internal elastic lamina. Conclusions NF-κB activation and VCAM-1 expression participate in the inflammation of rat denudated artery.Activation and inactivation of NF-κB occur before the expression and disappearance of VCAM-1.

Abstract:Aim To approach the relationship between inflammatory factors and glycosylated hemoglbinA1c(HbA1c) in patients with coronary heart disease(CHD). Methods 203 consecutive patients with CHD was recruited and took oral glucose tolerance test(OGTT).68 cases suffered from diabetes mellitus(DM),80 from impaired glucose homeostasis(IGH) and 55 were with normal glucose.White blood cell(WBC),fibrinogen(FIB),and C-reactive protein(CRP) were compared among the three groups.The relation between WBC,FIB,CRP and HbA1c was analyzed. Results Patients with DM or IGH had a higher level of WBC(P<0.05),FIB(P<0.05) and CRP(P<0.05) compared with the normal glucose.There was statistic positive relation between WBC(R2=0.158 9,P<0.05),CRP(R2=0.228 5,P<0.05),FIB(R2=0.302 4,P<0.05)and HbA1c. Conclusion Patients of CHD with DM and IGT suffer a more severe system inflammation.

Abstract:Aim To investigate the relationship of carotid artery segments-specific intima-media thickness(IMT),plaque summary score,brachial artery flow-media dilatation and extent of coronary artery atherosclerosis. Methods 31 consecutive eligible patients were divided into three groups with low,medium and high score.Intima-media thickness of the right and left carotid artery(the common carotid artery,internal carotid artery,bifurcation) were measured with external vascular ultrasound,the brachial artery flow-mediated dilatation of all subjects was measured noninvasively by the same ultrasound machine. Results A significant positive correlation between the intima-media thickness of various segments carotid artery and the extent of coronary atherosclerosis was found in all of the subjects,and a better correlation could be got between the intima-media thickness of bifurcation and the extent of coronary atherosclerosis(r=0.679,P<0.01).There was a significant positive correlation between plaque Crouse summary score and the extent of coronary atherosclerosis in all of the subjects,and it was easy formate plaque at the bifurcation(P<0.05).A significant negative correlation among percent FMD and the extent of coronary atherosclerosis was found in all of the subjects(r=-0.646,P<0.01).Nitroglycerin-induced endothelium-independent vasodilation among the three groups showed the trend of gradually weakening,but did not reach statistical significance(P>0.05). Conclusion Carotid IMT and brachial artery FMD may be a better reflection of the determination of coronary artery sclerosis.

Abstract:Aim To observe the effect of atorvastatin combined with probucol on the levels of serum lipids,oxidized low density lipoprotein(ox-LDL) and the activity of paraoxonase-1(PON1) in patients with acute coronary syndrome(ACS). Methods A randomized,open study was performed on a total of 38 patients(including 27 males and 11 females,the average age was 63.7±8.9 years) with ACS.The patients were randomly assigned to a control group(atorvastatin 10 mg/day,n=20) or a treatment group(atorvastatin 10 mg/day and probucol 1 000 mg/day,n=18).All of them were followed up for 4 weeks.Serum levels of total cholesterol(TC),low density lipoprotein cholesterol(LDLC),high density lipoprotein cholesterol(HDLC),triglyceride(TG),ox-LDL and PON1 activity were measured before and after treatment. Results After 4 weeks of treatment,LDLC levels reduced by 15.4% and HDLC increased by 13.7% in the control group compared with baseline(P<0.05),but the decreases in TC and TG were not significant(P>0.05);the serum levels of TC,LDLC,HDLC and TG in the treatment group decreased significantly(-28.1%,-28.5%,-14.2% and-23.3%,respectively,P<0.01 or 0.05);The decline of TC,and HDLC in treatment group was more significant than that in the control group(P<0.01).After treatment,serum ox-LDL levels declined significantly and PON1 activity increased significantly in both groups compared with baseline(P<0.01);The changes of ox-LDL levels and PON1 activity were more significant in the treatment group than those in the control group(P<0.01).No relationships were observed between TC,TG,LDLC,HDLC and ox-LDL or PON1 before and after treatment(P>0.05),but the serum levels of ox-LDL and PON1 had a significant negative correlation by Pearson correlation analysis(r=-0.669,P<0.01). Conclusion The addition of probucol to atorvastatin has a synergistic effect in lowing the cholesterol and antioxidant,but atorvastatin can not offset the HDLC decreasing effect of probucol.

Abstract:Aim To investigate the risk factors and clinical features of coronary lesions in patient with premature coronary heart disease. Methods 294 patients with coronary heart disease(CHD) were divided into premature CHD group(male<55 years old,n=104;female<65 years old,n=65) and aged CHD group(male≥55 years old,n=74;female≥65 years old,n=51).The risk factors of premature CHD and the features of coronary lesions were illustrated. Results The percentage of smoking,triglyceride(TG) level and family history in patients with premature CHD were higher than those in patients with aged CHD(P<0.05).But the patients with premature CHD had lower rate of hypertension and diabetes compared with the patients with aged CHD(P>0.05).There were significantly more premature CHD patients with acute coronary syndrome(66.3% vs 45.6%,P<0.05),more premature CHD patients had single vessel lesion(P<0.05),lower average lesion score(P<0.05). Conclusion Smoking,family history,increased TG level might play an important role in the development of premature coronary heart disease.

Abstract:Aim To investigate the effects of metoprolol succinate sustained-release tablets on heart rate turbulence(HRT) and heart rate variability(HRV) to silent ischemia with coronary heart disease. Methods The changes of heart rate turbulence and heart rate variability to silent ischemia with coronary heart disease in treatment with metoprolol were investigated. Results The TS and TO in treatment group were both lower than those of control group(P<0.05).The TS and TO after treatment were higher than those of before treatment.SDNN,SDANN and SDNNindex before treatment in treatment group except rMSSD and PNN50 were lower than those of control group(P<0.05).SDNN,SDANN and SDNNindex after treatment in treatment group were increased significantly(P<0.05). Conclusion HRT and HRV in the patients of silent ischemia with coronary heart disease is abnormal and metoprolol can improve the heart autonomic nerves function.

Abstract:Aim To observe the clinical effect of monosialotetrahexosylganglioside in treatment of ischemic stroke. Methods 106 cases of ischemic stroke were randomly divided into two groups,experimental group and control group,53 cases in each group.BI score were applied to assess the activities of daily living and level of awareness after a course of treatment to determine the efficacy.And serum S100β protein level changes were monitored before and after treatment. Results After one course of treatment,the total effective rate in experimental treatment group was 92.5% and 81.1% in the control group.BI score of the treatment group was significantly higher than that of the control group at 7th,14th and 21th days,and the differences were statistically significant(P<0.05).Compared with the control group,the experimental group achieved better nurological function after treatment,and the difference was statistically significant(P<0.05).The serum S100β protein levels in the treatment group decreased gradually at the 7th,14th and 21th days after treatment,significantly lower than the concentration of the same group before treatment,but also significantly lower than that of the control group.The differences were statistically significant(P<0.05). Conclusion Monosialotetrahexosylganglioside was effective in treatment of ischemic stroke,and without side effect,and deserved clinical application.

Abstract:Aim To explore the value of tissue doppler imaging in the evaluation of ventricular function in patients with end-stage renal disease. Methods 31 patients with end-stage renal disease of the normal eject factionand 31 healthy subjects were selected for routine 2D and tissue doppler imaging.Left ventricular eject faction,interventricular septum thickness,left ventricular posterior wall thickness,left ventricular internal dimensions and left ventricular internal dimensions were measured.Conventional left and right ventricular diastolic function parameters were acquired by pulsed doppler.Including to the mitral and tricuspid flow velocity,the ratio of the mitral and tricuspid early diastolic velocity and late diastolic velocity were calculated.The mitral and tricuspid annular early and late diastolic velocities were determined by tissue doppler imaging in apical views(4-and 2-chamber),and the ratio of the mitral and tricuspid early diastolic velocity and the mitral and tricuspid annular early diastolic velocities,and the ratio of the mitral and tricuspid annular early diastolic velocities and late diastolic velocities were calculated.Then function parameters of the end-stage renal disease group were compared with healthy group,and the corrections between the parameters were analyzed. Results The end-stage renal disease patients had lower ratio of the mitral and tricuspid early diastolic velocity and late diastolic velocity,the mean mitrial and tricuspid systolic velocities,the mean mitral and tricuspid annular early and late diastolic velocities,the mean ratio of the mitral and tricuspid annular early diastolic velocities and late diastolic velocities were significantly reduced,while the ratio of the mitral and tricuspid early diastolic velocity and the mitral and tricuspid annular early diastolic velocities was significantly increased. Conclusion Patients with end-stage renal disease had left and right ventriculars diastolic dysfunction,and so were systolic function.Systolic was impaired in patients with end-stage renal disease with normal ejection fraction.

Abstract:Aim To research the distribution of dyslipidemia population and related factors in Heilongjiang Province and provide a scientific basis for the prevention and treatment of dyslipidemia. Methods A population based investigation was carried out cross-sectionally in a sample of 3 481(1 509 men and 1 972 women,aged from 20~85).Total cholesterol(TC),triglyceride(TG),high density lipoprotein cholesterol(HDLC),low density lipoprotein(LDL) and glucose were measured and according to the diagnostic criteria dyslipidemia population were screened. Results Serum lipids abnormalities were found in 1 681 persons,and the detection rate was 48.3%,54.5% for men,43.6% for women.In addition to 20~,40~,50~ the age group of high TC and high LDL,the remaining incidence of dyslipidemia in different ages and genders were significantly different.By non-conditional Logistic regression analysis,the statistical significant risk factors for dyslipidemia were age(OR=1.771),gender(OR=1.384),body mass index(OR=1.666),glucose(OR=1.919),alcohol(OR=1.277),smoking(OR=1.515),DBP(OR=1.529),waist circumference(OR=1.283) and waist-hip ratio(OR=1.858),and physical exercise(OR=0.802) was protective factors of dyslipidemia. Conclusions It is very necessary to take measures to prevent dyslipidemia.Taking control of body weight and blood pressure,elimination of tobacco and alcohol,strengthening exercise,balanced diet and other key scientific measures are positive to reduce the prevalence of dyslipidemia.