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Objective·To explore the association of blood pressure variability (BPV),especially diurnal blood pressure rhythm with brachial ankle pulse wave velocity (baPWV) and left ventricular mass index (LVMI).Methods· A total of 184 hypertensive patients participated this cross sectional study.Patients were divided into dippers,non-dippers,inverted dippers and extreme dippers groups according to nocturnal systolic blood pressure (SBP) decline.baPWV and LVMI in different groups were compared.Correlation of baPWV and LVMI with blood pressure and BPV variables were analyzed by univariate and multivariate regression analysis.Results· After adjusted by age,BMI,hypertension duration,blood pressure in consulting room,SBP and diastolic blood pressure (DBP) in 24 h,total cholesterol,low density lipoprotein cholesterin,brain natriuretic peptide and ejection fraction,baPWV in non-dippers group and inverted-dippers group were significantly higher than that in dippers group and extreme dippers group (P=0.000),and LVMI was significantly higher in non-dippers group than in dippers group (P=0.001) and extreme-dippers group (P=0.022).baPWV and LVMI were both significantly correlated to age,24 h SBP and 24 h DBP,SD value of 24 h SBP and 24 h DBP,daytime SBP and DBP,nocturnal SBP and DBP,SD values of daytime SBP and DBP,SD values of nocturnal SBP and DBP in univariate linear regression models (P＜0.05).In multivariate linear regression model,baPWV was independently associated to SD value of nocturnal SBP (β=0.289,P=0.000),nocturnal SBP decline (β=0.398,P=0.000),daytime SBP (β=0.214,P=0.001) and SD value of daytime DBP (β=0.207,P=0.002),while LVMI was independently associated to 24 h SBP (β=0.348,P=0.000) and SD value of nocturnal SBP (β=0.196,P=0.026).Conclusion· baPWV was independently correlated to SD value of nocturnal SBP,nocturnal SBP decline,daytime SBP and SD value of daytime DBP,while LVMI was independently correlated to 24 h SBP and SD value of nocturnal SBP.
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One of the hot spots of nanomaterials research is the preparation of carbon-dots ( C-dots) by simple steps with cheap raw materials and looking for its potential application. In this study, coal-based C-dots was prepared from coal mined of Wucaiwan in Xinjiang by mixed acids ( H2 SO4+HNO3 )/ultrasound treatment, and at the same time of structural characterization, the coal-based C-dots were used as fluorescent probe to detect metal ions in water. It was found that the coal-based C-dots were polycyclic aromatic hydrocarbons with particle size of (8±4) nm linked with oxygen-containing groups such as nitro group, possessing the annulus wall of multilayer graphene fragment structures built up by sp2 carbons. This endowed the coal-based C-dots with good dispersity in water, high absorbance and strong fluorescence. The coal-based C-dots were used as viable probes in that their fluorescence was selectively quenching by CuⅡ. The finding was exploited to design a fluorometric assay for CuⅡ with a detection limit of 9. 6 nmol/L.
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One of the hot spots of nanomaterials research is the preparation of carbon-dots ( C-dots) by simple steps with cheap raw materials and looking for its potential application. In this study, coal-based C-dots was prepared from coal mined of Wucaiwan in Xinjiang by mixed acids ( H2 SO4+HNO3 )/ultrasound treatment, and at the same time of structural characterization, the coal-based C-dots were used as fluorescent probe to detect metal ions in water. It was found that the coal-based C-dots were polycyclic aromatic hydrocarbons with particle size of (8±4) nm linked with oxygen-containing groups such as nitro group, possessing the annulus wall of multilayer graphene fragment structures built up by sp2 carbons. This endowed the coal-based C-dots with good dispersity in water, high absorbance and strong fluorescence. The coal-based C-dots were used as viable probes in that their fluorescence was selectively quenching by CuⅡ. The finding was exploited to design a fluorometric assay for CuⅡ with a detection limit of 9. 6 nmol/L.
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<p><b>BACKGROUND</b>Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atherosclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution (sidestream whole, SSW), and discuss the possible mechanism of inflammatory injury induced by second-hand smoke.</p><p><b>METHODS</b>The biological markers (platelet endothelial cell adhesion molecule-1, PECAM-1; alpha-smooth muscle actin, alpha-SMA; collagen IV, Col IV) and inflammatory markers (vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1; interleukin-8, IL-8) of human aortal wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1:40 SSW group (VCAM-1: 0.35 +/- 0.04, MCP-1: 0.34 +/- 0.05, IL-8: 0.37 +/- 0.05) and the 1:20 SSW group (VCAM-1: 0.40 +/- 0.04, MCP-1: 0.52 +/- 0.09, IL-8: 0.51 +/- 0.07) were significantly stronger than the control group (VCAM-1: 0.12 +/- 0.04, MCP-1: 0.06 +/- 0.02, IL-8: 0.24 +/- 0.03) by semi-quantitative analysis of immunofluorescence (P < 0.001 vs control). MCP-1 mRNA expression in the 1:40 SSW (0.15 +/- 0.04) and the 1:20 SSW (0.19 +/- 0.06) group was significantly higher than in the control group (0.09 +/- 0.03) (P < 0.05, P < 0.01 vs control); IL-8 mRNA expression in the 1:40 SSW (0.64 +/- 0.12) and 1:20 SSW (0.72 +/- 0.13) groups was also significantly higher than that in the control group (0.49 +/- 0.13) (P < 0.05, P < 0.01 vs control) by RT-PCR.</p><p><b>CONCLUSIONS</b>It is implied that a second-hand smoke solution induces the inflammatory reaction of the arterial wall by release of inflammatory factors even though there is no distinct structural change on the arterial walls under light microscope, indicating that passive cigarette smoking is related to inflammatory injury in human arterial wall and could be closely related to the early inflammatory stage of atherosclerosis.</p>
Subject(s)
Adult , Humans , Male , Arteries , Cell Biology , Metabolism , Cells, Cultured , Fluorescent Antibody Technique , In Vitro Techniques , Inflammation , Reverse Transcriptase Polymerase Chain Reaction , Tobacco Smoke PollutionABSTRACT
Objective To investigate the accuracy of three-dimensional reconstruction coronary angiography with CardiOp-B system in the evaluation of coronary artery stenosis, and make comparison with conventional quantitative coronary angiography(QCA). Methods The imaging data of 33 patients (39 vessel segments) who underwent coronary angiography and received interventional therapy were collected. The vessel diameter, vessel area, diameter of reference vessel rate of stenosed area and lesion length detected by three-dimensional reconstruction coronary angiography and QCA were compared. Results There was no significant difference in the detected minimal vessel diameter, minimal vessel area, diameter of reference vessel, rate of stenosed area and lesion length between three-dimensional reconstruction coronary angiography and QCA in these 39 vessel segments (P > 0.05), while the lesion length detected by three-dimensional reconstruction coronary angiography was significantly longer than that detected by QCA(P < 0.05). Conclusion Three-dimentional reconstruction of coronary angiography with CardiOp-B system demonstrates higher accuracy in the quantitative analysis of coronary artery stenosis compared with conventional QCA.
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Objective To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats. Methods The models of acute myocardial infarction were established in 16 rata by ligation of left anterior descending branch of left coronary artery through chest incision, and the animal were divided into control group(n=8) and experiment group (n=8). The hearts of another 2 rats were obtained for normal myocardial tissue sections as controls. Monoclonal antibody of ICAM-1 was infused from the caudal vein in experimental group, and no invervention was conducted for control group. Blood samples were obtained from caudal vein on the first, third, seventh and fourteenth day after operation in these two groups. Serum concentration of ICAM-1 was measured by ELISA, positive rate of CD34 cells in peripheral blood was detected by flow cytometry, and the parameters of concentration of ICAM-1 and positive rate of CD34 cells at each time point were compared between groups. Results The concentration of ICAM-1 in peripheral blood of experiment group reached the lowest of (59.01±2.22) pg/mL on the seventh day. The concentrations of ICAM-1 in peripheral blood of experiment group were lower than those in control group, and there were significant differences between these two groups on the seventh and fourteenth day(P < 0.01). The positive rate of CD34 cells in peripheral blood of experiment group reached the highest of (12±2.11)% on the seventh day. The positive rates of CD34 cells in peripheral blood of experiment group were higher than those in control group, and there were significant differences between these two groups on the third, seventh and fourteenth day(P<0.05 or P<0.01). Conclusion ICAM-1 can inhibit the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats.
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Accumulating studies have proved that systemic inflammation is one of the important pathophysiologic mechanisms of heart failure. This article focuses on the sources of inflammation mediators and the causes of inflammation activation in heart failure including hemodynamic changes and oxidative stress, Toll-like receptors, microbial antigens and microorganisms, endotoxin hypothesis and neurohormonal activation. Furthermore, the effects of inflammation mediators such as cytokines and chemokines on heart failure are introduced. All lead to the conclusion that heart failure is a process with complex inflammation.
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Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells (VSMCs), which were regulated by sterol regulatory element binding proteins(SREBPs).Methods ① Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed, and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.② Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group (n=6), low concentration simvastatin group (n=6) and high concentration simvastatin group (n=6). Besides, normal control group (sham operation group, n=8) was established. Intragastric group and high concentration simvastation group, respectively, while those in normal control group and atherosclerotic injured group were given same amount of normal saline. Rats were sacrificed 4 weeks later. Plasma lipid levels were examined by enzymic method, ratios of intima/(intima + tunics media) of thoracic aorta and left common carotid artery were determined, and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR. Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs. Low concentration simvastatin didn't promote the proliferation and migration of VSMCs, while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs, which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs. Moreover, high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA. Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.
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<p><b>OBJECTIVE</b>The purpose of this study was to observe the endothelial progenitor cells (EPCs) related gene expression changes before and early after revascularization in patients with acute myocardial infarction.</p><p><b>METHODS</b>Peripheral blood samples were taken from patients with acute anterior myocardial infarction 6 hours and 7 days after PCI and stenting. Mononuclear cells (MNCs) were isolated by Ficoll-density centrifugation and cultured in M-199 medium. After 14 days culture, attaching cells incorporated DiI-acetylated low-density lipoprotein (EPCs) were collected and RNA was isolated by Trizol for microarray analysis on 24 genes associated with permissibility/vessel tone (angiotensin system: ACE, AGTR-1, AGTR-2; NO system: eNOS; prostacyclin system: COX-2; endothelin system: ET-1, ETA, ETB; superoxide anions system: SOD-1), angiogenesis (adhesion molecule: CDH5; growth factors and receptors: VEGFR1, VEGFR2, VEGF) and endothelial cell activation (adhesion molecules expression: ICAM1, ICAM2, ICAM3, PECAM-1, E-Selectin, L-Selection, VCAM1; change phenotype from antithrombotic to prothrombotic: tPA, uPA, PAI, vWF). VEGFR2, PECAM-1 and VE-cadherin positive cells were identified by flow cytometry.</p><p><b>RESULT</b>Eight gene expressions (AGTR-1, AGTR-2, COX-2, eNOS, ET-1, ETA, VEGF) were significantly downregulated 7 days post PCI compared to pre-PCI (P < 0.05). Flow cytometry results showed that VEGFR2 positive cells were also significantly reduced post PCI than that of before PCI (P < 0.05).</p><p><b>CONCLUSION</b>PCI down-regulated endothelial progenitor cells related gene expressions in patients with acute myocardial infarction.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Centrifugation, Density Gradient , Endothelial Cells , Cell Biology , Endothelium, Vascular , Cell Biology , Gene Expression , Myocardial Infarction , Metabolism , Therapeutics , Myocardial Reperfusion , Myocardial Revascularization , Oligonucleotide Array Sequence Analysis , Receptor, Angiotensin, Type 1 , Genetics , Receptor, Endothelin A , Genetics , Stem Cells , Cell Biology , Superoxide Dismutase , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To study the blood pressure (BP) changes in the liver transplant recipients.</p><p><b>METHODS</b>A total of 206 patients without preoperation hypertension received liver transplantation in our hospital from February 2001 to July 2005. The BP level and serum immunosuppressant concentration at preoperation and various time points post operation were determined.</p><p><b>RESULTS</b>Compared with the preoperation, the average systolic and diastolic pressure was significantly increased at the 2 week, 1, 2, 4 and 6 months post operation. The mobility of hypertension increased significantly after liver transplantation, with the highest mobility (46.49%) at the 1st month post operation. There was no linear correlation between the immunosuppressant (FK506) concentration and the BP level at any time point.</p><p><b>CONCLUSION</b>There was a high hypertension incidence after liver transplantation. Although the use of immunosuppressive drugs accompanied with the BP increase, there was no linear correlation between the immunosuppressant concentration and the BP level post operation.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Blood Pressure , Follow-Up Studies , Hypertension , Immunosuppressive Agents , Liver Transplantation , Postoperative Complications , Retrospective StudiesABSTRACT
Background Granulocyte colony-stimulating factor(G-CSF)has been reported to have beneficial effect on cardiac dysfunction in post infarction and doxorubicin-induced cardiomyopathy.Objective To investigate the effects of G-CSF on cardiac remodeling in cardiac hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ).Methods Thirty-six male wild type mice(WT)were allocated randomly to receive subcutaneously G-CSF(10 ?g/kg per day, n=9),or Ang Ⅱ(2.88 mg/kg per day,n=9),or Ang Ⅱ plus G-CSF(Ang Ⅱ 2.88 mg/kg+G-CSF 10 ?g/kg,n =9)for 4 weeks with untreated WT(n=9)as controls.Blood pressure and cardiac function were measured. Heart weight/body weight ratio,myocyte cross-sectional area and fibrosis area were determined.The mRNA ex- pression of osteopontin(OPN)in myocardium was detected by RT-PCR.The expressions of angiotensin converting enzyme(ACE),ACE2 and phosph-p70S6 kinase protein in myocardium were assessed by Western-Blot.Results Ang Ⅱ significantly elevated blood pressure(SBP,Ang Ⅱ:139.7?1.6 vs WT:108.7?2.3 mmHg,P0.05),but significantly attenuated the myocyte cross-sectional area(Ang Ⅱ+G-CSF:181.06?0.11 vs Ang Ⅱ:202.02?0.16 ?m~2,P
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Objective To explore the biphasic effects of simvastatin on vascular smooth muscle cells(VSMCs),which were regulated by sterol regulatory element binding proteins(SREBPs).Methods①Rat primary VSMCs were cultured,the effects of different concentrations of simvastatin on proliferation and migration of VSMCs were observed,and the expression of SREBP-1 and SREBP-2 mRNA on VSMCs was detected.②Rat models of atherosclerosis were established,and were divided into atherosclerotic injured group(n =6),low concentration simvastatin group(n=6) and high concentration simvastatin group(n=6).Besides,normal control group(sham operation group,n=8) was established.Intragastric administration of simvastation of 0.5 mg?kg~(-1)?d~(-1) and 2.5 mg?kg~(-1)?d~(-1) was conducted in low concentration simvastatin group and high concentration simvastation group,respectively,while those in normal control group and atherosclerotic injured group were given same amount of normal saline.Rats were sacrificed 4 weeks later.Plasma lipid levels were examined by enzymic method,ratios of intima/(intima+tunica media) of thoracic aorta and left common carotid artery were determined,and the expression of SREBP-1 and SREBP-2 mRNA on blood vessels was detected by RT-PCR.Results Simvastatin didn't show biphasic effects on the proliferation and migration of VSMCs.Low concentration simvastatin didn't promote the proliferation and migration of VSMCs,while high concentration simvastatin showed inhibition effect on the proliferation and migration of VSMCs,which was dose-dependent and independent of lipid regulation effect by simvastatin. Simvastatin could activate the expression of SREBP-1 and SREBP-2 mRNA of VSMCs.Moreover,high concentration simvastatin could significantly activate the expression of SREBP-1 and SREBP-2 mRNA.Conclusion Simvastatin can inhibit the proliferation and migration of VSMCs by activating SREBPs.
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<p><b>OBJECTIVE</b>To study the role of baseline risk factors in predicting the onset of diabetes among essential hypertensive patients with metabolic syndrome (MS) and to evaluate an ideal therapeutic regime that could reduce the risk factors and risk of onset of diabetes.</p><p><b>METHODS</b>A randomized parallel clinical trial in essential hypertensive patients of grade 1 or 2 was conducted. Two of the three components (1) increased waist circumference and/or BMI; (2) increased triglycerides (TG) and/or decreased high-density lipoprotein cholesterol; (3) impaired glucose tolerance (IGT) were present define the MS. The three intervention therapy groups were: indapamide + fosinopril (I + F, n = 151); atenolol + nitrendipine (A + N, n = 160); atenolol + nitrendipine + metformin (A + N + M, n = 152). Each case was followed-up monthly and the dosage of medicine taken be adjusted according to their BP level. The plasma glucose during fasting and two hours after taking 75 g glucose orally was also measured every six months. The new onset of diabetes was diagnosed according to the criteria. OGTT, insulin release test, lipid analysis, body weight and waist circumference were measured again at the last follow-up.</p><p><b>RESULTS</b>(1) The lowering of BP was similar among the three groups (P > 0.05). 23 new diabetes onsets occurred, being 10 in group I + F and 8 in group A + N and 5 in group A + N + M, respectively (P > 0.05); (2) Proportions of patients' risk factors decreased significantly in group A + N or A + N + M, e.g. the proportions of high TG in each group reduced by 14.7% and 9.3% respectively (P < 0.05), the central fat distribution reduced by 16.7% and 15.9% respectively (P < 0.05) and the IGT reduced by 6.6% and 29.6% respectively (P < 0.05). However no changes were found in group I + F; (3) After 1 year and 5 months' follow-up, the proportions of main risk factors (high TG, central fat distribution and IGT) in the three groups were 91%, 96%, 83% and 90%, 88%, 47%, respectively. The difference of IGT was significant between two groups (P < 0.01) and the proportions of having three risk factors were 70% and 31% in the two groups (P < 0.01); (4) I + F group was better than A + N group in reduction of TG and central fat distribution. And A + N + M group improved in all risk factors.</p><p><b>CONCLUSIONS</b>IGT alone or combined with increased TG plus abdominal obesity are the most important risk factors in predicting a new onset of diabetes among essential hypertensive patients with MS. Metformin in combination with atenolol plus nitrendipine can significantly prevent the onset of diabetes as well as improve patients' metabolic abnormality.</p>