3DPhenoFish: Application for two- and three-dimensional fish morphological phenotype extraction from point cloud analysis.

Fish morphological phenotypes are important resources in artificial breeding, functional gene mapping, and population-based studies in aquaculture and ecology. Traditional morphological measurement of phenotypes is rather expensive in terms of time and labor. More importantly, manual measurement is highly dependent on operational experience, which can lead to subjective phenotyping results. Here, we developed 3DPhenoFish software to extract fish morphological phenotypes from three-dimensional (3D) point cloud data. Algorithms for background elimination, coordinate normalization, image segmentation, key point recognition, and phenotype extraction were developed and integrated into an intuitive user interface. Furthermore, 18 key points and traditional 2D morphological traits, along with 3D phenotypes, including area and volume, can be automatically obtained in a visualized manner. Intuitive fine-tuning of key points and customized definitions of phenotypes are also allowed in the software. Using 3DPhenoFish, we performed high-throughput phenotyping for four endemic Schizothoracinae species, including Schizopygopsis younghusbandi, Oxygymnocypris stewartii, Ptychobarbus dipogon, and Schizothorax oconnori. Results indicated that the morphological phenotypes from 3DPhenoFish exhibited high linear correlation (>0.94) with manual measurements and offered informative traits to discriminate samples of different species and even for different populations of the same species. In summary, we developed an efficient, accurate, and customizable tool, 3DPhenoFish, to extract morphological phenotypes from point cloud data, which should help overcome traditional challenges in manual measurements. 3DPhenoFish can be used for research on morphological phenotypes in fish, including functional gene mapping, artificial selection, and conservation studies. 3DPhenoFish is an open-source software and can be downloaded for free at https://github.com/lyh24k/3DPhenoFish/tree/master.

Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart.

OBJECTIVE: To investigate the antioxidative effect and mechanism of luteolin on rat cardiomyocytes and isolated hearts followed by simulated ischemia/reperfusion (SI/R) injury. METHODS: The left ventricular cardiomyocytes and the isolated hearts from adult rats were subjected to SI/R injury. The experiment groups included control, SI/R, luteolin + SI/R (Lut + SI/R), vitamin E (Vit E) + SI/R, and LY294002 + luteolin + SI/R (LY + Lut + SI/R) groups. Cell viability, shortening amplitude, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity, the production of reactive oxygen species (ROS) and malondialdehyde (MDA), expression levels of Akt, phosphorylated Akt, NOX2 (gp91phox), NOX2 mRNA, mitogen-activated protein kinase (p38 MAPK) and phosphorylated p38MAPK were all measured after 3-h simulated ischemia and 2-h simulated reperfusion procedure in cardiomyocytes. Vit E was used as a standard control. The contractile function of isolated hearts was further observed after they were subjected to 30-min global ischemia and 120-min reperfusion. RESULTS: Pretreatment with 8-µmol/L luteolin substantially increased cell viability and shortening amplitude, while reducing evidence of oxidative stress-induced damage in the cells. In addition, the expression of NOX2, NOX2 mRNA and phosphorylation of p38MAPK were all downregulated. Furthermore, pretreatment with 40-µmol/L luteolin improved the recovery of myocardial contractile function following SI/R-induced injury, and luteolin markedly increased phosphorylation of Akt. However, all of the above effects were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002. CONCLUSIONS: Luteolin prevents SI/R-induced myocardial damage by reducing oxidative stress-induced injury in isolated rat hearts and cardiomyocytes, and the cardioprotection induced by luteolin was partially mediated by the PI3K/Akt pathway.

Luteolin Attenuates Foam Cell Formation and Apoptosis in Ox-LDL-Stimulated Macrophages by Enhancing Autophagy.

BACKGROUND: Our previous studies demonstrated that luteolin, which is rich in flavones, has various biological properties and can exert anti-oxidant, anti-inflammatory and anti-apoptotic activities. However, its effect on ox-LDL-induced macrophage lipid accumulation and apoptosis has not been revealed. AIMS: This study aimed to explore the role of luteolin in ox-LDL-induced macrophage-derived foam cell formation and apoptosis and to delineate the underlying mechanism. METHODS: Murine RAW264.7 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) (50 µg/ml) for 24 h and then pretreated with 25 µM luteolin for another 24 h. The effects of luteolin on lipid accumulation in RAW264.7 cells induced by ox-LDL were assayed using Oil red O staining and high performance liquid chromatography (HPLC). Apoptosis was confirmed by acridine orange/ethidium bromide (AO/EB) staining, flow cytometric analysis and the TUNEL assay. Immunofluorescence, Western blot and monodansylcadaverine (MDC) staining analyses were then used to further investigate the molecular mechanisms by which luteolin protects macrophages from ox-LDL-induced foam cell formation and apoptosis. 3-Methyladenine (3-MA), an autophagy inhibitor, was used as a positive control. RESULTS: Treatment with 25 µM luteolin not only significantly attenuated ox-LDL-induced macrophage lipid accumulation but also decreased the apoptotic rate of RAW264.7 cells, the number of TUNEL-positive macrophages and the expression of Bax, Bak, cleaved caspase-9 and cleaved caspase-3. In addition, luteolin pretreatment significantly increased autophagosome formation and Beclin-1 activity, thus increasing the ratio of LC3-II/LC3-I. Moreover, these effects were abolished by 3-MA. CONCLUSIONS: Taken together, these results highlight that luteolin treatment attenuates foam cell formation and macrophage apoptosis by promoting autophagy and provide new insights into the molecular mechanism of luteolin and its therapeutic potential in the treatment of atherosclerosis.

Coronary Plaque Characteristics Affect No-Reflow During Primary Percutaneous Coronary Intervention: A Pooled Analysis of 14 Observational Studies Using Intravascular Ultrasound.

The association between coronary plaque composition and no-reflow during percutaneous coronary intervention (PCI) is still debated. We performed a systematic literature search using MEDLINE, Embase, Cochrane, and Ovid databases for intravascular ultrasound (IVUS) studies evaluating the relationship between coronary plaque characteristics and no-reflow after PCI. Fourteen observational trials were included in the meta-analysis, including 1457 patients (237 in the no-reflow group, 1220 in the normal reflow group). Pooled analysis indicated that the no-reflow group had a significantly higher absolute volume of fibrofatty plaque (weighted mean differences [WMD], 4.94 mm(3); 95% confidence interval [CI], 1.83-l8.06; P = .002), external elastic membrane cross-sectional area (EEM-CSA) (WMD, 3.40 mm2; 95% CI, 2.22-4.58; P = .00001), plaque area (WMD, 4.06 mm(2); 95% CI, 2.24-5.89; P = .0001), and artery remodeling index (WMD, 0.09; 95% CI, 0.06-0.13; P = .00001), and a smaller percentage of fibrous plaque (WMD, -5.89 %; 95% CI, -0.66 to -11.12; P = .03) than in the normal reflow group. There were no significant differences in the other plaque components between the two groups. This meta-analysis confirmed that high absolute volume of fibrofatty plaque, EEM-CSA, plaque area, and coronary artery remodeling index, and a decreased percentage of fibrous plaque as detected by IVUS in culprit lesions, are linked with the development of the no-reflow phenomenon after PCI.

Detection of Vulnerable Atherosclerotic Plaques in Experimental Atherosclerosis with the USPIO-Enhanced MRI.

This study's goal was to assess the diagnostic value of the USPIO-(ultra-small superparamagnetic iron oxide) enhanced magnetic resonance imaging (MRI) in detection of vulnerable atherosclerotic plaques in abdominal aorta in experimental atherosclerosis. Thirty New Zealand rabbits were randomly divided into two groups, Group A and Group B. Each group comprised 15 animals which were fed with high cholesterol diet for 8 weeks and then subjected to balloon-induced endothelial injury of the abdominal aorta. After another 8 weeks, animals in Group B received adenovirus carrying p53 gene that was injected through a catheter into the aortic segments rich in plaques. Two weeks later, all rabbits were challenged with the injection of Chinese Russell's viper venom and histamine. Pre-contrast images and USPIO-enhanced MRI images were obtained after pharmacological triggering with injection of USPIO for 5 days. Blood specimens were taken for biochemical and serological tests at 0 and 18 weeks. Abdominal aorta was histologically studied. The levels of serum ICAM-1 and VCAM-1 were quantified by ELISA. Vulnerable plaques appeared as a local hypo-intense signal on the USPIO-enhanced MRI, especially on T2*-weighted sequences. The signal strength of plaques reached the peak at 96 h. Lipid levels were significantly (p < 0.05) higher in both Group A and B compared with the levels before the high cholesterol diet. The ICAM-1 and VCAM-1 levels were significantly (p < 0.05) higher in Group B compared with Group A. The USPIO-enhanced MRI efficiently identifies vulnerable plaques due to accumulation of USPIO within macrophages in abdominal aorta plaques.

Prevention of contrast-induced nephropathy with prostaglandin E1 in high-risk patients undergoing percutaneous coronary intervention.

PURPOSE: Contrast-induced nephropathy (CIN) is an important complication in the use of iodinated contrast media. The present study aimed to assess the safety and efficacy of prostaglandin E1 (PGE1) in prevention of CIN in patients with high-risk factors undergoing percutaneous coronary intervention (PCI). METHODS: The study group consisted of 163 patients who had undergone a coronary intervention procedure between January 1, 2012 and October 31, 2012. Study participants were randomly assigned to either the PGE1 group (82 patients) or the control group (81 patients). Patients in the PGE1 group received PGE1 intravenous infusion of 20 ng/kg/min for 6 h before and after the administration of contrast media. The control group received 0.9 % sodium chloride solution for routine hydration only. A nonionic, low-osmolality contrast agent was used in our laboratory at this time. Serum creatinine (Scr) values and estimated glomerular filtration rate were measured before and within 48 h of the administration of contrast agents. CIN was defined as an increase of ≥0.5 mg/dL or ≥ a 25 % increase in Scr concentrations over baseline within 48 h of angiography. RESULTS: The amount of contrast agent administered was similar for the PGE1 and control groups (156 ± 63 vs. 161 ± 68 mL, P > 0.05). The incidence of CIN was lower in the PGE1 group than in the control group (3.7 vs. 11.1 %, P < 0.05). No serious adverse effects were observed. CONCLUSIONS: In patients with high-risk factors undergoing PCI, the use of PGE1 for prevention of CIN is safe and efficacious.

A meta-analysis of the risk of total cardiovascular events of isosmolar iodixanol compared with low-osmolar contrast media.

BACKGROUND: The iso-osmolar contrast agent iodixanol may be associated with a lower incidence of cardiac events than low-osmolar contrast media (LOCM), but previous trials have yielded mixed results. OBJECTIVE: To compare the risk of total cardiovascular events of the iso-osmolar contrast medium, iodixanol, to LOCM. METHODS: Medical literature databases were searched to identify comparisons between iodixanol and LOCM with cardiovascular events as a primary endpoint. A random-effects model was used to obtain pooled odds ratio (OR) for within-hospital and 30-day events. RESULTS: A total of 2 prospective cross-sectional studies and 11 randomized controlled trials (RCTs) (covering 6859 subjects) met our criteria. There was no significant difference in the incidence of within-hospital and 30-day cardiovascular events when iodixanol was compared with LOCM, with pooled OR of 0.72 (95%CI 0.49-1.06, p=0.09) and 1.19 (95%CI 0.70-2.02, p=0.53), respectively. Subgroup analysis showed no relative difference when iodixanol was compared with ioxaglate (OR=0.92, 95%CI 0.50-1.70, p=0.80) and iohexol (OR=0.75, 95%CI 0.48-1.17, p=0.21). However, a reduction in the within-hospital cardiovascular events was observed when iodixanol was compared with LOCM in the RCT subgroup (OR=0.65, 95%CI 0.44-0.96, p=0.03). Sensitivity analyses revealed that three studies had a strong impact on the association of within-hospital cardiovascular events between iodixanol and LOCM. Meta-regression analysis failed to account for heterogeneity. No publication bias was detected. CONCLUSIONS: This meta-analysis demonstrates that there is no conclusive evidence that iodixanol is superior to LOCM overall with regard to fewer cardiovascular events.

The value of quantitative real-time myocardial contrast echocardiography for detection of angiographically significant coronary artery disease.

BACKGROUND: Real-time (RT) myocardial contrast echocardiography (MCE) is a novel method for the assessment of regional myocardial perfusion. We sought to evaluate the feasibility and diagnostic accuracy of quantitative RT-MCE in predicting significant coronary stenosis, with reference to quantitative coronary angiography. HYPOTHESIS: RT-MCE can identify anatomically significant coronary artery stenosis in selected patients. RT-MCE is probably an effective method for detection of angiographically significant coronary artery stenosis. METHODS: Thirty-five patients (mean age, 59.94 ± 10.63 years; 25 males) scheduled for coronary angiography underwent RT-MCE at rest, and shortly afterward underwent gated single-photon emission computed tomography (gated-SPECT). Coronary angiography was performed within 1 week after RT-MCE in all patients. The observing indexes included the images of RT-MCE that were analyzed quantitatively from microbubble replenishment curves for myocardial perfusion by using the Q-Lab software. The sensitivity and specificity of RT-MCE for quantitative detection of coronary artery disease (CAD) were obtained. The receiver operator characteristic (ROC) curves were used to assess the differences of accuracy in ischemic segments with A, ß and A × ß respectively. The sensitivity and specificity of gated-SPECT and RT-MCE for assessment of CAD were calculated using a 4-score method. RESULTS: A total of 513 segments among 595 segments in 35 patients were obtained. The cutoffs for A, ß and A × ß were 4.58, 0.64, and 2.73, and the sensitivity and specificity of quantitative RT-MCE for detection of CAD were 86.0%, 80.2%, 88.9%, and 84.1%, 64.6%, 79.9%, respectively. Meanwhile, the sensitivity and specificity of semiquantitative analysis for assessment of CAD were 66.7% and 61.8%. The ROC curve area of A and A × ß was 0.91 and 0.90 in the middle segments. The ROC area of A was 0.52 in the base segments. The sensitivity and specificity of gated-SPECT for assessment of CAD were 84.8% and 82.7%, respectively. The sensitivity of multi-indexes RT-MCE increased. The sensitivity was 89.1%, 90.4%, and 96.3% by A + ß, A + A × ß, and ß + A × ß. CONCLUSIONS: Quantitative RT-MCE is an effective method for the detection of coronary artery stenosis. Quantitative RT-MCE is segmented for assessment to ischemic myocardium. RT-MCE with multi-indexes has a valuable application for assessment of CAD surpassing SPECT.

Impact of anemia on contrast-induced nephropathy (CIN) in patients undergoing percutaneous coronary interventions.

BACKGROUND: The aim of the present study was to assess the influence of anemia on the risk of developing contrast-induced nephropathy after percutaneous coronary angioplasty. METHODS: Serum creatinine values were measured before and within 48 h after the administration of contrast agents. Contrast-induced nephropathy (CIN) was defined as an increase of ≥ 0.5 mg/dl or ≥ 25 % in serum creatinine concentration over baseline within 48 h after administration. Anemia was defined as hemoglobin <120 g/l in women and <130 g/l in men. RESULTS: Among the 1,026 patients studied, 32 (3.1 %) developed CIN after procedure. CIN occurred in 6.3 % of the anemic patients and in 2.2 % of the non-anemic patients (P < 0.01). The incidence of CIN increased with decreasing of baseline estimated glomerular filtration rate (eGFR) in both the anemia and non-anemia groups. In patients with baseline eGFR <30 ml/min, a high proportion of both anemic and non-anemic patients experienced CIN (24.6 vs. 17.5 %). When baseline eGFR was 30-59 ml/min, the incidence of CIN in anemic patients was twofold higher than in non-anemic patients (7.9 vs. 3.8 %; P < 0.05). Multivariate logistic regression analysis found that baseline eGFR and baseline hemoglobin were independent predictors of CIN. CONCLUSION: Anemia is associated with a higher incidence of CIN in patients with moderate renal dysfunction. Patients with both preexisting renal insufficiency and anemia are at high risk of CIN. Baseline eGFR and baseline hemoglobin are independent predictors of CIN.

[Efficacy and safety of aranidipine in Chinese patients with mild-to-moderate essential hypertension].

OBJECTIVE: To assess the efficacy and safety of aranidipine versus retard-released felodipine in Chinese patients with mild-to-moderate essential hypertension. METHODS: This was a multicenter, randomized, double-blind, placebo and active antihypertensive drug parallel-controlled study. After 2 weeks of placebo run-in period, 315 patients at 6 centers with diastolic blood pressure (DBP) between 95 to 109 mm Hg (1 mm Hg = 0.133 kPa) while systolic blood pressure (SBP) below 180 mm Hg were randomized to receive aranidipine 5-20 mg/d (n = 126) or retard-released felodipine 5-10 mg/d (n = 126) for 12 weeks. Others (n = 63) received placebo for 4 weeks. Their blood pressures were evaluated at baseline and the end of Weeks 4, 8 and 12. RESULTS: After a 12-week treatment, SBP decreased from 148.8 ± 10.7 mm Hg to (132.8 ± 11.2) mm Hg while DBP dropped from ( 98.4 ± 2.8) mm Hg to (83.9 ± 7.5) mm Hg. There were significant differences with the baseline values (P < 0.0001). After a 4-week treatment, the reductions of SBP in aranidipine and retard-released felodipine groups were (12.1 ± 11.0) mm Hg and (12.2 ± 11.2) mm Hg while the reductions of DBP in two groups (11.8 ± 6.9) mm Hg and (12.1 ± 7.9) mm Hg respectively. The reductions of SBP and DBP in two groups were (2.3 ± 8.4) mm Hg and (4.0 ± 5.1) mm Hg and they were significantly superior to that in placebo group (P < 0.0001). But no significant difference existed between aranidipine and retard-released felodipine groups. Also no significant differences were found between these two antihypertensive therapy groups at the end of Weeks 4, 8 and 12 in the reduction of blood pressure, total response rate and blood pressure control rate. But 20 mg daily aranidipine was significantly superior to 10 mg daily retard-released felodipine in the control rates of SBP and DBP. Adverse events occurred at 24.22% and 29.92% in aranidipine and retard-released felodipine groups respectively (P = 0.305). CONCLUSION: Administration of aranidipine 5-20 mg/d can effectively control blood pressure and is not inferior to retard-released felodipine 5-10 mg/d. The efficacy of 20 mg/d aranidipine is superior to that of retard-released felodipine 5-10 mg/d. And the effectiveness and safety of aranidipine are similar to those of retard-released felodipine.

Real-time three-dimensional echocardiographic evaluation of left ventricular systolic synchronicity in patients with chronic heart failure: comparison with tissue Doppler imaging.

BACKGROUND: To investigate the clinical value of real-time three-dimensional echocardiography (RT-3DE) for assessing of left ventricular systolic synchronicity. METHODS: Thirty healthy volunteers and 62 patients with congestive heart failure (CHF) were enrolled. The SD of time to peak systolic motion (TDI-Ts12-SD) was measured with tissue Doppler imaging in 12 myocardial segments. The SD and maximal difference of the time to minimal systolic volume (Tmsv) between 16, 12, or 6 myocardial segments, expressed as a percentage of cardiac cycle duration, were measured with RT-3DE and labeled Tmsv16-SD%, Tmsv12-SD%, Tmsv6-SD%, Tmsv16-D%, Tmsv12-D%, and Tmsv6-D%, respectively. The Spearman coefficient and Kappa value were calculated, and Bland-Altman analysis was performed to investigate the correlation and agreement between the two methods. Tmsv values were compared with ejection fraction (EF). RESULTS: There was a moderately positive (p< 0.01) correlation between TDI-Ts12-SD and Tmsv16-SD%, Tmsv12-SD%, Tmsv16-D%, and Tmsv12-D% (r = 0.65, 0.64, and 0.65, respectively, with Kappa values of 0.66, 0.65, 0.72, and 0.74, respectively, p< 0.01). Tmsv16-SD%, Tmsv12-SD%, and Tmsv12-D% were significantly different between CHF patients with EF ≤ 35% and those with EF > 35%. CONCLUSIONS: RT-3DE can be used in patients with CHF to quantify left ventricular mechanical dyssynchrony. Tmsv12-SD% and Tmsv12-D% were the best indices of left ventricular systolic synchronicity in relation to the severity of CHF as evaluated from EF.

Clinical usefulness of low-dose dobutamine stress real-time myocardial contrast echocardiography for detection of viable myocardium.

OBJECTIVES: To evaluate and compare the diagnostic accuracy of semi-quantitative and quantitative real-time myocardial contrast echocardiography (RT-MCE) with low-dose dobutamine stress echocardiography (LD-DSE) in detecting viable myocardium. METHODS: Thirty in-patients with coronary artery disease and regional wall motion abnormalities underwent RT-MCE without and with LD-DSE. Percutaneous coronary intervention was performed within 1 week after RT-MCE in all patients. Myocardial perfusion was evaluated from A, ß, and A × ß indices from microbubble replenishment curves. The motion of each myocardium segment was observed by routine echocardiography 1, 3, and 6 months after percutaneous coronary intervention and its improvement over time was the criterion of viable myocardium. RESULTS: RT-MCE sensitivity and specificity for the assessment of viable myocardium were 71.7% and 69.8%, rising to 81.3% and 76.7% (p < 0.05) when combined with LD-DSE. Using quantitative RT-MCE with cutoff values of A, ß, and A × ß, the sensitivity and specificity were 75.6%, 78.8%, 82.1%, and 82.4%, 77.9%, 78.6%, respectively. When combined with LD-DSE, the sensitivity and specificity were 86.0%, 83.2%; 88.9% and 84.1%; 89.6%, 79.9%, respectively. CONCLUSIONS: Quantitative RT-MCE analysis yielded higher sensitivity and specificity than semi-quantitative RT-MCE with or without LD-DSE for the detection of viable myocardium.

Salvianolic acid A inhibits angiotensin II-induced proliferation of human umbilical vein endothelial cells by attenuating the production of ROS.

AIM: To investigate the action of salvianolic acid A (SalA) on angiotensin II (Ang II)-induced proliferation of human umbilical vein endothelial cells (HUVECs) and the possible signaling pathways mediating this action. METHODS: Cell proliferation was examined with MTT assay. The expression levels of Src phosphorylation (phospho-Src), Akt phosphorylation (phospho-Akt), and NADPH oxidase 4 (Nox4) in HUVECs were determined by Western blot. The production of reactive oxygen species (ROS) was estimated using fluorescence-activated cell sorting (FACS). RESULTS: SalA (6.25-50 µmol/L) did not affect the viability of HUVECs. Treatment of HUVECs with Ang II (1 µmol/L) markedly increased the cell viability; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) prevented Ang II-induced increase of the cell viability in a concentration-dependent manner. Treatment of HUVECs with Ang II (1 µmol/L) markedly up-regulated the protein expression levels of phospho-Src, phospho-Akt (473) and Nox4; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) blocked all the effects in a concentration-dependent manner. Treatment of HUVECs with Ang II (1 µmol/L) dramatically increased ROS production in HUVECs; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) blocked the ROS production in a concentration-dependent manner. CONCLUSION: SalA inhibits Ang II-induced proliferation of HUVECs via reducing the expression levels of phospho-Src and phospho-Akt (473), thereby attenuating the production of ROS.

[Clinical significance of matrix metalloproteinase-9 and tissue factors secreted by cultured monocyte-derived macrophage of patients with coronary heart disease in vitro and the intervenient effect of puerarin on them].

OBJECTIVE: To investigate the clinical significance of matrix metalloproteinase-9 (MMP-9) and tissue factor (TF) secreted by cultured monocyte-derived macrophages (HMDM) from patients with coronary heart disease (CHD) in vitro, and to evaluate the intervenient effect of puerarin (Pur) on them. METHODS: A total of 40 patients were enrolled, including 12 patients with acute myocardial infarction (AMI), 16 patients with unstable angina pectoris (UAP), 12 patients with stable angina pectoris (SAP). Besides, 8 healthy subjects with normal coronary arteriograph were set as controls. Monocytes acquired from their peripheral blood were incubated for 48 h and induced to differentiate into macrophages by phorbolester 12-myristate 13-acetate (PMA), the contents of MMP-9 and TF in supernatant were assayed, and the relationship of them with patients' age, risk factors of CHD and coronary artery lesion scores were analyzed. HMDMs randomly from selected 12 patients with acute coronary syndrome (ACS) were arranged for observing the intervenient effects of different concentrations of Pur on the levels and activity of MMP-9 and TF. RESULTS: The levels of MMP-9 and TF in UAP and AMI patients were significantly higher than those in SAP patients and healthy subjects (P < 0.01), but no statistical correlation was found between levels of MMP-9 and TF with different CHD risk factors, as well as patients' age and coronary artery lesion scores. The levels and activity of MMP-9 and TF in the 12 ACS patients were significantly decreased in a dose-dependent manner after Pur intervention when compared with the controt group. CONCLUSION: The levels of MMP-9 and TF secreted in vitro by HMDM from CHD patients could be taken as indexes for evaluating patient's condition of ACS. Pur can inhibit the expression and the activity of MMP-9 and TF secreted by HMDM, stabilize the plaque and improve the vulnerability of blood to certain extent.

[Study on the relationship between compositions of hyperuricemia and metabolic syndrome].

OBJECTIVE: To study the relationship between compositions of hyperuricemia and metabolic syndrome among residents aged > or =20 years. METHODS: A stratified cluster sampling was conducted with 7887 dwellers recruited and examinaed. Blood samples were then collected for serum detection. Available data was analyzed using SPSS 13.0. RESULTS: The incidence rates of obesity, hypertension and hyperglycemia for hyperuricemia were 53.4% with OR = 2.568 (95% CI: 2.103-3.137), 38.8% with OR= 2.157 (95% CI: 1.856-2.508) and 21.9% with OR = 1.850 (95% CI: 1.552-2.205) respectively. Along with the increase of uric acid, body mass index changed the most followed by triglyceridemia. The change of hyperglycemia for men and cholesterol for women were not prominent. Conclusion The relationship between compositions of hyperuricemia and metabolic syndrome was close, suggesting that hyperuricemia might serve as one of the compositions of metabolic syndrome and could contribute to the prevention and control of cardiovascular and cerebrovascular diseases.