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91.
Cardiovascular disease is the leading cause of death worldwide, with an especially devastating impact in low-to-medium income countries. Cardiovascular disease has been elevated to this position by a combination of factors that include urbanization and its attendant effects, such as obesity, a sedentary lifestyle, changes in dietary habits, and smoking. Given the enormous extent of the problem and the complexity of its causes, which include cultural, social, political, and health care factors, an equally sophisticated and comprehensive strategy is required to combat cardiovascular disease on a global scale. Because exposure to cardiovascular risk factors occurs from early ages, this strategy must be expanded and adjusted throughout the life of an individual. Thus, our efforts should be concentrated not only on cardiovascular disease treatment and prevention, but also on health promotion and primordial prevention. In this review, we present different strategies yielding encouraging results at the population level, from childhood until old age, that aim to protect against the challenges facing the scientific community when combating cardiovascular disease.  相似文献   
92.
本实验用连续测定法观察了细菌的生长率的变化,结果表明:三株卟啉菌在3d的生长率基本相似,均以指数方式生长,其中PgW50在以后的几天中仍基本保持平衡,Pg381在5~6d后开始呈下降趋势,而Pe在3~4d到达顶点后,即开始呈下降趋势。SDS-PAGE显示:ECV的泳带要比同菌OMPC的泳带多,且大多集中在20KD到100KD之间.各带的含量(峰高)亦不相同。  相似文献   
93.
目的探讨痂囊腔菌素A光动力学疗法(EA-PDT)对ECV304细胞的杀伤效应,并与竹红菌乙素光动力学疗法(HB-PDT)进行比较。方法以不同浓度的痂囊腔菌素A(elsinochromeA,EA)及竹红菌乙素(hypocrellinB,HB)分别孵育人脐静脉血管内皮ECV304细胞4h,然后分别用波长532nmKTP激光,以20mW/cm2功率密度照射1000s。照光后置于37℃、5%CO2的孵育箱中继续孵育24h后,用MTT法分别测定不同浓度下的细胞存活率,绘制杀伤曲线并拟合曲线方程,根据方程求出不同光敏剂对细胞的半数杀伤浓度(IC50)。结果EA-PDT和HB-PDT对ECV304细胞的IC50分别为50·97ng/ml和85·20ng/ml,二者比较差异有统计学意义(P<0·05),EA-PDT对ECV304细胞有较强的杀伤效应。结论EA-PDT对ECV304细胞株的杀伤效应强于HB-PDT,在血管性病变治疗方面可能有广阔的应用前景。  相似文献   
94.
碱性成纤维细胞成长因子对ECV304细胞迁移的影响   总被引:3,自引:0,他引:3  
目的:观察不同浓度的碱性成纤维细胞生长因子(bFGF)对体外培养中划痕损伤后ECV304细胞迁移的影响。方法: 在体外细胞划痕损伤模型中应用显微电视电脑图像处理系统定量测定不同浓度(0、5、10、15 μg/L)bFGF引起的ECV304细胞迁移的变化,用光镜与扫描电镜观察bFGF引起的迁移细胞的形态变化。结果: 与不加bFGF的对照组比较,低浓度(5 μg/L)时bFGF对ECV304细胞的迁移呈促进作用;高浓度时(15 μg/L)呈抑制作用。迁移细胞表面有众多丝状伪足。结论: bFGF对体外培养的ECV304细胞的迁移有双相调节作用,低浓度时(5 μg/L)促进细胞迁移,高浓度时(15 μg/L)抑制细胞迁移。迁移细胞表面伪足丰富,以丝状伪足为主。  相似文献   
95.
目的 检测内皮细胞中与低密度脂蛋白氧化可能相关的信号传导相关蛋白基因,期望获得阐明氧化机制的有价值的线索.方法 利用低密度脂蛋白作用人血管内皮细胞系ECV304,通过基因芯片分析人信号传导相关蛋白的表达谱.结果 在被检测的1 990个基因中,52个基因的表达变化超过了2倍以上,其中23个基因表达增加,29个基因表达减少.在表达发生改变的基因中,有7个已在最新的报道中认为可能和动脉粥样硬化相关.结论 我们的发现可能给内皮细胞氧化低密度脂蛋白的机制的揭示提供全新的思路.  相似文献   
96.
目的 研究3种常见的非白色假丝酵母菌对人脐静脉内皮细胞株ECV304细胞增殖及细胞周期的影响。方法 制备热带假丝酵母菌、克鲁斯假丝酵母菌和光滑假丝酵母菌上清液并行倍比稀释,设1、4、16倍3个稀释度以及对照组。体外培养ECV304细胞,分别将3种非白色假丝酵母菌不同稀释度的上清液与ECV304细胞共培养,采用 MTT法测定培养24、48、72 h后的细胞增殖率;倒置显微镜观察培养48 h后细胞密度的变化;流式细胞术测定培养 48h后对ECV304细胞周期的影响。结果 培养24 h后,3种假丝酵母菌1倍稀释的上清液均可促进细胞增殖,4倍稀释的克鲁斯假丝酵母菌也可促进细胞增殖(P<0.05);培养48、72 h后,克鲁斯假丝酵母菌和光滑假丝酵母菌上清液仍可促进ECV304细胞增殖,而热带假丝酵母菌上清液无论稀释度高低均不能促进ECV304细胞增殖。培养48 h后,克鲁斯假丝酵母菌和光滑假丝酵母菌上清液组的细胞密度明显增高,同时其G/G1期细胞所占比例降低,细胞增殖指数(P)升高(P<0.05);而热带假丝酵母菌组的细胞密度和PI均无明显变化(P>0.05)。结论 克鲁斯假丝酵母菌和光滑假丝酵母菌的代谢产物对ECV304细胞的增殖有诱导作用,临床上应加强非白色假丝酵母菌感染的检测和治疗。  相似文献   
97.
周娟  杨予白  奥沛源  雷立权 《医学争鸣》2004,25(20):1843-1845
目的:观察脱氢表雄酮对内皮细胞NO合成、ET-1分泌及细胞表面ICAM-1表达的影响.方法:培养的人脐静脉内皮细胞系ECV304经不同浓度和不同作用时间DHEA处理后,采用硝酸还原酶及放免法分别测定培养液中NO及ET-1水平,用SABC免疫组化法观察细胞表面ICAM-1的表达.结果:与对照组相比,随着DHEA浓度的增加,培养液中NO的含量从(387±12)降至(242±11)μmol/L(P<0.05),而ET-1的浓度却从(397±13)增至(626±29)ng/L(P<0.05).随着时间的延长,各对照组培养液中NO含量均无明显变化(P>0.05),而DHEA组NO生成量却逐渐降低(P<0.05),呈时间依赖.培养液中ET-1浓度无论是对照组还是DHEA组均随时间的延长而升高(P<0.05),但DHEA组升高的更为明显.无论是增加浓度还是延长时间,DHEA均不影响细胞表面ICAM-1的表达.结论:DHEA可通过调节内皮细胞NO及ET-1生成量对血管功能进行调控.  相似文献   
98.

Background

Prognosis in light-chain (AL) and transthyretin (ATTR) amyloidosis is influenced by cardiac involvement. ATTR amyloidosis has better prognosis than AL amyloidosis despite more amyloid infiltration, suggesting additional mechanisms of damage in AL amyloidosis.

Objectives

The aim of the study was to assess the presence and prognostic significance of myocardial edema in patients with amyloidosis.

Methods

The study recruited 286 patients: 100 with systemic AL amyloidosis, 163 with cardiac ATTR amyloidosis, 12 with suspected cardiac ATTR amyloidosis (grade 1 on 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid), 11 asymptomatic individuals with amyloidogenic TTR gene mutations, and 30 healthy volunteers. All subjects underwent cardiovascular magnetic resonance with T1 and T2 mapping and 16 underwent endomyocardial biopsy.

Results

Myocardial T2 was increased in amyloidosis with the degree of elevation being highest in untreated AL patients (untreated AL amyloidosis 56.6 ± 5.1 ms; treated AL amyloidosis 53.6 ± 3.9 ms; ATTR amyloidosis 54.2 ± 4.1 ms; each p < 0.01 compared with control subjects: 48.9 ± 2.0 ms). Left ventricular (LV) mass and extracellular volume fraction were higher in ATTR amyloidosis compared with AL amyloidosis while LV ejection fraction was lower (p < 0.001). Histological evidence of edema was present in 87.5% of biopsy samples ranging from 5% to 40% myocardial involvement. Using Cox regression models, myocardial T2 predicted death in AL amyloidosis (hazard ratio: 1.48; 95% confidence interval: 1.20 to 1.82) and remained significant after adjusting for extracellular volume fraction and N-terminal pro–B-type natriuretic peptide (hazard ratio: 1.32; 95% confidence interval: 1.05 to 1.67).

Conclusions

Myocardial edema is present in cardiac amyloidosis by histology and cardiovascular magnetic resonance T2 mapping. T2 is higher in untreated AL amyloidosis compared with treated AL and ATTR amyloidosis, and is a predictor of prognosis in AL amyloidosis. This suggests mechanisms additional to amyloid infiltration contributing to mortality in amyloidosis.  相似文献   
99.

Objectives

The purpose of this study was to examine the histological correlation of native myocardial T1 and extracellular volume fraction (ECV) measurement at 3-T for the assessment of diffuse pathological changes in the myocardial tissue, including myocardial fibrosis and extracellular space in dilated cardiomyopathy (DCM).

Background

Cardiac magnetic resonance T1 techniques allow the quantification of diffuse myocardial fibrosis. However, there are no definitive head-to-head studies of native T1 versus ECV for the detection, quantification, and characterization of pathological changes in the myocardial tissue in DCM by using histological samples for confirmation.

Methods

A total of 36 subjects with DCM (31 men, mean age 56 ± 16 years) underwent pre- and post-contrast T1 mapping as well as late gadolinium enhancement (LGE) cardiac magnetic resonance at 3-T. Biopsy samples were used for the quantification of collagen volume fraction using picrosirius red staining and an extracellular space component from hematoxylin and eosin–stained myocardium.

Results

Nonischemic LGE was observed in 14 of 36 patients. Although patients with LGE had significantly greater biopsy-proven collagen volume fraction than those without LGE (21 ± 12% vs. 11 ± 8%; p < 0.01), there was substantial overlap of collagen volume fraction values between patients with and without LGE. Both native T1 value and ECV were similarly and significantly associated with biopsy-proven collagen volume fraction (r = 0.77 and r = 0.66, respectively; p < 0.05). Furthermore, ECV had a strong correlation with the biopsy-proven extracellular space component (r = 0.86), whereas native T1 had only a moderate correlation (r = 0.55). Interobserver and intraobserver reproducibility for native T1 and ECV were 0.89, 0.95, 0.96, and 0.98, respectively.

Conclusions

Native T1 exhibited comparable ability as ECV measurement in the detection and quantification of histological collagen volume fraction, with high reproducibility, and therefore diffuse myocardial fibrosis in DCM may be reliably assessed by native T1 mapping without the administration of gadolinium contrast agent. In addition, cardiac magnetic resonance–derived ECV showed excellent agreement with histological extracellular space.  相似文献   
100.

Objectives

The goal of this study was to demonstrate that cardiac magnetic resonance could reveal anthracycline-induced early tissue remodeling and its relation to cardiac dysfunction and left ventricular (LV) atrophy.

Background

Serum biomarkers of cardiac dysfunction, although elevated after chemotherapy, lack specificity for the mechanism of myocardial tissue alterations.

Methods

A total of 27 women with breast cancer (mean age 51.8 ± 8.9 years, mean body mass index 26.9 ± 3.6 kg/m2), underwent cardiac magnetic resonance before and up to 3 times after anthracycline therapy. Cardiac magnetic resonance variables were LV ejection fraction, normalized T2-weighted signal intensity for myocardial edema, extracellular volume (ECV), LV cardiomyocyte mass, intracellular water lifetime (τic; a marker of cardiomyocyte size), and late gadolinium enhancement.

Results

At baseline, patients had a relatively low (10-year) Framingham cardiovascular event risk (median 5%), normal LV ejection fractions (mean 69.4 ± 3.6%), and normal LV mass index (51.4 ± 8.0 g/m2), a mean ECV of 0.32 ± 0.038, mean τic of 169 ± 69 ms, and no late gadolinium enhancement. At 351 to 700 days after anthracycline therapy (240 mg/m2), mean LV ejection fraction had declined by 12% to 58 ± 6% (p < 0.001) and mean LV mass index by 19 g/m2 to 36 ± 6 g/m2 (p < 0.001), and mean ECV had increased by 0.037 to 0.36 ± 0.04 (p = 0.004), while mean τic had decreased by 62 ms to 119 ± 54 ms (p = 0.004). Myocardial edema peaked at about 146 to 231 days (p < 0.001). LV mass index was associated with τic (β = 4.1 ± 1.5 g/m2 per 100-ms increase in τic, p = 0.007) but not with ECV. Cardiac troponin T (mean 4.6 ± 1.4 pg/ml at baseline) increased significantly after anthracycline treatment (p < 0.001). Total LV cardiomyocyte mass, estimated as: (1 ? ECV) × LV mass, declined more rapidly after anthracycline therapy, with peak cardiac troponin T >10 pg/ml. There was no evidence for any significant interaction between 10-year cardiovascular event risk and the effect of anthracycline therapy.

Conclusions

A decrease in LV mass after anthracycline therapy may result from cardiomyocyte atrophy, demonstrating that mechanisms other than interstitial fibrosis and edema can raise ECV. The loss of LV cardiomyocyte mass increased with the degree of cardiomyocyte injury, assessed by peak cardiac troponin T after anthracycline treatment. (Doxorubicin-Associated Cardiac Remodeling Followed by CMR in Breast Cancer Patients; NCT03000036)  相似文献   
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