老年冠心病患者L-选择素P213S基因多态性研究

目的 探讨L-选择素P213S基因多态性在老年冠心病患者和正常人群中的分布及与冠心病的相关性.方法 应用聚合酶链反应-限制性片断长度多态性技术对汉族116例老年冠心病患者及108例正常人L-选择素基因P213S多态性位点进行研究,同时检测血脂和L-选择素水平.结果 L-选择素P等位基因频率在老年冠心病和正常人群中分别为77.6%和67.1%,S等位基因频率分别为22.4%和32.9%.冠心病患者PP基因型频率和P等位基因频率均明显高于正常对照组（P＜0.05）.结论 L-选择素P213S位点多态性与老年冠心病呈相关性.P等位基因可能是老年冠心病的易感性标志.     

慢性阻塞性肺疾病患者白细胞L-选择素的表达及意义

目的探讨L-选择素在慢性阻塞性肺疾病(COPD)气道炎症发展中的作用及意义。方法采用流式细胞术定量测定38例COPD患者(观察组)急性期及稳定期外周血白细胞L-选择素的表达率,与30例查体健康者(对照组)进行比较,并与PaO2、PaCO2、肺功能FEV1占预计值的百分比(FEV1%)进行相关性分析。结果观察组急性期粒细胞、淋巴细胞L-选择素的表达率明显低于对照组(P均<0.01),稳定期淋巴细胞L-选择素的表达率仍低于对照组。中性粒细胞L-选择素表达与FEV1%、PaO2呈正相关(r=0.602,r=0.671,P均<0.01),与PaCO2呈负相关(r=-0.427,P<0.01)。结论L-选择素参与了COPD气道炎症的发生和发展,检测外周血白细胞L-选择素表达率有助于判断COPD病情及预后。     

急性冠状动脉综合征患者血清中可溶性L-选择素的变化规律

目的 :观察急性冠状动脉综合征 (ACS)不同分型患者血清中可溶性L 选择素 (sL selectin)水平的变化规律及心肌梗死 (MI)患者sL selectin水平与肌酸激酶 同工酶 (CK MB)和MI面积的相关性。方法 :将 5 9例冠心病患者分为 3组 :急性MI组 2 6例 ,不稳定型心绞痛 (UAP)组 18例 ,稳定型心绞痛 (SAP)组 15例 ;另设正常对照组 19例。血清sL selectin水平应用ELISA方法测定 ;预测MI面积应用Michelle等公式。结果 :①SAP组血清sL selectin水平为 (0 .84± 0 .12 )mg/L ,明显低于正常对照组 (1.0 5± 0 .18)mg/L ,P <0 .0 5 ;②UAP组和急性MI组sL selectin测定值分别为 (1.0 9± 0 .19)、(1.4 0± 0 .6 4 )mg/L ,与SAP组相比明显增高 (P <0 .0 5 ) ;③sL se lectin与CK MB无相关性 ,与MI面积亦无相关性。结论 :sL selectin与ACS的发生发展密切相关 ,sL selectin不能反映心肌坏死的程度     

肺癌组织中CCR7和L-选择素的表达及意义

目的 探讨CC趋化因子受体7(CCR7)和黏附分子L-选择素在肺癌组织中的表达及其临床意义.方法 采用免疫组化法检测110例肺癌组织和30例癌旁正常肺组织中CCR7和L-选择素的表达.结果 110例肺癌组织中CCR7阳性表达77例(70.0%),L-选择素阳性表达37例(33.6%);30例癌旁正常肺组织中CCR7阳性表达5例(16.7%),I广选择素阳性表达0例.肺癌组织中CCR7、L-选择索阳性率明显高于癌旁正常肺组织(P<0.05),且CCR7表达与L-选择素表达有关(P<0.05).有淋巴结转移者(68例)CCR7、L-选择索阳性率分别为83.8%、41.2%,无淋巴结转移者(42例)CCR7、L-选择素阳性率分别为47.6%、21.4%(P均<0.05).Ⅰ、Ⅱ、Ⅲ、Ⅳ期肺癌患者CCR7阳性率分别为59.5%、76.2%、69.2%、100.O%(P<0.05),L-选择素阳性率分别为21.6%、31.0%,46.2%、80.O%(P<0.05).结论 肺癌组织中CCR7与L-选择索表达有关,二者可能共同参与了肺癌的发生及淋巴结的转移过程,检测二者表达情况有利于判断肺癌患者的TNM分期和预后.     

高密度脂蛋白与心血管保护的研究进展

多项大规模临床研究显示,血清高密度脂蛋白(HDL)的水平与冠心病存在着密切的联系。HDL胆固醇对心血管的保护作用,体现在可介导胆固醇逆向转运、抗氧化作用、调节内皮功能、抗炎及影响凝血系统等。本文对HDL的结构和代谢进行了回顾,并对其心血管保护作用的新进展进行了综述。     

L-选择素与慢性髓细胞白血病的相关性研究

黏附分子是存在于细胞间的精细网状结构,与细胞相互接触进而传递细胞内信息有关,包括Ig超基因家族,整合素β1、β2家族及选择素家族。L-选择素(L-selectin,又称CD62L)是选择素家族成员之一,表达于大多数白细胞和白血病细胞表面,是白细胞移出血管外过程中早期与内皮细胞黏附的主     

削弱高密度脂蛋白胆固醇心血管保护作用的影响因素分析

目的研究高水平高密度脂蛋白胆固醇(HDL-C)冠心病患者的临床特征及血脂水平,分析削弱HDL-C心血管保护作用的影响因素。方法选择80例HDL-C≥1.56 mmol/L(60 mg/dl)的患者,按冠状动脉造影结果分为冠心病组46例,对照组34例,测定血脂和血糖指标,详细记录临床特征并进行分析。结果与对照组比较,冠心病组的体重指数(BMI)显著大于对照组(P<0.01),甘油三酯(TG)和低密度脂蛋白胆固醇(LDL-C)水平显著高于对照组(P<0.01),总胆固醇(TC)和载脂蛋白B(ApoB)水平亦高于对照组(P<0.05);HDL-C与饮酒呈正相关(r=0.227,P<0.001),与BMI、TG呈负相关(r=-0.159、-0.287,均P<0.001);LDL-C、BMI及年龄与冠心病发病的危险性独立相关。结论部分高水平HDL-C人群受BMI、TG等因素的影响,削弱了HDL-C的心血管保护作用而发生冠心病。     

高密度脂蛋白胆固醇与心血管剩余风险

血脂异常是动脉粥样硬化的最主要危险因素之一.从20世纪60年代开始,大量的降低胆固醇临床试验均为“越低越好”的降脂理念奠定了坚固的循证医学基石.他汀类药物可通过降低低密度脂蛋白胆固醇而显著减低心血管事件发生.然而在一些低密度脂蛋白胆固醇已经达标,甚至已降至70 mg/dL以下的患者中,仍然存在着较高的心血管剩余风险.低水平的高密度脂蛋白胆固醇是其最主要的原因之一.因此目前,即使大剂量的强化他汀治疗仍不能完全解决剩余风险的存在.而解决剩余风险的存在对进一步降低心血管病患者的风险又尤为重要.文章主要就高密度脂蛋白胆固醇与心血管剩余风险之间的关系及最新研究进展作进一步归纳和阐述.     

L-选择素P213S基因多态性与甘肃汉族、东乡族2型糖尿病的关系

目的 探讨L-选择素P213S基因多态性在甘肃汉族、东乡族人群中的分布及其与2型糖尿病的关系.方法 2006至2008年入选汉族2型糖尿病患者143例和正常对照者152名,东乡族2型糖尿病患者116例和正常对照者126名,应用聚合酶链反应-高温连接酶检测反应检测L-选择素P213S基因型,采用氧化酶法或放免法测定血糖、胰岛素及血脂水平.采用卡方检验进行统计学分析.结果 L-选择素基因型PP、PS和SS频率在汉族2型糖尿病患者为55.9%、37.8%及6.3%,在汉族正常对照者为41.4%、50.7%及7.9%,在东乡族2型糖尿病患者为44.8%、48.3%及6.9%,在东乡族正常对照者为38.1%、44.4%及17.5%.等位基因P、S频率在汉族2型糖尿病患者为74.8%及25.2%,在汉族正常对照者为66.8%及33.2%,在东乡族2型糖尿病患者为69.0%及31.0%,在东乡族正常对照者为60.3%及39.7%(均P<0.05).汉族人群P等位基因携带者2型糖尿病患病风险是S等位基因携带者的1.479倍,东乡族人群P等位基因携带者2型糖尿病患病风险是S等位基因携带者的1.462倍.结论 L-选择素P213S基因多态性与2型糖尿病发病相关,P等位基因可能是罹患2型糖尿病的危险因素之一.     

火把花根片对EAE大鼠模型VCAM-1和L-选择素的影响

目的探讨火把花根片对实验性自身免疫性脑脊髓炎(EAE)大鼠模型的治疗作用以及对VCAM-1和L-选择素的影响。方法模型组采用豚鼠髓鞘蛋白匀浆和福氏完全佐剂诱发大鼠急性EAE模型;治疗组在模型组基础上予以火把花根(300mg·kg-1·d-1,每日2次),观察动物表现并评分,HE染色和Loyez氏髓鞘染色观察病理和髓鞘改变,免疫组化技术测定脑和脊髓的VCAM-1和L-选择素(L-selectin)水平。结果治疗组未出现临床症状,VCAM-1为(2.13±0.99),L-selectin为(1.88±0.64),与模型组比较差异有统计学意义(P<0.05);脑和脊髓小血管周围炎症细胞浸润明显减少,髓鞘结构完整。结论火把花根片对EAE有治疗作用,其作用机制与抑制VCAM-1及L-selectin表达有关。     

高密度脂蛋白胆固醇与心脑血管病相关性前瞻研究

目的 探讨我国35～64岁人群血清HDL-C水平与急性冠心病事件和急性卒中事件发病危险的关系.方法 采用前瞻性队列研究的方法 ,对11省市35～64岁队列人群共30 384人基线HDL-C水平和1992-2003年发生的急性冠心病和急性卒中事件关系进行分析.应用Cox比例风险模型对HDL-C水平与心血管病发病危险进行多因素分析.结果 (1)与对照组相比,随着HDL-C水平的降低,缺血性心血管病(ICVD)事件发病危险呈持续增加.(2)HDL-C水平与不同类型的心血管病发病危险的关系有所差别,随着HDL-C水平的降低,急性冠心病事件发病危险及缺血性卒中事件发病危险明显上升;而出血性卒中事件与HDL-C水平的关系差异无统计学意义.低HDL-C血症组急性冠心病发病的危险增加45%(RR=1.45,P＜0.05),缺血性卒中发病的危险增加53%(RR=1.53,P＜0.01).(3)在缺血性心血管病事件中,6.4%可归因于HDL-C水平降低;其中6.2%的急性冠心病事件和7.3%的急性缺血性卒中事件可归因于低HDL-C血症.结论 从HDL-C≥1.56mmol/L开始,随着HDL-C水平的降低,ICVD的发病危险明显上升.在血脂异常的防治中,对于低HDL-C应予以足够重视.     

Improved risk assessment of coronary artery disease by substituting paraoxonase 1 activity for HDL-C: Novel cardiometabolic biomarkers based on HDL functionality

Background and aimsDeveloping laboratory assays to evaluate HDL functions and improve cardiovascular disease (CVD) risk assessment has recently emerged as a challenge. The present study was conducted to help predict the risk of coronary artery disease (CAD) by investigating new cardiometabolic risk factors based on substituting paraoxonase 1 (PON1) as a critical enzyme in the functionality of HDL for that of HDL-C.Methods and resultsThe present study recruited 274 subjects undergoing diagnostic coronary angiography, 92 without significant CAD (non-CAD), and 182 with a severe CAD. The diagnostic accuracy of the new biomarkers in non-CAD versus multi-vessel disease was obtained in descending order of AUC as 0.72 (P < 0.001) for log (TG/PON1), 0.70 (P < 0.001) for nonHDL-C/PON1, and 0.67 (P < 0.001) for LDL-C/PON1. After performing a multivariate adjustment for age, gender, BMI, statin therapy, and diabetes mellitus, the increased odds of CAD remained significant for the new cardiometabolic ratios as independent variables [adjusted OR = 1.47 (1.15–1.88), p = 0.002 for LDL-C/PON1; adjusted OR = 2.15 (1.41–3.5), p = 0.009 for nonHDL-C/PON1; adjusted OR = 5.03 (2.14–13.02), p = 0.004 for log (TG/PON1)]. CAD was diagnosed with an optimal discriminating cutoff of 1.84 for LDL-C/PON1, 2.8 for nonHDL-C/PON1, and 0.48 for log (TG/PON1).ConclusionsTo improve CAD's risk assessment, the PON1 activity was proposed as an alternative to HDL-C in the commonly used atherogenic lipid ratios. Substituting the PON1 activity for the HDL-C concentration can provide an index of the HDL activity. The present study sought to exploit the lipoprotein-related risk factors of CAD from a more effective perspective.     

高密度脂蛋白对血管内皮依赖性舒张功能的影响

目的　探讨血清高密度脂蛋白 胆固醇 (HDL C)水平与肱动脉内皮依赖性舒张功能之间的关系。方法　测定 71例血清总胆固醇水平相对正常的冠心病患者和 34例对照者的血脂水平以及在反应性充血时和含服硝酸甘油后肱动脉的内径变化。结果　冠心病组血流介导的肱动脉舒张和硝酸甘油所致的肱动脉舒张均低于对照组 [分别为 (2 6 1± 2 91) %比 (8 0 1± 4 72 ) %和 (17 2 2± 6 76 ) %比 (2 3 13± 8 6 1) % ,P均 <0 0 0 1]。多因素线性逐步回归分析显示 :血流介导的肱动脉舒张与血清HDL C水平呈正相关 (r=0 32 4,P =0 0 0 2 ) ,与血清总胆固醇、甘油三酯和低密度脂蛋白水平无关 ;硝酸甘油所致的肱动脉舒张也与上述血脂水平无关。根据血流介导的肱动脉舒张程度将两组受试者合并再分为A、B两组 ,A组肱动脉舒张≤ 4% ,B组肱动脉舒张 >4%。结果显示 ,A组HDL C水平明显低于B组 [(1 15± 0 2 6 )mmol/L对 (1 38± 0 5 0 )mmol/L ,P <0 0 1) ]。结论　冠心病患者内皮依赖性及非内皮依赖性的血管舒张功能均受损。HDL C对血管内皮依赖性舒张功能有保护作用 ,该作用可能与其抗动脉粥样硬化作用有关     

High density lipoproteins, genetic polymorphism for apo A-I and coronary artery disease

HDL cholesterol and apolipoprotein A-I are associated with the development of coronary artery-disease (CAD). The presence of a PstI site polymorphism adjacent to the gene encoding apo A-I (known as P₂) has also been shown to be associated with CAD but this relationship is controversial. A case control study was conducted in an Australian population to re-examine whether the rare P₂ allele is associated with CAD. Data were derived from 159 cases of angiographically confirmed CAD and 99 healthy controls. The proportion of CAD cases carrying the P₂ allele did not differ significantly from controls (11% versus 9%). In a multiple logistic regression model controlling for the effects of age, country of birth, hypertension and hypotensive drugs, body mass index and lipid variables, the P₂ allele failed to predict significantly the presence of CAD (odds ratio 1.83; 95% confidence interval 0.65–5.19).     

Role of high density lipoproteins (HDL) in reverse cholesterol transport

The atheromatous risk is negatively correlated with the plasma concentration of HDL cholesterol. This might be due to the role of HDL in the reverse cholesterol transport. In the first stage, free cholesterol molecules from peripheral cells are taken up by HDL through a receptor-dependent mechanism. In HDL, the esterification of cholesterol is catalysed by the lecithin: cholesterol acyl transferase. The progressive accumulation of cholesterol esters leads to the formation of HDL2. Through the action of cholesterol ester transfer protein, HDL2 become enriched in triglycerides and transfer cholesterol esters to LDL. Finally, cholesterol may be taken up by the liver through two routes which are: the receptor-mediated LDL endocytosis and the direct uptake of cholesterol esters which occurs during the degradation of HDL2 by hepatic lipase.     

Smoking, lipoproteins and coronary heart disease risk: Data from the Munster Heart Study (PROCAM)

Aims The mechanism of the increase in coronary heart disease riskassociated with smoking is unclear, but may partly be due tosmoking-related changes in intermediate risk factors such aslipid levels, fibrinogen and blood pressure. We therefore examinedthe distribution of these variables among smokers and non-smokersin the Münster Heart Study. Methods 20696 men, aged 41·7±2·7 years (mean±SD)and 10212 women, aged 37·0±2·6 years, wereenrolled between 1978 and 1995. Thirty-two percent of womenand 36% of men smoked. Compared to non-smokers, mean levelsof low density lipoprotein cholesterol, total cholesterol, triglyceridesand fibrinogen were increased, respectively, by 1·4%,0·9%, 15% and 12·1% in male and by 2·0%,5·5%, 12% and 3·4% in female smokers. Mean highdensity lipoprotein cholesterol levels, body mass index andblood pressure were reduced, respectively, by 6·4%, 3·8%,and 2% in male, and by 6·7% 1·2% and 2% in femalesmokers. In the subgroup of 4639 men aged 40 to 65 with 8 yearsof follow-up, the coronary event rate (definite myocardial infarction,sudden cardiac death) in cigarette smokers was more than twicethat of non-smokers with otherwise identical risk factors. Conclusion In the Münster Heart Study, smoking was associated withadverse changes in lipids (of greater magnitude in women), andfibrinogen (of greater magnitude in men). However, these changesexplained only a small part of the smoking-related increasein coronary heart disease risk.The European Society of Cardiology     

高密度脂蛋白胆固醇酯化速率与冠心病的相关性

目的 研究高密度脂蛋白胆固醇酯化速率(FERHDL)与冠心病的相关性,探讨其在冠心病中的临床应用价值.方法 按冠状动脉造影结果将131例研究对象分为冠心病组(n=76)与非冠心病组(n=55),进行临床资料收集、生化指标检测、FERHDL及脂蛋白亚类的测定,分析FERHDL与冠心病的相关性.结果 冠心病组FERHDL明显高于非冠心病组(21.70±8.73比18.65±6.26.P<0.05).FERHDL在非冠心病、单支病变、双支病变、三支病变组间有升高趋势,FERHDL随病变支数增加而逐渐增高,其中非冠心病组和三支病变组比较差异有统计学意义(18.65±6.26比24.00±9.22,P<0.05).FERHDL与甘油三酯(r=0.647,P<0.01)、LDLb-C(r=0.441,P<0.01)呈显著正相关,与HDL-C(r=-0.708,P<0.01)、HDIJ2-C(r=-0.748,P<0.01))呈显著负相关.结论 冠心病患者FERHDL明显高于非冠心病者,FERHDL随冠状动脉病变支数增加而呈增高趋势.FERHDL与HDL和LDL颗粒大小相关.

Abstract：

Objective To assess the relationship between fractional esterification rate of high density lipoprotein cholesterol(FERHDL)and coronary artery disease.Methods A total of 131 hospitalized patients underwent coronary angiography due to chest pain were included in the study and Datients were divided into CAD group(n=76)and non CAD group(n=55)according to coronary allgiograrn.Clinical and laboratory data including biochemical laboratory,FERHDL and lipid subclasses were analyzed.Results The FERHDL value of CAD group was significantly higher than that of the non CAD group(21.70±8.73 vs.18.65 4±6.26,P<0.05).There was an increased trend of FERHDL with numbers of diseased coronary arteries,significant difference was evidenced between non CAD group and 3-vessel group(18.65±6.26 vs.24.00±9.22,P<0.05).FERHDL was positively correlated with TG(r=0.647,P<0.001).LDLb-C(r=0.441,P<0.001)and negatively correlated with HDL-C(r=-0.708,P<0.001)and HDL2-C(r=-0.748,P<0.001).Conclusion Our data showed that the values of FERHDL were significantly increased in CAD patients and correlated with the severity of the CAD.     

甘油三酯/高密度脂蛋白胆固醇比值对冠心病的诊断价值的探讨

目的　探讨甘油三酯 /高密度脂蛋白胆固醇 (TG/HDL C)比值对冠心病 (CHD)的诊断价值。方法　分析 173例选择性冠状动脉造影 (冠脉造影 )确诊的CHD患者 (CHD组 )及 118例冠脉造影阴性者 (对照组 )的TG/HDL C比值水平与CHD之间的关系。结果　CHD组患者的TG/HDL C比值水平及异常率均明显高于对照组 (2 0 2± 1 19vs 1 4 0± 0 97,P <0 0 1,2 8 9%比 11 8% ,P <0 0 1)。经多元逐步回归分析显示 :与TG、HDL C相比 ,该比值与CHD之间显示了更有意义的回归关系 (β值 0 2 5 ,P值 =0 0 0 0 1,复相关系数为 0 4 5 )。结论　TG/HDL C比值对于CHD诊断是一有临床使用价值的指标。     

冠心病患者血脂水平与血清高密度脂蛋白亚类组成关系的研究

目的 :探讨冠心病 (CHD)患者血脂水平与血清高密度脂蛋白 (HDL)亚类组成的关系。方法 :采用双向电泳 免疫印迹检测法分析了 83例CHD患者血清HDL亚类组成及相对百分含量。结果 :按血清三酰甘油 (TG)浓度将CHD患者分为 4组 ,各组患者血清中前β1 HDL、HDL3c(除TG <1.35mmol L组外 )、HDL3b水平显著高于对照组 (P <0 .0 0 1) ,HDL2b水平显著低于对照组 (P <0 .0 1)。随着血清TG浓度的升高 ,前 β1 HDL、HDL3c及HDL3b颗粒逐渐增加 ,而HDL2a及HDL2b颗粒逐渐减少。按血清HDL胆固醇 (HDL C)浓度将CHD患者分为 3组 ,各组患者中 ,前 β1 HDL(除HDL C≥ 1.30mmol L组外 )、HDL3c及HDL3b水平显著高于对照组 (P <0 .0 5～ <0 .0 1) ,HDL2b水平显著低于对照组 (P <0 .0 1)。随着血清HDL C浓度的升高 ,前 β1 HDL、HDL3c、HDL3b及HDL3a颗粒逐渐减少 ,而HDL2b颗粒逐渐增加。结论 :CHD患者血清HDL颗粒直径呈变小趋势 ,并且随着TG水平的升高和HDL C水平的降低 ,其HDL颗粒的变小程度更加明显。     

Effect of genistein against copper-induced lipid peroxidation of human high density lipoproteins (HDL)

Several studies have demonstrated that the isoflavone genistein exerts a protective effect against lipid peroxidation of low density lipoproteins (LDL). Aim of our study was to investigate whether genistein protects high density lipoproteins (HDL), isolated from normolipemic subjects, against Cu(++)-induced lipid peroxidation. Our results demonstrated that genistein exerts an inhibitory effect against Cu(++)-induced lipid peroxidation of HDL, as shown by the lower increase in the levels of conjugated dienes in lipoproteins oxidized after preincubation with different concentrations of genistein (0.5-2.5microM). Moreover the analysis of fluorescence emission spectra of tryptophan (Trp) and Laurdan (6-dodecanoyl-2-dimethyl-aminonaphthalene) demonstrated that genistein prevents the alterations of apoprotein structure and physico-chemical properties, associated with Cu(++)-triggered lipid peroxidation of lipoproteins. The protective effect exerted by genistein against oxidative damage of lipoproteins was realized at concentrations similar to those observed in plasma of human subjects consuming a traditional soy diet or receiving a soy supplement. Therefore, we suggested that antioxidant activity exerted by genistein against lipid peroxidation of HDL in vitro could be of physiological relevance.