Cardiovascular risk factors in people with different genotypes in the insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE)

The deletion (D) allele of an insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE) has been reported to be an independent risk factor for myocardial infarction (MI), particularly in people lacking traditional risk factors. Furthermore, a borderline association between Lp(a) lipoprotein level and the I/D polymorphism at the ACE locus was reported in one study. We have searched for possible "level gene" or "variability gene" effects of ACE genes on Lp(a) lipoprotein, total cholesterol (TC), high density lipoprotein (HDL) cholesterol (HDLC), low density lipoprotein (LDL) cholesterol (LDLC), triglycerides (TG), apolipoprotein B (apoB), apolipoprotein A-I (apoA-I), and body mass index (BMI). None of these variables differed significantly between genotypes in the I/D polymorphism in any of three population samples. A single population sample created by combining the three series, exhibited an insignificant trend towards individuals carrying the D-allele having a higher level of Lp(a) lipoprotein than those lacking it, and DD homozygotes had a significantly higher Lp(a) lipoprotein level than the combined group of ID/II individuals (p = 0.03). These results may indicate that the D-allele of the I/D polymorphism at the ACE locus could influence the level of Lp(a) lipoprotein.     

Lp(a) lipoprotein is a major risk factor for cardiovascular disease: pathogenic mechanisms and clinical significance

The results of two previous and two recent studies of middle-aged males and females are presented to exemplify the clinical importance of lipoprotein (a) (Lp(a)) as a risk factor for atherosclerosis and coronary heart disease. In these studies various conventional and recently suggested risk factors were included and different methods for Lp(a) quantification were used. Lp(a) was a significant risk factor in all four studies. In the recent prospective case-control study, Lp(a) and cholesterol were found to act synergistically and predict primary acute myocardial infarction in Swedish males. A cholesterol level above 6.5 mmol/1 increased the risk of acute myocardial infarction if the Lp(a) level was above 200 mg/1. The plasma apo A-I level was a protective factor. In the other recent case-control study, an Lp(a) level above 500 mg/1 was a highly significant risk factor in Black and White US women with myocardial infarction or advanced coronary artery disease in addition to low density lipoprotein cholesterol levels above 130 mg/dl. A high apo A-I level was a protective factor. In these studies no other factors tested reached significance in multivariate logistic regression analysis. A hypothetical association between high Lp(a) levels and intracellular infection with Chlamydia pneumoniae is discussed. The results suggest that the Lp(a) level is useful in identifying high-risk individuals. Lowering low density lipoprotein cholesterol below 100 mg/dl (7lt;2.6 mmol/1) seems to be most important in both males and females with high-risk Lp(a) levels.     

High levels of Lp(a) lipoprotein in a family ith cases of severe pre-eclampsia

We report a family with two cases of severe pre-eclampsia/eclampsia in which very high levels of Lp(a) lipoprotein were found. The serum level of Lp(a) lipoprotein is genetically determined and the Lp(a) apolipoprotein has a close homology to plasminogen. Very high levels of Lp(a) lipoprotein might interfere with the fibrinolytic/thrombolytic process in man. A previous report suggested that a high maternal serum Lp(a) lipoprotein level can cause fetal growth retardation, and it is proposed that very high levels might lead to increased deposition of fibrin in the uterine spiral arteries in pregnancy, which is central in the pathogenesis of pre-eclampsia. If confirmed, a very high Lp(a) lipoprotein level could be one risk factor for pre-eclampsia that is genetically determined.     

Restriction site polymorphism at the LPA (Lp(a) apoliprotein; apoliprotein(a)) locus

A restriction site polymorphism in the Lp(a) apolipoprotein gene (the LPA gene) is reported. The basis for the polymorphism is presence or absence of an MspI restriction site that appears to be 3' to the last kringle IV structure of the gene. The "1" gene (presence of the restriction site) has a frequency of 0.316 and the "2" gene (absence of the restriction site) has a frequency of 0.684. Both members of each of 67 monozygotic (MZ) twin pairs had the same genotype and there was Mendelian segregation of the DNA variants in 40 families with a total of 75 children. There was a lower proportion of people with genotype 1-1 in the top quartile than in the 3 bottom quartiles of the population distribution of Lp(a) lipoprotein levels but the difference did not reach statistical significance.     

Classifying cases of fetal wolff-parkinson-white syndrome by estimating the accessory pathway from fetal magnetocardiograms

The paper presents an evaluation of the possibility of using fetal magnetocardiogram (FMCG) signals to estimate and classify the accessory pathway in fetal Wolff-Parkinson-White (WPW) syndrome. The FMCG signals of two fetuses with WPW syndrome (type A) were detected using a 64-channel superconducting quantum-interference device system. An average across the cycles of these signals was taken to obtain clear WPW signals. To determine the direction and position of the accessory pathway in a fetal heart accurately, the accessory pathway and activated pathway at the peak of the QRS complex thus obtained were estimated for each fetus, using a single-dipole model. The phase angle (about 90^o) between the equivalent current dipoles (ECDs) was the same for both fetuses. This angle suggested that the accessory pathway is in the left side of the heart, i.e. that the pathway exists in the position of the accessory pathway in a fetus with WPW syndrome from the angle between the ECD of the accessory pathway and the ECD of the peak in the QRS complex was thus demonstrated.     

Frequency domain models of the EEG

The structure of the normal resting EEG crosspectrum SVV(omega) is analyzed using complex multivariate statistics. Exploratory data analysis with Principal Component Analysis (PCA) is followed by hypothesis testing and computer simulations related to possible neural generators. The SVV(omega) of 211 normal individuals (ages 5 to 97) may be decomposed into two types of processes: the xi process with spatial isotropicity reflecting diffuse, correlated cortical generators with radial symmetry, and processes that seem to be generated by more spatially concentrated, correlated sources. The latter are reflected as spectral peaks such as the process. The eigenvectors of the xi process are the Spherical Harmonic Functions which explains the recurring pattern of maps characteristic of the spatial PCA of qEEG data. A new method for estimating sources in the frequency domain which fits dipoles to the whole crosspectrum is applied to explain the characteristics of the localized sources.     

Reflex testing I: algorithm for lipid and lipoprotein measurement in coronary heart disease risk assessment

We reviewed the current literature in order to construct a reflex testing algorithm that maximizes clinical utility and cost-effectiveness of lipid and lipoprotein testing. The algorithm was based on the 2nd Report of the National Cholesterol Education Program Adult Treatment Panel guidelines for use of total cholesterol (TC), triglycerides (TG), HDL-C, and LDL-C, and published reports describing the clinical use of apolipoprotein B and lipoprotein (a). The success of this algorithm was tested in a low-risk general and a high-risk hyperlipidemic patient population. Lipid data and non-lipid risk factors were obtained from a national database and from patients seen at two lipid clinics. A total of 16 968 individuals from the National Health and Nutrition Examination Survey III database comprised the low-risk group, and 239 patients examined in the Hartford Hospital and Washington University Lipid Clinics comprised the high-risk group. We found a solid scientific base to support the NCEP guidelines and reasonable support for limited testing of apoB and Lp(a). According to the algorithm, the direct LDL-C assay was deemed unnecessary in 98% and 91% of low- and high-risk subjects, respectively, if one assumes that the Friedewald equation is adequate with TG≤4.00 g/l. With a more conservative cutoff of TG≤2.50 g/l, the algorithm canceled 92% and 81% of direct LDL tests, respectively. The algorithm also limited TG to 20 and 64%, apoB to 6 and 20%, and Lp(a) to 15 and 56%, of low- and high-risk groups, respectively. Use of a comprehensive, reflex algorithm for coronary heart disease risk assessment will substantially reduce the utilization of laboratory services without diminishing the clinical value of these tests. The algorithm will prevent the overuse of certain expensive tests (direct LDL) while promoting the limited use of underutilized tests [apoB and Lp(a)].     

水中嗜肺军团菌分布规律研究

目的　探讨水环境中嗜肺军团菌分布规律及分型特征。方法　采集自然环境及生活环境中各主要水体样品 ,浓缩后经常规细菌培养后的疑似菌株 ,用血清学鉴定与 1 6SrRNA半套式PCR技术双重鉴定进行军团菌和嗜肺军团菌的分型。结果　全部 1 2 6个监测点水样有 2 8个出现军团菌阳性 (其中嗜肺军团菌 2 1个 ) ;自然环境及生活环境监测点军团菌阳性率分别为 32 1 %、2 2 2 % (其中嗜肺军团菌阳性率分别为2 1 4 %、1 6 7% ) ;全年 4 30份水样有 36份军团菌阳性 (其中 2 3份为嗜肺军团菌 ) ,夏、秋季检出率较高 ,春、冬季也有检出 ;空调冷却塔水、淋浴喷头水、公园湖水检出率较高。结论　嗜肺军团菌在自然环境及生活环境各水体中分布广泛。环境温度是军团菌污染的重要因素 ,夏、秋季是军团菌污染和军团病传播的高发季节 ,春、冬季也可发生。公园娱乐水体、空调冷却水、淋浴喷头水等与人群密切接触水体是军团菌污染和军团病传播的高危水体。应尽快采取预防与控制措施以保护广大人群身体健康     

冠心病患者血清中胆红素、脂蛋白(a)的检测

目的通过对冠心病(CHD)患者血清中脂蛋白(a)[Lp(a)]、胆红素的检测,探讨它们之间存在的内在关联。方法用全自动生化分析仪对104例冠心病患者和120例正常对照者分别进行总胆红素(TBil)、直接胆红素(DBil)、间接胆红素(IBil)和Lp(a)的检测。结果冠心病组胆红素明显低于对照组,而Lp(a)显著高于对照组。结论胆红素、Lp(a)的联合检测在冠心病诊断中具有重要意义。