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Biomedical subjects

C Gerdes

Publications and source records attributed to C Gerdes.

At least 19 recordsLinked to original sources
PubMed2001

[Clinic admission?--but not without my child!].

Since the end of the 1990s the Westfälische Klinik Lengerich has offered an inpatient psychiatric treatment of an psychiatric ill parent--combined with a pedagogic attendance of the child taken along. The following article describes our experience in that matter, from a ward concentrated on psychotherapy. In selected examples supposed patterns of interaction--following the specific disease--are represented from both the psychotherapeutic und the pedagogic point of view. In practice our plan of treatment and attendance has proved successful for the wellbeing of the patients and their children. Remains to be hoped that--despite difficulties in organisation which will have to be overcome--similar offers can be made in regional psychiatric attendance.

Adult↗
PubMed2000

The apolipoprotein epsilon4 allele determines prognosis and the effect on prognosis of simvastatin in survivors of myocardial infarction : a substudy of the Scandinavian simvastatin survival study.

BACKGROUND: Carriers of the epsilon4 allele of the apolipoprotein E gene are at a higher risk of coronary heart disease than individuals with other genotypes. We examined whether the risk of death or a major coronary event in survivors of myocardial infarction depended on apolipoprotein E genotype and whether the benefits of treatment with simvastatin differed between genotypes. METHODS AND RESULTS: Cox proportional hazards models were used to analyze 5.5 years of follow-up data from 966 Danish and Finnish myocardial infarction survivors enrolled in the Scandinavian Simvastatin Survival Study. A total of 16% of the 166 epsilon4 carriers in the placebo group died compared with 9% of the 312 patients without the allele, which corresponds to a mortality risk ratio of 1.8 (95% confidence interval, 1.1 to 3.1). The risk ratio was unaffected by considerations of sex, age, concurrent angina, diabetes, smoking, and serum lipids in multivariate analyses. Simvastatin treatment reduced the mortality risk to 0.33 (95% confidence interval, 0.16 to 0.69) in epsilon4 carriers and to 0.66 (95% confidence interval, 0. 35 to 1.24) in other patients (P=0.23 for treatment by genotype interaction). Apolipoprotein E genotype did not predict the risk of a major coronary event. Baseline serum levels of lipoprotein(a) also predicted mortality risk and could be combined with epsilon4-carrier status to define 3 groups of patients with different prognoses and benefits from treatment. CONCLUSIONS: Myocardial infarction survivors with the epsilon4 allele have a nearly 2-fold increased risk of dying compared with other patients, and the excess mortality can be abolished by treatment with simvastatin.

Adult↗
PubMed2000

Postprandial response to a fat tolerance test in young adults with a paternal history of premature coronary heart disease - the EARS II study (European Atherosclerosis Research Study).

BACKGROUND: The European Atherosclerosis Research Study (EARS) I had shown that fasting plasma concentrations of apolipoprotein B (apo B) and triglycerides were the most discriminant variables between offspring with a paternal history of coronary heart disease (CHD) and controls. The EARS II study was undertaken to investigate whether a paternal history of CHD was associated with differences in postprandial lipemia. DESIGN: Male subjects with a paternal history of CHD (cases, n = 407) and age-matched male controls (n = 415) were recruited from 14 European universities. All subjects had an oral fat tolerance test. RESULTS: In the sample as a whole, the postprandial triglyceride responses did not significantly differ between the two groups. However, in the upper tertile of fasting triglycerides, cases displayed a higher area under the curve (5.71 vs. 4.49 mmol.h L-1, P < 0.001), a higher peak (1.76 vs. 1.43 mmol L-1, P < 0.001) and a more delayed time to peak (3.15 vs. 2.91 h, P < 0.05) than controls. In the upper tertile, fasting apo B levels (P < 0.05) and triglyceride area under the curve (P = 0.002) significantly discriminated cases from controls in a multivariate analysis. Cases had also higher Lp C-III:B levels at 4 h than controls (11.2 vs. 9.9 mg dL-1, P < 0.01) and this difference remained significant after adjustment for apo B and triglyceride levels. CONCLUSIONS: These results indicate that in subjects with a moderate elevation of fasting triglycerides, an impaired postprandial response to a fat load constitutes an early biological expression of a paternal history of premature CHD.

Administration, Oral↗
PubMed1999

Two common mutations (D9N, N291S) in lipoprotein lipase: a cumulative analysis of their influence on plasma lipids and lipoproteins in men and women.

We assessed the effect of two common mutations in the lipoprotein lipase gene (LPL), D9N and N291S, which have been shown to modulate plasma lipids in a wide spectrum of patients. A total of 1114 men and 1 144 women from the Framingham Offspring Study (FOS) were analyzed for these two LPL variants. Subsequently, the association with fasting plasma lipids and risk of coronary artery disease (CHD) was determined. We extended our study by calculating weighed means of lipids and lipoproteins in carriers and non-carriers for these LPL mutations in patients with genetic dyslipidemias, CHD patients and healthy controls. In the FOS sample, the D9N and N291S alleles were associated with lower high-density lipoprotein-cholesterol (HDL-C) (delta = - 0.07 mmol/ 1, p = 0.03) and a trend towards increased triglycerides (delta = 0.25 mmol/ 1, p = 0.07). In women, a trend towards the high triglyceride, low HDL-C phenotype was evident (delta = - 0.02 mmol/1 for HDL-C and delta = 0.14 mmol/l for triglycerides, respectively). Cumulative analysis of other studies of male carriers of the D9N and N291S revealed higher levels of triglycerides (D291N; 2.60(1.85) mmol/l vs. 1.62(1.18) mmol/l: p < 0.0001) (D9N; 1.94 (1.19) mmol/l vs. 1.74(1.17) mmol/l: p < 0.001) and lower HDL-C (N291S; 1.04(0.32) mmol/l vs. 1.15(0.28) mmol/l: p < 0.0001) (D9N; 1.08(0.24) mmol/l vs. 1.16(0.28) mmol/l: p < 0.0001). In females, results differed with higher TG levels (N291S; 1.70(0.99) mmol/l vs. 1.10(0.63) mmol/l: p < 0.001) (D9N; 1.08(0.76) mmol/l vs. 0.96(0.51) mmol/l: p < 0.01) and lower HDL-C levels (N291S; 1.27(0.33) mmol/l vs. 1.51(0.32) mmol/l: p < 0.0001); however, the HDL-C levels for D9N carriers were similar to non-carriers (D9N; 1.52(0.29) mmol/l vs. 1.53(0.35) mmol/l: p = 0.83). Our data provide evidence that common variants of the LPL gene are significant modulators of lipid and lipoprotein levels in both men and women.

Cholesterol, HDL↗
PubMed1999

The intrinsic factor-vitamin B12 receptor, cubilin, is a high-affinity apolipoprotein A-I receptor facilitating endocytosis of high-density lipoprotein.

Cubilin is the intestinal receptor for the endocytosis of intrinsic factor-vitamin B12. However, several lines of evidence, including a high expression in kidney and yolk sac, indicate it may have additional functions. We isolated apolipoprotein A-I (apoA-I), the main protein of high-density lipoprotein (HDL), using cubilin affinity chromatography. Surface plasmon resonance analysis demonstrated a high-affinity binding of apoA-I and HDL to cubilin, and cubilin-expressing yolk sac cells showed efficient 125I-HDL endocytosis that could be inhibited by IgG antibodies against apoA-I and cubilin. The physiological relevance of the cubilin-apoA-I interaction was further emphasized by urinary apoA-I loss in some known cases of functional cubilin deficiency. Therefore, cubilin is a receptor in epithelial apoA-I/HDL metabolism.

Anemia, Megaloblastic↗
PubMed1999

A comparison of lifestyle, genetic, bioclinical and biochemical variables of offspring with and without family histories of premature coronary heart disease: the experience of the European Atherosclerosis Research Studies.

BACKGROUND: Lifestyle, genetic, bioclinical and biochemical factors of European university students aged 18-26 years, with and without documented paternal histories of premature coronary heart disease, have been compared in the European Atherosclerosis Research Studies (EARS) I and II. OBJECTIVE: To highlight consistencies and inconsistencies between findings in the two studies. METHODS: All measurements were made according to strict protocols, by trained technicians using validated methods. The results for men in EARS I are compared with those from EARS II which was confined to men. RESULTS: In both studies we found no differences between cases and controls in lifestyle factors and bioclinical factors except that controls were taller. We found inconsistent differences between obesity indices and antecedents of arterial hypertension. In both studies we found consistent differences between cases and controls in levels of total cholesterol and apolipoprotein B, both levels being higher in cases. The lack of any difference between levels of high-density lipoprotein cholesterol and apolipoprotein A1 was also found consistently. Inconsistent differences were found for levels of triglycerides and apolipoprotein E. For most of the candidate genes that were studied, no differences between cases and controls were found, but different polymorphisms were associated with levels of lipids, apoproteins and fibrinogen independently of case-control status. Some of these associations were potentiated by lifestyle factors. The interaction between genetic and environmental factors is further illustrated with results from the association of apolipoprotein E polymorphism with the level of apolipoprotein B and a variety of other determinants of apolipoprotein B level. CONCLUSIONS: In the EARS studies a documented family history of premature coronary heart disease was mainly expressed in terms of biochemical factors that are determined both by nature and by nurture.

Adolescent↗
PubMed1997

Lipoprotein lipase variants D9N and N291S are associated with increased plasma triglyceride and lower high-density lipoprotein cholesterol concentrations: studies in the fasting and postprandial states: the European Atherosclerosis Research Studies.

BACKGROUND: Variations at the DNA level with moderate effects on biochemical variables may be important for the occurrence of disease at the population level, if they are common. Two mutations in the LPL gene, N9 and S291, are associated with variation in fasting plasma concentrations of HDL cholesterol (HDL-C) and triglycerides (TG). We investigated whether these mutants were more frequent in offspring of cases with premature coronary disease and analyzed the effects on fasting plasma lipids and postprandial TG. METHODS AND RESULTS: Students with and without paternal history of myocardial infarction (cases and control subjects [controls]) were studied in the European Atherosclerosis Research Studies I and II (EARS-I and -II). Allelic frequencies for the N9 and S291 mutations did not differ between cases and control subjects. The N9 mutation was identified in 4.2% of all subjects in EARS-I, and carriers had higher fasting TG levels (P<.001) than noncarriers. In an oral fat tolerance test, there were no differences in postprandial TG between carriers and noncarriers of the N9 allele. The S291 mutation was identified in 3.1% of all subjects in EARS-I, and carriers had lower fasting HDL-C levels (P<.005) than noncarriers. There was a significant interaction between S291 genotype and body mass index on fasting TG levels (P<.01). In the cases, carriers of the S291 allele had higher TG levels 6 hours postprandially (P<.04) than did noncarriers. CONCLUSIONS: The two LPL mutations are common and may predispose to elevated TG and decreased HDL-C concentrations, even in young subjects. In the case of the S291 mutation, this effect appears to be mediated via delayed postprandial TG clearance. Moreover, even moderate obesity potentiates the TG-raising and HDL-lowering effects associated with the S291 allele.

Adolescent↗
PubMed1997

Isoform-specific binding of human apolipoprotein E to the non-amyloid beta component of Alzheimer's disease amyloid.

The non-A beta component (NAC) of Alzheimer's disease amyloid is a newly discovered 35 amino acid peptide found to be closely linked to the beta-amyloid fibrils in senile plaques. Apolipoprotein E (apoE) is another prominent constituent of senile plaques. In vitro studies have shown that apoE binds beta-amyloid (A beta) with high avidity, but it is unknown to what extent apoE interacts with NAC. We examined the interactions between apoE and NAC and found that apoE bound synthetic NAC, forming a complex that resisted reducing agents and separation on SDS-PAGE. The complex could be formed using apoE from either purified human very low density lipoprotein (VLDL) particles, unfractionated human cerebrospinal fluid (CSF), or recombinant protein. The binding was established within 15 min upon mixing, and the interaction between NAC and apoE was dose-dependent and specific as revealed by competition experiments. The NAC-apoE complex was affected by non-physiological pH, but not by reducing agents such as DTT or beta-mercaptoethanol. ApoE exists in different isoforms of which the apoE3 genotype is the most frequent. Notably, the apoE4 genotype has been linked to late-onset Alzheimer's disease. This study presents evidence that apoE3 as well as apoE4 bind NAC, but the binding to apoE4 is about twice as strong as to apoE3. The isoform-specific binding of NAC to apoE may thus play an important role in amyloidogenesis and in the sequestering of apoE in senile plaques during the progress of Alzheimer's disease.

Alzheimer Disease↗
PubMed1997

Patients' perceptions of outcomes of a Canadian hospitalization.

Notes that with health care reform moving at tremendous speed throughout Canada, a great deal of interest in outcomes research has been generated. States that the research team consisted of 17 professional practice leaders from eight disciplines. Proposes, through the research, to identify from the perspective of former patients what results they hoped to achieve prior to discharge from hospital and what facilitated and hindered them in achieving these results. Reports that a representative sample was selected for the study. Forty-one former patients each participated in up to two focus groups, with a total of 16 focus groups conducted. Hierarchical analysis revealed themes that fell within the framework of structure, process and outcomes. The findings will assist in ensuring that more appropriate and effective care is offered to patients by a variety of disciplines.

Adult↗
PubMed1997

Phenotypic variation in patients heterozygous for familial defective apolipoprotein B (FDB) in three European countries.

A glutamine-for-arginine substitution at amino acid position 3500 of apolipoprotein B (apo B) causes synthesis of LDL with reduced binding affinity to the LDL receptor (LDLR). The associated clinical syndrome has been named familial defective apolipoprotein B- 100 (FDB). In 205 FDB patients from Germany (n = 73). The Netherlands (n = 87), and Denmark (n = 45), we tried to assess determinants of variation in lipid concentrations. Besides age, sex, and geographic origin, variation in the LDLR gene was the most powerful determinant of variation in total cholesterol and LDL cholesterol levels. Polymorphic variation in the LDLR gene (SfaNI, exon 2; Nco I, exon 18) was associated with total cholesterol (TC) and LDL cholesterol (LDL-C) variation in women (SfaNI: P = .04 and .03 for TC and LDL-C, respectively; Nco I; P = .003 and .006, respectively), whereas the Ava II (exon 13) and the Pvu II (intron 15) polymorphisms were not. Combined information from all three LDLR exon polymorphisms showed that subjects with at least one S + A + N + allele had 13% to 20% higher TC than non-S + A + N + subjects (P = .02 [TC, men]; P = .01 [LDL-C, men]; P = .005 [TC, women]; and P = .004 [LDL-C, women]) and, together with age and geographic origin, accounted for 20% (women) and 19% (men) of the variation in LDL-C. The expected association of the apo E genotypes (e3e2, e3e3, and e3e4) with cholesterol concentrations was seen in S + A + N + but not in non-S + A + N + subjects and in P-P- but not in P + P + or P + P- subjects. With regard to clinical expression, FDB patients had lower TC and LDL-C levels and a lower prevalence of cardiovascular disease than 101 Danish patients with familial hypercholesterolemia.

Adult↗
PubMed1996

Effects of apoE gene polymorphism on Lp(a) concentrations depend on the size of apo(a): a study of 466 white men.

Polymorphisms in the genes for the low-density lipoprotein (LDL) receptor ligands, apolipoprotein E (apoE), and apolipoprotein B (apoB) are associated with variation in plasma levels of LDL cholesterol. Lp(a) lipoprotein(a) [Lp(a)] is LDL in which apoB is attached to a glycoprotein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined isoforms differing in molecular weight, which are inversely correlated with Lp(a) concentrations in blood. The interaction of apo(a) with triglyceride-rich lipoproteins differs with the size of apo(a), and therefore the effects of apoE gene polymorphism on Lp(a) levels could also depend on apo(a) size. We have investigated the possible effect of genetic variation in the apoE and apoB genes on plasma Lp(a) concentrations in 466 white men with different apo(a) phenotypes. Overall there was no significant association between the common apoE polymorphism and Lp(a), but in the subgroup with apo(a)-S4, concentrations of Lp(a) differed significantly among the apoE genotypes (P = 0.05). Lp(a) was highest in the apoE genotypes epsilon 2 epsilon 3 and epsilon 3 epsilon 3 and lowest in genotype epsilon 3 epsilon 4, and the apoE polymorphism was estimated to account for about 2.4% of the variation in Lp(a). In contrast, in the subgroup with apo(a)-S2 Lp(a) was significantly lower (P = 0.04) in apoE genotype epsilon 2 epsilon 3 than in genotype epsilon 3 epsilon 3. Lp(a) concentrations did not differ among the XbaI (P = 0.65) or SP 24/27 (P = 0.26) polymorphisms of the apoB gene. The expected effects of both apoE and apoB polymorphism on LDL levels were significant in the whole population sample and in subjects with large-sized apo(a) isoforms (P < 0.01), whereas no effect was seen in those with low molecular weight apo(a) isoforms. We conclude that the influence of apoE genotypes on Lp(a) concentrations depends on the size of the apo(a) molecule in Lp(a), possibly because both apo(a)-S4 and apoE4 have high affinity for triglyceride-rich lipoproteins and may be taken up and degraded rapidly by remnant receptors.

Apolipoproteins A↗
PubMed1996

Are men carrying the apolipoprotein epsilon 4- or epsilon 2 allele less fertile than epsilon 3 epsilon 3 genotypes?

The epsilon 3 allele in the human gene coding for apolipoprotein E (apoE) is the most common worldwide, but epsilon 4 is probably the ancestral allele. Since apoE is involved in many important biological processes, selection forces could have favoured epsilon 3. We hypothesized that apoE genotypes may affect reproductive efficiency, and we therefore compared the distributions of 40-year-old married men with known genotypes by the numbers of their biological children. The distributions were statistically significantly different (P = 0.0026). On average, men with the epsilon 3 epsilon 3 genotype (n = 212) had 1.93 children, men with the epsilon 3 epsilon 4 or epsilon 4 epsilon 4 genotype (n = 105) had 1.50, and men with the epsilon 3 epsilon 2 or epsilon 2 epsilon 2 genotypes (n = 53) had 1.66 children. Of the men in the three groups, 6%, 26% and 19%, respectively, reported being childless. These findings are unlikely to be due to gross error in the reported prevalence of childlessness, differences in socioeconomic status or other likely sources of bias. They are compatible with higher fertility in men with the epsilon 3 epsilon 3 genotype than in those with the other common apoE genotypes.

Adult↗
PubMed1996

The apolipoprotein E polymorphism in Greenland Inuit in its global perspective.

Apolipoprotein E (apoE) genotypes were determined in Inuit population samples from Nuuk on the south-west coast of Greenland (n = 100) and from the Ammassalik region on the south-east coast (n = 78). The epsilon 2 allele was absent in the latter sample, and the epsilon 4 allele frequency was relatively high, about 23%. As in most other populations, mean plasma lipoprotein-related variables, except high-density lipoprotein (HDL) cholesterol, were higher in both Inuit men and women with epsilon 4 than in epsilon 3 epsilon 3 genotypes (P < 0.05 for triglycerides in men, and for non-HDL cholesterol and apolipoprotein B in women). The estimated apoE allele frequencies were combined with data from other studies of aboriginal peoples to outline a world map of apoE allele frequencies. A recent study of non-human primates suggests that epsilon 4, and not epsilon 3, is the ancestral allele in humans and we have used the map to generate additional hypotheses regarding the history of the apoE polymorphism in humans.

Alleles↗
PubMed1996

Expression and purification of an Epstein-Barr virus encoded 23-kDa protein and characterization of its immunological properties.

Serodiagnosis of Epstein-Barr virus (EBV) infection is currently based on the detection of antibodies to distinct EBV antigens by immunofluorescence and enzyme-linked immunosorbent assay-based tests, or in part on the detection of heterophile antibodies by the Paul-Bunnell-Davidson heterophile assay. In the past few years, the specificity and the sensitivity of serodiagnostic assay systems has been improved considerably by the use of purified recombinant EBV antigens. Screening of EBV-positive sera for antigenic reactivities by immunoprecipitation with extracts of EBV-positive cells revealed a 23-kDa protein (p23) that was recognized by antibodies from all EBV carriers tested. Open reading frame BLRF2 was identified as the coding region for this protein. After cloning and high-level expression of the BLRF2 open reading frame as DHFR fusion protein in Escherichia coli, the recombinant protein was purified to near homogeneity with the help of continuous elution electrophoresis. Sera from both EBV-positive and -negative donors were screened by immunoblot analysis and enzyme-linked immunosorbent assay for IgM and IgG antibodies against the EBV-encoded protein p23. Since anti-p23 antibodies were not detectable in 30 of 30 EBV-negative sera, and 294 of 302 EBV-positive sera had either IgM and/or IgG antibody responses to this protein, recombinant p23 seems to be a useful diagnostic marker for EBV-infection.

Antibodies, Viral↗
PubMed1996

Lymphoproliferative responses after infection with human parvovirus B19.

Immunity after infection with the parvovirus B19 is assumed to be conferred by a humoral immune response with development of neutralizing antibody. In contrast, little is known about the nature of T-cell-mediated responses to parvovirus B19 infection in humans. We used recombinant proteins VP1, VP2, and NS1, as well as a recombinant VP1-specific amino-terminal sequence, to test the proliferative responses of peripheral blood mononuclear cells after infection of otherwise healthy individuals with parvovirus B19. These proteins were used as antigens for the stimulation of freshly isolated cells. The results show that a B19 virus-specific cellular immunity develops that is directed against the capsid proteins VP1 and VP2. We also demonstrate that viral determinants are presented to CD4+ T cells by HLA class II molecules.

Antigens, Viral↗
PubMed1996

Comparison of the effects of the thrombin inhibitor r-hirudin in four animal models of neointima formation after arterial injury.

Thrombin has been implicated as a contributing factor to restenosis after vessel reopening procedures. We compared the ability of the direct thrombin inhibitor recombinant (r-) hirudin to reduce neointimal growth in different animal models of arterial injury. Carotid arteries of rats, rabbits, and hypercholesterolemic minipigs were injured by withdrawal of an inflated balloon catheter. In addition, we used a double-lesion model in rabbits, which involved balloon angioplasty of a preexisting lesion induced by carotid denudation 4 weeks earlier. r-Hirudin was given in all four animal models as a short-term application (bolus of 1 mg/kg i.v. immediately before injury, followed by infusion of 1 mg.kg-1.h-1 for 2 hours, and an injection of 6 mg/kg SC). Additionally, we investigated the effects of prolonged treatment (intravenous infusion for 3 and 14 days) in rats. Inhibition of thrombin was monitored by determination of activated partial thromboplastin time, and histomorphometric analysis of the arteries was performed after 2 (rats) or 4 (rabbits and minipigs) weeks. In rabbits, short-term r-hirudin treatment reduced neointimal area by 59% (single-injury model, P = .05) and 44% (double-injury model, P = .02). In rats and minipigs no inhibition of neointimal growth was observed after short-term r-hirudin application. A 3- or 14-day infusion of r-hirudin in rats, however, resulted in 25% (P = .007) and 27% (P = .003) reductions in neointimal area, respectively. In conclusion, there is considerable interspecies variation in the time frame of susceptibility for reduction of neointimal growth by inhibition of thrombin after arterial injury. These results demonstrate the importance of testing potential antirestenotic treatments in an array of different animal models.

Animals↗
PubMed1995

Polymorphisms in the lipoprotein lipase gene and their associations with plasma lipid concentrations in 40-year-old Danish men.

BACKGROUND: In some previous studies, HindIII and Pvu II restriction fragment length polymorphisms (RFLPs) in the lipoprotein lipase (LPL) gene were associated with coronary heart disease and plasma concentrations of HDL cholesterol and triglycerides. However, the populations studied were relatively small and heterogeneous in regard to age, sex, and ethnic background. METHODS AND RESULTS: Associations of a HindIII (intron 8) and a Pvu II (intron 6) RFLP in the LPL gene with plasma concentrations of cholesterol, HDL cholesterol, non-HDL cholesterol, and triglycerides were studied in 457 randomly selected 40-year-old Danish men. The HindIII and the Pvu II sites were in strong linkage disequilibrium. The frequencies of the H+ and P+ alleles (+ denotes presence of cutting site) were 0.717 and 0.464, respectively. In multivariate analysis, there was a clear gene dosage effect of the H+ allele on HDL. The lowest HDL cholesterol concentration was in the H+H+ group, the highest concentration was in the H-H- group, and the H+H- group had intermediate HDL concentrations (P = .03). There was a similar, but not statistically significant gene dosage effect on triglyceride concentrations, with the highest value seen in the H+H+ group. There were no other associations between LPL RFLPs and lipoprotein components. In males reporting family history of premature ischemic heart disease, the H+H+ genotype was overrepresented (odds ratio, 2.75; 95% confidence interval, 1.37 to 5.53). CONCLUSIONS: The results suggest that genetic variation in or near the LPL gene plays a role in interindividual differences in HDL cholesterol concentration and in risk of atherosclerosis and ischemic heart disease in men.

Adult↗