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Biomedical subjects

J J Albers

Publications and source records attributed to J J Albers.

At least 19 recordsLinked to original sources
PubMed1998

Use of niacin, statins, and resins in patients with combined hyperlipidemia.

Patients in the original Familial Atherosclerosis Treatment Study (FATS) cohort were subgrouped into those with triglyceride levels < or = 120 mg/dL (n = 26) and those with triglyceride levels > or = 190 mg/dL (n = 40). Their therapeutic responses to niacin plus colestipol, lovastatin plus colestipol, colestipol alone, or placebo were determined. Therapeutic response was also determined in the same 2 triglyceride subgroups (n = 12 and n = 27, respectively) of patients selected for low levels of high-density lipoprotein (HDL) cholesterol and coronary artery disease. These triglyceride criteria were chosen to identify patient subgroups with high likelihood of "pattern A" (normal-size low-density lipoprotein [LDL] particles and triglyceride < or = 120 mg/dL) or "pattern B" (small dense LDL and triglyceride > or = 190 mg/dL). Our findings in these small patient subgroups are consistent with the emerging understanding that coronary artery disease patients presenting with high triglyceride levels have lower HDL-C, smaller less buoyant LDL-C, and greater very low-density lipoprotein (VLDL) cholesterol and VLDL apolipoprotein B, and are more responsive to therapy as assessed by an increase in HDL-C and reduction in triglycerides, VLDL-C, and VLDL apolipoprotein B. In the FATS high-triglyceride subgroup with these characteristics, a tendency toward greater therapeutic improvement in coronary stenosis severity was observed among those treated with either of the 2 forms of intensive cholesterol-lowering therapy. This improvement is associated with therapeutic reduction of LDL-C and elevation of HDL-C, but also appears to be associated with drug-induced improvement in LDL buoyancy.

Anticholesteremic Agents↗
PubMed1998

Transmission of two novel mutations in a pedigree with familial lecithin:cholesterol acyltransferase deficiency: structure-function relationships and studies in a compound heterozygous proband.

Two novel mutations were identified in a compound heterozygous male with lecithin:cholesterol acyltransferase (LCAT) deficiency. Exon sequence determination of the LCAT gene of the proband revealed two novel heterozygous mutations in exons one (C110T) and six (C991T) that predict non-conservative amino acid substitutions (Thr13Met and Pro307Ser, respectively). To assess the distinct functional impact of the separate mutant alleles, studies were conducted in the proband's 3-generation pedigree. The compound heterozygous proband had negligible HDL and severely reduced apolipoprotein A-I, LCAT mass, LCAT activity, and cholesterol esterification rate (CER). The proband's mother and two sisters were heterozygous for the Pro307Ser mutation and had low HDL, markedly reduced LCAT activity and CER, and the propensity for significant reductions in LCAT protein mass. The proband's father and two daughters were heterozygous for the Thr13Met mutation and also displayed low HDL, reduced LCAT activity and CER, and more modest decrements in LCAT mass. Mean LCAT specific activity was severely impaired in the compound heterozygous proband and was reduced by 50% in individuals heterozygous for either mutation, compared to wild type family members. It is also shown that the two mutations impair both catalytic activity and expression of the circulating protein.

Adult↗
PubMed1997

Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men. The Dietary Alternatives Study.

CONTEXT: The long-term effect of aggressively vs moderately fat-restricted diets has not been studied extensively in free-living subjects with different types of hyperlipidemia. OBJECTIVE: To compare the cholesterol-lowering effects of 4 levels of dietary fat intake restriction after 1 year. DESIGN: Randomized, parallel, comparison trial. SETTING: Male employees of a large industry. PARTICIPANTS: A total of 444 men had low-density lipoprotein cholesterol (LDL-C) levels above the 75th age-specific percentile. Subjects with triglyceride (TG) levels less than the 75th age-specific percentile were defined as hypercholesterolemic (HC) and those with TG levels at or above the 75th age-specific percentile were defined as combined hyperlipidemic (CHL). INTERVENTIONS: Hypercholesterolemic subjects were randomized to diets 1, 2, 3, and 4 taught to contain 30%, 26%, 22%, and 18% fat, and the CHL subjects were randomized to diets 1, 2, and 3. All 4 diets were taught to subjects and spouses or partners in 8 weekly 2-hour classes. MAIN OUTCOME MEASURES: Plasma lipoprotein levels after 1 year. RESULTS: Fat intake after 1 year declined from a mean of 34% to 36% of energy to 27%, 26%, 25%, and 22% in the 4 HC diet groups and 28%, 26%, and 25% in the 3 CHL diet groups. Mean+/-SD percent LDL-C reductions were 5.3%+/-16.2%, 13.4%+/-12.6%, 8.4%+/-11.2%, and 13.0%+/-15.7% in the HC diet groups and 7.0%+/-16.2%, 2.8%+/-15.8%, and 4.6%+/-13.5% in the CHL diet groups (P<.01 in all but 1 instance). Apoprotein B levels decreased 8.6%, 10.7%, 4.3%, and 5.3% in the HC groups and 14.6%, 11.4%, and 9.9% in the CHL groups (P<.05-.01 in each instance). Triglyceride levels increased significantly in subjects following HC diets 3 and 4, 21.7% and 38.7% (P<.05 and .01), but not in any CHL subjects. High-density lipoprotein cholesterol decreased 2.8% and 3.2% in subjects on HC diets 3 and 4, respectively (P<.05 in both cases). CONCLUSIONS: After 1 year, moderate restriction of dietary fat intake attains meaningful and sustained LDL-C reductions in HC subjects and apoprotein B reductions in both HC and CHL subjects. More extreme restriction of fat intake offers little further advantage in HC or CHL subjects and potentially undesirable effects in HC subjects.

Apolipoproteins↗
PubMed1997

Moderate dose, three-drug therapy with niacin, lovastatin, and colestipol to reduce low-density lipoprotein cholesterol <100 mg/dl in patients with hyperlipidemia and coronary artery disease.

The efficacy, safety, and tolerability of a moderate dose, 3-drug lipid-lowering regimen were evaluated among 29 male patients with hyperlipidemia and coronary artery disease. In an initial 12-month phase, regular niacin, 500 mg qid, lovastatin, 20 mg bid, and colestipol, 10 g/bid, were given with dose adjustment for lipid targets and side effects. This was followed by 2 random sequence crossover phases (8 months each) alternating regular niacin with a polygel controlled-release formulation of niacin for use in this regimen. Lipid, lipoprotein, apoprotein, and clinical chemistry determinations were obtained at baseline, during the initial phase, at the 2 crossover phases, and at 6 weeks after therapy. A final questionnaire queried specific side effects and overall preferences. Low-/high-density lipoprotein (LDL/HDL) changed from means of 215/46 mg/dl at baseline, to 94/59 mg/dl after run-in, to 85/52 mg/dl after 8 months of controlled-release niacin, and to 98/56 mg/dl after 8 months of regular niacin (regular niacin vs controlled-release niacin, p <0.005/<0.05). The target of LDL < or = 100 mg/dl was achieved at 8 months by 83% of these patients with controlled-release niacin and by 52% with regular niacin (p <0.01). Compliance was 95% with controlled-release niacin versus 85% with regular niacin (p <0.001). The controlled-release niacin and regular niacin regimens did not differ in terms of uric acid, glucose, insulin, or asparate aminotransferase levels. Overall, 21% of patients called the 3 drugs "very easy" and 72% "fairly easy" to take. The controlled-release niacin-containing regimen was preferred by 21 patients and the regular niacin by 4. In conclusion, these regimens achieve striking lipid changes among hyperlipidemic patients. Controlled release is the preferred niacin preparation in terms of LDL reduction, compliance, patient preference, and achieving the National Cholesterol Education Program guideline of LDL < or = 100 mg/dl. The 2 niacin preparations did not differ in evidence of toxicity.

Cholesterol, LDL↗
PubMed1997

Characterization of the mouse gene encoding phospholipid transfer protein.

The mouse gene encoding phospholipid transfer protein (PLTP) was cloned from 129/SvJ lambdaFIX(R) II library and characterized for the first time. It is comprised of 16 exons separated by 15 introns. Its gene organization strikingly resembles that encoding the human PLTP; the exon-intron junctions in these two genes are completely conserved. Sequencing analysis reveals that the putative promoter of mouse PLTP gene consists of a TATA-box, a high GC region, and several consensus sequences for the binding of transcription factors. Within the first 200 bp of the 5'-flanking region, the mouse and human PLTP genes share 81.1% identity of nt sequences and contain the consensus sequences for the transcription factors AP-2 and Sp1 at the same locations.

Animals↗
PubMed1997

Molecular and macromolecular specificity of human plasma phospholipid transfer protein.

Phospholipid transfer protein (PLTP), also known as lipid transfer protein 2 (LTP-2), mediates a transfer of phospholipids between high-density lipoproteins (HDL). The molecular and macromolecular specificities of recombinant human PLTP were studied using a fluorometric assay based on the excimer fluorescence of pyrenyl lipids. To determine lipoprotein specificity of PLTP, donor very low density lipoproteins (VLDL), low-density lipoproteins (LDL), and HDL were labeled with 1-palmitoyl-2-[10-(1-pyrenyl)decanoyl]phosphatidylcholine (PPyDPC) and incubated with unlabeled acceptor VLDL, LDL, and HDL in every pairwise combination. The highest rate of PPyDPC transfer mediated by PLTP occurred between donor HDL and acceptor HDL. Reassembled HDL (rHDL) consisting of 1-palmitoyl-2-oleoylphosphatidylcholine, apolipoprotein A-I, and pyrene lipids (100:1:4) were used to demonstrate that PLTP transfers diacylglyceride > phosphatidic acid > sphingomyelin > phosphatidylcholine (PC) > phosphatidylglycerol > cerobroside > phosphatidylethanolamine. Thus, PLTP transfers a variety of lipids with two carbon chains and a polar head group. Unsaturation of one PC acyl chain greatly increased transfer rate, whereas increasing chain length and exchanging sn-1/sn-2 position had only small effects. The rate of PPyDPC transfer by PLTP decreases with increasing free cholesterol content in rHDL and with decreasing HDL size. In contrast to spontaneous transfer, PLTP mediates the accumulation of PC in small rHDL particles. PLTP may be important in vivo in the recycling of PC from mature HDL to nascent HDL, the latter of which are the initial acceptors of cholesterol from peripheral tissue for reverse cholesterol transport to the liver.

Ca(2+) Mg(2+)-ATPase↗
PubMed1997

DNA sequences essential for transcription of human phospholipid transfer protein gene in HepG2 cells.

The present study was conducted to determine the essential DNA sequences required for the transcription of the human phospholipid transfer protein gene. Truncation studies revealed that DNA sequences between -230 and -159, particularly those at the upstream region, were responsible for the full promoter activity. This region was able to compete with AP-2 and GRE oligonucleotides for the binding to HepG2 cell nuclear extract as shown by gel mobility shift assay. Further analysis, using site-directed mutagenesis, indicated that DNA sequences identical to Sp1 and highly homologous to GRE and Ap-2 consensus sequences were essential for the transcription. These findings support the concept that several elements, spread over the entire functional promoter, synergistically drive the basal transcription.

Carcinoma, Hepatocellular↗
PubMed1997

Secondary prevention of heart disease amongst patients with lipid abnormalities: practice and trends in the United States.

Patients with established coronary disease and abnormalities of lipid metabolism represent a particularly important subgroup, since their mortality risk is typically 10 times greater than that amongst-subjects with comparable risk factors but no clinical history. Such patients are commonly treated initially with anti-anginal therapy; if ischaemic symptoms persist they often undergo revascularization (bypass or angioplasty). While invasive procedures restore blood flow and relieve ischemia, they do not, in most cases, reduce risk of subsequent MI or death, or alter the underlying atherogenic process(es). Despite this, there has been a progressive 54% decline in age-adjusted cardiac mortality over the period 1960-1995, which appears best attributable to US lifestyle changes. In particular, the past decade has provided compelling evidence for the merits of a fourth approach: comprehensive risk factor management. Clinical outcome studies have confirmed the substantial merit of aspirin prophyllaxis and of intensive lipid-lowering therapy in secondary prevention. Prospective angiographic trials and evidence from studies of vascular biology have provided insight into mechanisms of benefit. As a consequence, lipid therapy and aspirin use have increased greatly among middle aged and older US citizens, especially those with CAD. The growth of comprehensive medical management now rivals that of invasive revascularization in secondary prevention.

Aspirin↗
PubMed1997

Molecular basis of fish-eye disease in a patient from Spain. Characterization of a novel mutation in the LCAT gene and lipid analysis of the cornea.

The genetic and biochemical basis of fish-eye disease (FED) was investigated in a 63-year-old female proband with low plasma HDL cholesterol. Analyses of corneal and plasma lipids of the proband were consistent with impaired lecithin:cholesterol acyltransferase (LCAT) activity. Free cholesterol and phospholipid levels were elevated relative to control values, whereas cholesteryl ester levels were greatly reduced. Fatty acid compositions of corneal lipids from the proband and control subjects differ from the respective fatty acid compositions of their plasma lipids. This suggests that the metabolic pathways and acyl chain specificities for phospholipid, cholesteryl ester, and triglyceride metabolism within the cornea are distinct from those of plasma. Sequencing of the LCAT gene from the proband revealed a novel mutation at nucleotide 399, corresponding to an Arg99-->Cys substitution. Secretion of LCAT (Arg99-->Cys) by transfected COS-6 cells was approximately 50% of that of the wild type, but its specific activity against reassembled HDL was 93% lower than that of wild-type LCAT. The specific activities of wild-type and LCAT (Arg99-->Cys) against LDL were reduced similarly, suggesting that the appearance of the FED phenotype does not require enhanced activity against LDL. Our data support the hypothesis that FED is a partial LCAT deficiency in which poor esterification in specific types of HDL particles may contribute to the appearance of the corneal opacities.

Animals↗
PubMed1997

Catalytically inactive lecithin: cholesterol acyltransferase (LCAT) caused by a Gly 30 to Ser mutation in a family with LCAT deficiency.

Plasma lecithin:cholesterol acyltransferase (LCAT) plays an important role in early steps of reverse cholesterol transport, i.e., cholesterol efflux from peripheral tissues and cholesterol esterification in HDL. However, structural and functional relationships of LCAT have not been fully elucidated. We described a missense mutation of Gly 30-to-Ser in a patient with classical LCAT deficiency. The proband was homozygous for the mutation and had a very low level of HDL cholesterol (2 mg/dl), with a half of normal LCAT mass (2.75 micrograms/ml), but no detectable or very low LCAT activity in endogenous and exogenous substrate assays. Both his mother and sister were heterozygous for the mutation, and had slightly decreased levels of HDL cholesterol (34 and 36 mg/dl, respectively). Transient expression study using COS cells indicated that mutant cDNA produces similar amounts of media protein as compared to wild type, but no detectable LCAT activity. The missense mutation may result in a near-native conformation without large effects on cellular secretion but a catalytically defective protein. Thus, the N-terminal domain appears crucial for enzymatic activity, in addition to the catalytically active consensus sequence of Gly179 to Gly183 and a putative sterol binding domain of Glu154 to Lys173.

Animals↗
PubMed1996

Plasma phospholipid mass transfer rate: relationship to plasma phospholipid and cholesteryl ester transfer activities and lipid parameters.

Human plasma phospholipid transfer protein (PLTP) has been shown to facilitate the transfer of phospholipid from liposomes or isolated very low and low density lipoproteins to high density lipoproteins. Its activity in plasma and its physiological function are presently unknown. To elucidate the role of PLTP in lipoprotein metabolism and to delineate factors that may affect the rate of phospholipid transfer between lipoproteins, we determined the plasma phospholipid mass transfer rate (PLTR) in 16 healthy adult volunteers and assessed its relationship to plasma lipid levels, and to phospholipid transfer activity (PLTA) and cholesteryl ester transfer activity (CETA) measured by radioassays. The plasma PLTR in these subjects was 27.2 +/- 11.8 nmol/ml per h at 37 degrees C (mean +/- S.D.), and their PLTA and CETA were 13.0 +/- 1.7 mumol/ml per h and 72.8 +/- 15.7 nmol/ml per h, respectively. Plasma PLTR was correlated directly with total, non-HDL, and HDL triglyceride (rs = 0.76, P < 0.001), total and non-HDL phospholipid (rs > 0.53, P < 0.05), and inversely with HDL free cholesterol (rs = -0.54, P < 0.05), but not with plasma PLTA and CETA. When 85% to 96% of the PLTA in plasma was removed by polyclonal antibodies against recombinant human PLTP, phospholipid mass transfer from VLDL and LDL to HDL was reduced by 50% to 72%, but 80% to 100% of CETA could still be detected. These studies demonstrate that PLTP plays a major role in facilitating the transfer of phospholipid between lipoproteins, and suggest that triglyceride is a significant modulator of intravascular phospholipid transport. Furthermore, most of the PLTP and CETP in human plasma is associated with different particles. Plasma PLTA and CETA were also measured in mouse, rat, hamster, guinea pig, rabbit, dog, pig, and monkey. Compared to human, PLTA in rat and mouse was significantly higher and in rabbit and guinea pig was significantly lower while the remaining animal species had PLTA similar to humans. No correlation between PLTA and CETA was observed among animal species.

Adult↗
PubMed1996

Neutralization and transfer of lipopolysaccharide by phospholipid transfer protein.

Phospholipid transfer protein (PLTP) and lipopolysaccharide-binding protein (LPB) are lipid transfer proteins found in human plasma. PLTP shares 24% sequence similarity with LBP. PLTP mediates the transfer and exchange of phospholipids between lipoprotein particles, whereas LBP transfers bacterial lipopolysaccharide (LPS) either to lipoprotein particles or to CD14, a soluble and cell-surface receptor for LPS. We asked whether PLTP could interact with LPS and mediate the transfer of LPS to lipoproteins or to CD14. PLTP was able to bind and neutralize LPS: incubation of LPS with purified recombinant PLTP (rPLTP) resulted in the inhibition of the ability of LPS to stimulate adhesive responses of neutrophils, and addition of rPLTP to blood inhibited cytokine production in response to LPS. Transfer of LPS by rPLTP was examined using fluorescence dequenching experiments and native gel electrophoresis. The results suggested that rPLTP was able to mediate the exchange of LPS between micelles and the transfer of LPS to reconstituted HDL particles, but it did not transfer LPS to CD14. Consonant with these findings, rPLTP did not mediate CD14-dependent adhesive responses of neutrophils to LPS. These results suggest that while PLTP and LBP both bind and transfer LPS, PLTP is unable to transfer LPS to CD14 and thus does not mediate responses of cells to LPS.

Boron Compounds↗
PubMed1996

A novel missense mutation (Asn5-->Ile) in lecithin: cholesterol acyltransferase (LCAT) gene in a Japanese patient with LCAT deficiency.

We identified a novel missense mutation in the lecithin:cholesterol acyltransferase gene in a new case of lecithin:cholesterol acyltransferase (LCAT) deficiency. The patient was a 64-year-old diabetic Japanese male who showed an extremely low level of serum high-density lipoprotein-cholesterol, corneal opacities, anemia, and proteinuria. Both the patient's LCAT activity and mass were markedly low. DNA sequence analysis of the LCAT gene showed an A-to-T transition at base 97 in exon 1, and predicted a change in asparagine to isoleucine at the 5th amino acid of the protein. Restriction analysis of polymerase chain reaction-amplified DNA using Ase I showed that the patient was homozygous for this mutation. Our results suggested that asparagine 5 was an important amino acid and substitution with isoleucine caused marked reduction of LCAT activity and mass, resulting in LCAT deficiency.

Amino Acid Sequence↗
PubMed1996

Transgenic mice expressing human phospholipid transfer protein have increased HDL/non-HDL cholesterol ratio.

The role of plasma phospholipid transfer protein (PLTP) in lipoprotein metabolism is poorly understood. In vitro studies suggest that PLTP influences HDL size and composition and transfers phospholipids among lipoproteins. To provide an in vivo model for studies of PLTP physiology, transgenic mice that express human PLTP were generated. Human PLTP transcripts were detected in total RNA from adipose tissue, lung, heart, and spleen of the two distinct lines (A and C) of transgenic mice. Despite minimal expression of human PLTP in the liver of these transgenic mice and similar plasma phospholipid transfer activity in transgenic and non-transgenic mice (19.1 +/- 3.1 vs 18.9 +/- 2.7 mumol/ml/h), differences in lipoprotein levels were observed between transgenic and control mice receiving the same chow diet. Male transgenic mice of line C had significantly higher HDL cholesterol than control mice (76.4 +/- 4.6 vs 71.9 +/- 7.0 mg/dl, p < 0.05) and the male transgenic mice of lines A and C had a significantly lower non-HDL cholesterol (15.1 +/- 4.1 and 15.6 +/- 4.7 vs 20.9 +/- 5.5 mg/dl, P < 0.01 and P < 0.02) and a significantly higher HDL cholesterol/non-HDL cholesterol ratio than the control mice (5.3 +/- 1.3 and 5.5 +/- 2.2 vs 3.9 +/- 1.9 mg/dl, P < 0.01 and P < 0.02). Female mice from transgenic line C had higher HDL cholesterol than control mice (64.6 +/- 4.8 vs 57.4 +/- 5.1 mg/dl, P < 0.01) while female mice from line A tended to have higher HDL cholesterol/non-HDL cholesterol ratio than control mice (5.5 +/- 3.7 vs 3.8 +/- 1.4). These observations suggest that expression of PLTP in peripheral tissues play an important role in lipoprotein metabolism. Expression of human PLTP produced a more favorable lipoprotein profile and thus, enhanced expression of PLTP could potentially retard atherosclerosis.

Animals↗
PubMed1996

Molecular biology of phospholipid transfer protein.

Lipid transfer proteins play an essential role in the intravascular dynamics of lipids among lipoproteins and between lipoproteins and cell membranes. Phospholipid transfer protein has been known for over a decade but, unlike cholesteryl ester transfer protein, has been investigated relatively little with regard to its physiological importance. The recent determination of the phospholipid transfer protein complementary DNA sequence as well as the further characterization of its gene structure will direct future studies toward the understanding of its structure-function correlations, physiological regulation, and clinical assessment at the molecular level. As a member of the lipid-transfer lipopolysaccharide-binding protein gene family, phospholipid transfer protein will attract investigators to studying its possible involvement in lipopolysaccharide or endotoxin interactions in addition to its phospholipid transfer activity.

Animals↗
PubMed1996

A cysteine-containing truncated apo A-I variant associated with HDL deficiency.

We identified a 50-year-old Japanese woman with a novel mutation in the apolipoprotein (apo) A-I gene causing high-density lipoprotein (HDL) deficiency. The patient had extremely low HDL cholesterol and apo A-I levels (0.14 mmol/L and 0.8 mg/dL, respectively) but no evidence of coronary heart disease. However, she had bilateral xanthomas of the Achilles tendon, elbow, and knee joint as well as corneal opacities. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of serum followed by immunoblotting revealed that the patient's apo A-I had a lower molecular weight (24,000) than normal apo A-I. A partial gene duplication encompassing 23 nucleotides was found by DNA sequence analysis, resulting in a tandem repeat of bases 333 to 355 from the 5' end of exon 4. This tandem repeat caused a frameshift mutation with premature termination after amino acid 207. The frameshift gives rise to a predicted protein sequence that contains two cysteines. We designated this mutant as apo A-ISasebo. Apo A-ISasebo formed heterodimers with apo A-II and apo E in the patient's plasma and was associated with both the low-density lipoprotein and HDL fractions. The patient's cholesterol esterification rate and lecithin-cholesterol acyltransferase activity were reduced to about 30% of normal, although specific enzyme activity was unaffected, suggesting that it remained functionally normal. In addition, cholesteryl ester transfer activity was reduced to about half of normal. Thus, apo A-ISasebo was associated with complex derangements of lipoprotein metabolism.

Amino Acid Sequence↗
PubMed1996

Relation between number of apolipoprotein(a) kringle 4 repeats and mobility of isoforms in agarose gel: basis for a standardized isoform nomenclature.

The size of apolipoprotein(a) [apo(a)] varies from 187 to 648 kDa because of interallelic differences in the number of kringle 4-encoding sequences in the apo(a) gene. Plasma apo(a) isoform sizes were determined by a high-resolution sodium dodecyl sulfate-agarose gel electrophoretic method, followed by immunoblotting. The relation between the number of apo(a) kringle 4-encoding sequences in the apo(a) gene, as assessed by pulsed-field gel electrophoresis and genomic blotting, and the mobility of apo(a) isoforms in agarose gel was evaluated in 29 individuals who had 48 expressed apo(a) isoforms that contained between 12 and 41 kringle 4 repeats. The log of the kringle number was linearly related to the distance the isoform migrated on the agarose gel (r= 0.999). A nomenclature is proposed to designate apo(a) isoforms by the respective number of kringle 4 repeats.

Alleles↗