Evidence map›Paper›PMID 1928089›Full record

ArticleAmerican journal of human genetics1991

Expressed hypervariable polymorphism of apolipoprotein (a).

M I Kamboh, R E Ferrell, B A Kottke

2 registry-linked trialsAbstract read
In one paragraph

Article in American journal of human genetics, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
29.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT00005147 completednot on this map

Epidemiology of Atherosclerosis

TypeobservationalSponsorNational Heart, Lung, and Blood Institute (NHLBI)Ran1979 to 1991ConditionsAtherosclerosis, Cardiovascular Diseases, Heart Diseases, Coronary Arteriosclerosis
NCT00005209 completednot on this map

Genetic Epidemiology of Coronary Heart Disease

TypeobservationalSponsorNational Heart, Lung, and Blood Institute (NHLBI)Ran1987 to 2007ConditionsCardiovascular Diseases, Heart Diseases, Coronary Disease
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 215 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Lipoprotein (a): a Unique Independent Risk Factor for Coronary Artery Disease.Indian journal of clinical biochemistry : IJCB · 2016
    Review
  10. Article
  11. Lipoprotein(a): an elusive cardiovascular risk factor.Arteriosclerosis, thrombosis, and vascular biology · 2004
    Review
  12. Article
  13. Article
  14. Article
  15. The role of lipoprotein[a] in atherosclerosis.Current atherosclerosis reports · 2000
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

M I KambohDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, PA 15621.
R E Ferrell
B A Kottke
University of Pittsburgh · US

Funding

GENETIC EPIDEMIOLOGY OF CORONARY HEART DISEASER01HL039107 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SING, CHARLES F · 1987 to 2005
$5.8M
GENETIC EPIDEMIOLOGY OF LIPOPROTEIN/LIPID LEVELSR01HL044672 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMBOH, M. ILYAS · 1991 to 2000
$294k
EPIDEMIOLOGY OF ATHEROSCLEROSISR01HL024489 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI KOTTKE, BRUCE A. · 1985 to 1990
–
NHLBI NIH HHS HL24489NHLBI NIH HHS HL39107NHLBI NIH HHS HL44672
6 · The paper itself

Abstract

Elevated plasma lipoprotein (a) (LP(a] levels are an independent predictor of the development of premature atherosclerosis in humans. The LP(a) particle consists of two disulfide-linked proteins, apolipoprotein (APO) B and APO(a). The APO(a) is a highly glycosylated protein which carries the LP(a) antigen. Genetic polymorphism in the APO(a) molecule has been reported, and, depending on the sensitivity of the method used, 6-11 alleles at the APO(a) structural locus have been documented in the literature. In this investigation, we have used a high-resolution SDS-agarose electrophoresis method followed by immunoblotting to screen APO(a) polymorphism in 54 families with 130 offspring. This method identified a total of 23 different APO(a) isoforms, and their genetic basis was confirmed in families. In addition to the detectable products of 23 APO(a) alleles, the family data predict the existence of a "null" allele. Of the total 270 individuals tested, 209 (77.4%) revealed double-banded phenotypes and 61 (22.6%) revealed single-banded phenotypes. In the unrelated sample of 140 individuals, however, 114 (81.4%) and 26 (18.6%) had double- and single-banded phenotypes, respectively. When the segregation pattern of single-banded phenotypes in the unrelated sample was followed in families, only nine (6.4%) were found to be true homozygotes, and the remaining 17 (12.2%) were classified as heterozygotes for the null allele. Of the 276 possible phenotypes predicted for 23 alleles in a large population, we observed 115 (42%) phenotypes in our restricted sample. On the basis of our results from the family data, we hypothesize the existence of at least 24 alleles, including a null allele, at the APO(a) structural locus.(ABSTRACT TRUNCATED AT 250 WORDS)

Indexed as

Polymorphism, GeneticAdultAllelesApolipoproteins AChildElectrophoresis, Agar GelFemaleGene FrequencyHumansImmunoblottingMalePedigreeRandom AllocationSensitivity and SpecificityTerminology as TopicApolipoproteins A

Identifiers

PMID1928089
PMCPMC1683273
OpenAlexW2417365582

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.