Evidence map›Paper›PMID 9463319›Full record

ArticleAmerican journal of human genetics1998

Candidate-gene studies of the atherogenic lipoprotein phenotype: a sib-pair linkage analysis of DZ women twins.

M A Austin, P J Talmud, L A Luong, L Haddad, I N Day, B Newman, K L Edwards, R M Krauss, S E Humphries

Registry-linked trialOpen access · bronzeAbstract readTwin Study
In one paragraph

Article in American journal of human genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00005465 (Genetic Mapping of Atherogenic Lipoprotein Phenotypes), which is not on this map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.8field-weighted citation impact, top 4% 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.

NCT00005465 completednot on this map

Genetic Mapping of Atherogenic Lipoprotein Phenotypes

TypeobservationalSponsorUniversity of WashingtonRan1991 to 1996ConditionsAtherosclerosis, Cardiovascular Diseases, Heart Diseases
3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. A cholesterol-lowering gene maps to chromosome 13q.American journal of human genetics · 2000
    Article
  10. 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

9 authors at 4 institutions in 2 countries.

M A AustinDepartment of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, WA 98195, USA. maustin@u.washington.edu
P J Talmud
L A Luong
L Haddad
I N Day
B Newman
K L Edwards
R M Krauss
S E Humphries
University College London · GBUniversity of Washington · USLawrence Berkeley National Laboratory · USUniversity of North Carolina at Chapel Hill · US

Funding

X-LINKED EXTENSION OF THE REVISED HASEMAN-ELSTON ALGORITHM FOR LINKAGE ANALYSISP41RR003655 · NCRR · LOUISIANA STATE UNIV HSC NEW ORLEANS · PI ELSTON, ROBERT C. · 1987 to 2011
$11.5M
Identification of Issues and Expectations of Subjects Participating in Genetic StR01CA149051 · NCI · UNIVERSITY OF WASHINGTON · PI EDWARDS, KAREN L · 2011 to 2013
$1.2M
GENETIC EPIDEMIOLOGY OF CHD RISK FACTORS IN WOMEN TWINSR01HL041830 · NHLBI · KAISER FOUNDATION HOSPITALS · PI SELBY, JOE V · 1989 to 1991
–
GENETIC MAPPING OF ATHEROGENIC LIPOPROTEIN PHENOTYPESR01HL046880 · NHLBI · UNIVERSITY OF WASHINGTON · PI AUSTIN, MELISSA A · 1991 to 1994
–
NCI NIH HHS R01 CA149051NCRR NIH HHS 1 P41 RR03655NHLBI NIH HHS HL-41830NHLBI NIH HHS HL-46880
6 · The paper itself

Abstract

There is a growing body of evidence supporting the roles of small, dense LDL and plasma triglyceride (TG), both features of the atherogenic lipoprotein phenotype, as risk factors for coronary heart disease. Although family studies and twin studies have demonstrated genetic influences on these risk factors, the specific genes involved remain to be determined definitively. The purpose of this study was to investigate genetic linkage between LDL size, TG, and related atherogenic lipoproteins and candidate genes known to be involved in lipid metabolism. The linkage analysis was based on a sample of 126 DZ women twin pairs, which avoids the potentially confounding effects of both age and gender, by use of a quantitative sib-pair linkage-analysis approach. Eight candidate genes were examined, including those for microsomal TG-transfer protein (MTP), hepatic lipase, hormone-sensitive lipase, apolipoprotein (apo) B, apo CIII, apo E, insulin receptor, and LDL receptor. The analysis suggested genetic linkage between markers for the apo B gene and LDL size, plasma levels of TG, of HDL cholesterol, and of apo B, all features of the atherogenic lipoprotein phenotype. Furthermore, evidence for linkage was maintained when the analysis was limited to women with a major LDL-subclass diameter >255 A, indicating that the apo B gene may influence LDL heterogeneity in the intermediate-to-large size range. In addition, linkage was found between the MTP gene and TG, among all the women. These findings add to the growing evidence for genetic influences on the atherogenic lipoprotein phenotype and its role in genetic susceptibility to atherosclerosis.

Indexed as

Polymorphism, GeneticApolipoproteins BApolipoproteins EArteriosclerosisCarrier ProteinsDiseases in TwinsDisease SusceptibilityFemaleGenetic LinkageHumansLipoproteins, LDLMicrosomesMiddle AgedPhenotypeReceptors, LDLRegression AnalysisApolipoproteins BApolipoproteins ECarrier ProteinsLipoproteins, LDLmicrosomal triglyceride transfer proteinReceptors, LDLTriglycerides

Identifiers

PMID9463319
PMCPMC1376888
OpenAlexW1992445024

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.