Evidence map›Paper›PMID 18971955›Full record

ArticleHeredity2009

Determinants of variation in human serum paraoxonase activity.

D L Rainwater, S Rutherford, T D Dyer, E D Rainwater, S A Cole, J L Vandeberg, L Almasy, J Blangero, J W Maccluer, M C Mahaney

Abstract read
In one paragraph

Article in Heredity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Paraoxonase 1 polymorphisms and ischemic stroke risk: A systematic review and meta-analysis.Genetics in medicine : official journal of the American College of Medical Genetics · 2010
    Pooled it
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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

10 authors.

D L RainwaterDepartment of Genetics, Southwest Foundation for Biomedical Research, San Antonio, TX 78245-0549, USA. david@sfbrgenetics.org
S Rutherford
T D Dyer
E D Rainwater
S A Cole
J L Vandeberg
L Almasy
J Blangero
J W Maccluer
M C Mahaney

Funding

PEDIGREE ANALYSIS OF LIPOPROTEIN PHENOTYPESP01HL045522 · NHLBI · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI MAHANEY, MICHAEL CHARLES · 1991 to 2012
$27.6M
Quantitative Trait Locus Mapping in Human PedigreesR37MH059490 · NIMH · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI BLANGERO, JOHN · 2001 to 2010
$6.8M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR017515 · NCRR · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI SHADE, ROBERT E · 2003 to 2003
$3.1M
QUANTITATIVE TRAIT LOCUS MAPPING IN HUMAN PEDIGREESR01MH059490 · NIMH · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI BLANGERO, JOHN · 1998 to 2000
$426k
MOLECULAR AND BIOCHEMICAL GENETICS LABORATORY RENOVATIONC06RR013556 · NCRR · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI SHADE, ROBERT E · 1998 to 1998
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NCRR NIH HHS C06 RR013556NCRR NIH HHS C06 RR017515NCRR NIH HHS C06RR017515NHLBI NIH HHS P01 HL045522NIMH NIH HHS R01 MH059490NIMH NIH HHS R37 MH059490NIMH NIH HHS R37MH059490
6 · The paper itself

Abstract

Paraoxonase-1 (PON1) is associated with high-density lipoprotein (HDL) particles and is believed to contribute to antiatherogenic properties of HDLs. We assessed the determinants of PON1 activity variation using different substrates of the enzyme. PON1 activity in serum samples from 922 participants in the San Antonio Family Heart Study was assayed using a reliable microplate format with three substrates: paraoxon, phenyl acetate and the lactone dihydrocoumarin. There were major differences among results from the three substrates in degree of effect by various environmental and genetic factors, suggesting that knowledge of one substrate activity alone may not provide a complete sense of PON1 metabolism. Three significant demographic covariates (age, smoking status and contraceptive usage) together explained 1-6% of phenotypic variance, whereas four metabolic covariates representing lipoprotein metabolism (apoAII, apoAI, triglycerides and non-HDL cholesterol) explained 4-19%. Genes explained 65-92% of phenotypic variance and the dominant genetic effect was exerted by a locus mapping at or near the protein structural locus (PON1) on chromosome 7. Additional genes influencing PON1 activity were localized to chromosomes 3 and 14. Our study identified environmental and genetic determinants of PON1 activity that accounted for 88-97% of total phenotypic variance, suggesting that few, if any, major biological determinants are unrepresented in the models.

Indexed as

Genetic VariationAryldialkylphosphataseGenetic LinkageGenotypeHumansLipoproteinsMexican AmericansPolymorphism, GeneticSubstrate SpecificityTexasAryldialkylphosphataseLipoproteins

Identifiers

PMID18971955
PMCPMC2643132

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.