Evidence map›Paper›PMID 24954085›Full record

ArticleJournal of the neurological sciences2014

Novel genetic variants modify the effect of smoking on carotid plaque burden in Hispanics.

David Della-Morte, Liyong Wang, Ashley Beecham, Susan H Blanton, Hongyu Zhao, Ralph L Sacco, Tatjana Rundek, Chuanhui Dong

Open access · greenAbstract read
In one paragraph

Article in Journal of the neurological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 21% 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.

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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Genetic susceptibility to cerebrovascular disease.Current opinion in lipidology · 2016
    Review
  6. Article
  7. 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

8 authors at 4 institutions in 2 countries.

David Della-MorteDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States; Department of Systems Medicine, School of Medicine, University of Tor Vergata Rome, Italy; IRCCS San Raffaele Pisana, Rome, Italy.
Liyong WangJohn T. McDonald Department of Human Genetics, John P Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL, United States.
Ashley BeechamJohn T. McDonald Department of Human Genetics, John P Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL, United States.
Susan H BlantonDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States; John T. McDonald Department of Human Genetics, John P Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL, United States.
Hongyu ZhaoDepartment of Biostatistics, Yale School of Public Health, New Haven, CT, United States.
Ralph L SaccoDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States; John T. McDonald Department of Human Genetics, John P Hussman Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL, United States; Department of Public Health Sciences, Miller School of Medicine, University of Miami, Miami, FL, United States.
Tatjana RundekDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States; Department of Public Health Sciences, Miller School of Medicine, University of Miami, Miami, FL, United States.
Chuanhui DongDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States. Electronic address: cdong@med.miami.edu.
Dr. John T. Macdonald Foundation · USUniversity of Miami · USIRCCS Ospedale San Raffaele · ITYale University · US

Funding

Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
FAMILY STUDY OF STROKE RISK AND CAROTID ATHEROSCLEROSISR01NS040807 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BLANTON, SUSAN HALLORAN, RUNDEK, TATJANA · 2002 to 2022
$12.2M
Stroke Incidence and Risk Factors in a Tri-Ethnic RegionR37NS029993 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ELKIND, MITCHELL S, SACCO, RALPH L. · 2008 to 2014
$12.1M
NOVEL FACTORS FOR UNEXPLAINED PHENOTYPES OF SUBCLINICAL CAROTID ATHEROSCLEROSISR01NS065114 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BLANTON, SUSAN HALLORAN, RUNDEK, TATJANA · 2010 to 2014
$1.7M
Genetics Determinants of Extreme Phenotypes of Subclinical AtherosclerosisK24NS062737 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI RUNDEK, TATJANA · 2009 to 2013
$975k
NCATS NIH HHS UL1 TR000142NINDS NIH HHS K24 NS062737NINDS NIH HHS K24NS062737NINDS NIH HHS R01 NS040807NINDS NIH HHS R01 NS065114NINDS NIH HHS R01NS065114NINDS NIH HHS R37 NS029993NINDS NIH HHS R37NS029993
6 · The paper itself

Abstract

background and purposeSmoking greatly increases the risk of atherosclerotic plaque and the effect may vary from individual to individual. A genome-wide scan was performed for smoking×single nucleotide polymorphism (SNP) interactions on carotid plaque burden (CPB) to identify the potential genetic moderators in Hispanics.

methodsCarotid B-mode ultrasonography and genotyping by the Affymetrix 6.0 chip were performed in a discovery sample of 665 Caribbean Hispanics, followed by replication analyses in 264 Caribbean Hispanics. CPB was expressed as the sum of plaque areas over the segments in common and internal carotid arteries and bifurcation. Smoking was classified as 0, <20, and ≥20 cigarette pack-years. Assuming an additive genetic model, regression analysis was conducted to test for smoking×SNP interaction on the cube root transformed CPB while controlling for age, sex, and the top 3 principal components of ancestry.

resultsTwo SNPs showed a significant interaction with smoking on CPB with the similar effects in both discovery (P<1.0E-5) and replication (P<0.05) populations. Specifically, for SNP rs10205487 within MXD1, more smoking was significantly associated with greater CPB in A allele carriers (beta±SE: 0.24±0.08, P=0.005 in AG carriers; beta±SE: 0.48±0.12, P=0.0002 in AA carriers) but not in GG (P=0.06). For SNP rs7001413 within LY96 and JPH1, more smoking was significantly associated with greater CPB in GG carriers (beta±SE: 0.24±0.06, P=6.8E-5) but not in T carriers (P=0.06).

conclusionsOur study suggests that genetic variants may modulate the effect of smoking on CPB and highlights several genes for further investigation of their role in atherosclerosis, especially in smoking population.

Indexed as

SmokingAgedBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsFemaleGene FrequencyGenetic Predisposition to DiseaseHispanic or LatinoHumansLymphocyte Antigen 96MaleMembrane ProteinsMiddle AgedPhenotypePlaque, AtheroscleroticPolymorphism, Single NucleotideRepressor ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsjunctophilinLY96 protein, humanLymphocyte Antigen 96Membrane ProteinsMXD1 protein, humanRepressor ProteinsAtherosclerosisCarotid plaqueCarotid ultrasonographyHispanicsSmokingSmoking-gene interaction

Identifiers

PMID24954085
PMCPMC4143440
OpenAlexW2061277998

What OpenQuestion holds

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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.