Evidence map›Paper›PMID 18948608›Full record

ArticleStroke2009

Genome screen to detect linkage to common susceptibility genes for intracranial and aortic aneurysms.

Bradford B Worrall, Tatiana Foroud, Robert D Brown, E Sander Connolly, Richard W Hornung, John Huston, Dawn Kleindorfer, Daniel L Koller, Dongbing Lai, Charles J Moomaw and 4 more

Erratum issuedAbstract read
In one paragraph

Article in Stroke, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Spontaneous arterial dissection: phenotype and molecular pathogenesis.Cellular and molecular life sciences : CMLS · 2010
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

14 authors.

Bradford B WorrallUniversity of Virginia Health System, Department of Neurology, Box 800394, Charlottesville, VA 22908, USA. bbw9r@virginia.edu
Tatiana Foroud
Robert D Brown
E Sander Connolly
Richard W Hornung
John Huston
Dawn Kleindorfer
Daniel L Koller
Dongbing Lai
Charles J Moomaw
Laura Sauerbeck
Daniel Woo
Joseph P Broderick
Familial Intracranial Aneurysm Study Investigators

Funding

Familial Intracranial Aneurysm Study II (FIA II)R01NS039512 · NINDS · UNIVERSITY OF CINCINNATI · PI BRODERICK, JOSEPH PAUL · 2002 to 2010
$24.6M
Genetic Epidemiology of Complex TraitsZIAHG200327 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BAILEY-WILSON, JOAN ELLEN · 2009 to 2022
$10.5M
Genetic and Environmental Risk Factors for Hemorrhagic StrokeU01NS036695 · NINDS · UNIVERSITY OF CINCINNATI · PI ROSAND, JONATHAN, WOO, DANIEL · 2016 to 2020
$7.0M
GENOTYPING FOR LOCATING HUMAN DISEASE GENESN01HG065403 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID L · 1996 to 2000
$1.7M
Cerebrovascular Atherosclerosis: Genes &Gene ExpressionK08NS045802 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WORRALL, BRADFORD B · 2005 to 2009
$841k
NHGRI NIH HHS N01 HG065403NINDS NIH HHS K08 NS045802NINDS NIH HHS R01 NS039512NINDS NIH HHS R01 NS39512NINDS NIH HHS U01 NS036695
6 · The paper itself

Abstract

background and purposeRisk for both intracranial aneurysms (IAs) and aortic aneurysms (AAs) is thought to be heritable with mounting evidence for genetic predisposition. The concept of shared risk for these conditions is challenged by differences in age of diagnosis and demographic characteristics. We performed a genomewide linkage analysis in multiplex families with both IA and AA from the Familial Intracranial Aneurysm study.

methodsAvailable medical records of subjects who reported IA or abdominal/thoracic AA were reviewed with adjudication as definite/probable, possible, or not a case. To identify genes contributing to the susceptibility for IA and AA, genomewide linkage analysis was performed in the 26 multiplex IA families who had members who also had thoracic or abdominal AA. Individuals (n=91) were defined as affected if they had an IA (definite/probable) or an aortic or thoracic AA (definite/probable).

resultsMaximum logarithm of odds (LOD) scores were found on chromosomes 11 (144 cM; LOD=3.0) and 6 (33 cM; LOD=2.3). In both chromosomal regions, analyses of these same 26 families considering only IA as the disease phenotype produced LOD scores of 1.8 and 1.6, respectively.

conclusionsOur linkage analysis in these 26 families using the broadest disease phenotype, including IA, abdominal AA, and thoracic AA, supports the concept of shared genetic risk. The chromosome 11 locus appears to confirm earlier independent associations in IA and AA. The chromosome 6 finding is novel. Both warrant further investigation.

Indexed as

AdultAgedAortic AneurysmChromosome MappingChromosomes, Human, Pair 11Chromosomes, Human, Pair 6DNA Mutational AnalysisFemaleGenetic Predisposition to DiseaseGenetic TestingGenotypeHumansInheritance PatternsIntracranial AneurysmMaleMiddle Aged

Identifiers

PMID18948608
PMCPMC2629798

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Registered trials

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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.