Evidence map›Paper›PMID 24176416›Full record

ReviewNeurologic clinics2013

Clinical neurogenetics: stroke.

Natalia S Rost

Abstract readReview
In one paragraph

Review in Neurologic clinics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Article
  2. 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

1 author.

Natalia S RostDepartment of Neurology, JP Kistler Stroke Research Center, Massachusetts General Hospital, 175 Cambridge Street, Suite 300, Boston, MA 02114, USA. Electronic address: nrost@partners.org.

Funding

Genetic variation in white matter hyperintensity and risk of ischemic strokeK23NS064052 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROST, NATALIA S · 2009 to 2013
$915k
NINDS NIH HHS K23 NS064052NINDS NIH HHS K23NS064052
6 · The paper itself

Abstract

Understanding the genetic architecture of cerebrovascular disease holds promise of novel stroke prevention strategies and therapeutics that are both safe and effective. Apart from a few single-gene disorders associated with cerebral ischemia or intracerebral hemorrhage, stroke is a complex genetic phenotype that requires careful ascertainment and robust association testing for discovery and validation analyses. The recently uncovered shared genetic contribution between clinically manifest stroke syndromes and closely related intermediate cerebrovascular phenotypes offers effective and efficient approaches to complex trait analysis.

Indexed as

Brain IschemiaCerebrovascular DisordersHumansRisk FactorsStrokeCerebrovascular diseaseGeneticsGenome-wide association studyIntracerebral hemorrhageIschemic strokePhenotypeStroke subtypeWhite matter hyperintensity

Identifiers

PMID24176416
PMCPMC3815700

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.