ArticleTranslational stroke research2010
Genetics studies in ischaemic stroke.
Article in Translational stroke research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- An rs13293512 polymorphism in the promoter of let-7 is associated with a reduced risk of ischemic stroke.Journal of thrombosis and thrombolysis · 2016Trial
- Two Novel SNPs in the PLCL2 Gene Associated with Large Artery Atherosclerotic Stroke Identified by Fine-Mapping.Journal of molecular neuroscience : MN · 2020Article
- Genome-wide association study identifies a variant in HDAC9 associated with large vessel ischemic stroke.Nature genetics · 2012Article
- Opportunities and challenges in omics.Translational stroke research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conventional risk factors such as high blood pressure account for a significant proportion of stroke risk, but much stroke risk remains unexplained. Epidemiological evidence suggests genetic predisposition accounts for some of this unexplained risk. Many candidate genes association studies have been performed but have lead to largely disappointing results. The genome-wide association study (GWAS) approach allows novel associations to be identified with as many as one million polymorphisms (genetic variants) across the genome. It has been successfully applied to other complex diseases, including other cardiovascular diseases, but stroke has lagged behind. A number of GWAS projects in stroke are now underway. Genetic variants originally identified using the GWAS approach in atrial fibrillation and coronary artery disease have been shown to also confer an increased risk of stroke. These associations have been with specific subtypes of stroke, emphasising the importance of accurate stroke subtyping. The use of intermediate phenotypes for stroke, such as white matter hyperintensities on MRI and carotid intima-media thickness, is also discussed.
Identifiers
What OpenQuestion holds
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.