Evidence map›Paper›PMID 24435185›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2014

Epistatic effects of multiple receptor genes on pathophysiology of asthma - its limits and potential for clinical application.

Takahiro Yoshikawa, Hiroshi Kanazawa, Shigeo Fujimoto, Kazuto Hirata

Open access · bronzeAbstract readReview
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.

  1. Association of TLR4 (896A/G and 1196C/T) Gene Polymorphisms with Asthma Risk: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
  2. A meta-analysis of IL-13 polymorphisms and pediatric asthma risk.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Pooled it
  3. Article
  4. Have recent investigations into remission from childhood asthma helped in understanding the pathogenesis of this disease?Medical science monitor : international medical journal of experimental and clinical research · 2015
    Review
  5. Lung diffusion capacity in children with respiratory symptoms and untreated GERD.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  6. Letter to the Editor regarding: epistatic effects in pathophysiology of asthma and the "missing heritability" of this disease.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Takahiro YoshikawaDepartment of Sports Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Hiroshi KanazawaDepartment of Respiratory Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Shigeo FujimotoDepartment of Sports Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Kazuto HirataDepartment of Respiratory Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Osaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To date, genome-wide association studies (GWAS) permit a comprehensive scan of the genome in an unbiased manner, with high sensitivity, and thereby have the potential to identify candidate genes for the prevalence or development of multifactorial diseases such as bronchial asthma. However, most studies have only managed to explain a small additional percentage of hereditability estimates, and often fail to show consistent results among studies despite large sample sizes. Epistasis is defined as the interaction between multiple different genes affecting phenotypes. By applying epistatic analysis to clinical genetic research, we can analyze interactions among more than 2 molecules (genes) considering the whole system of the human body, illuminating dynamic molecular mechanisms. An increasing number of genetic studies have investigated epistatic effects on the risk for development of asthma. The present review highlights a concept of epistasis to overcome traditional genetic studies in humans and provides an update of evidence on epistatic effects on asthma. Furthermore, we review concerns regarding recent trends in epistatic analyses from the perspective of clinical physicians. These concerns include biological plausibility of genes identified by computational statistics, and definition of the diagnostic label of 'physician-diagnosed asthma'. In terms of these issues, further application of epistatic analysis will prompt identification of susceptibility of diseases and lead to the development of a new generation of pharmacological strategies to treat asthma.

Indexed as

Models, BiologicalPhenotypeAsthmaBayes TheoremEpistasis, GeneticGenotypeHumansReceptors, ImmunologicSignal TransductionReceptors, Immunologic

Identifiers

PMID24435185
PMCPMC3907491
OpenAlexW2042165473

What OpenQuestion holds

Textmetadata
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.