Evidence map›Paper›PMID 25010442›Full record

ReviewCurrent opinion in rheumatology2014

Genetics of juvenile idiopathic arthritis: new tools bring new approaches.

Halima Moncrieffe, Sampath Prahalad, Susan D Thompson

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. New or vanishing frontiers:International journal of pediatrics & adolescent medicine · 2021
    Article
  7. Review
  8. Review of environmental factors and juvenile idiopathic arthritis.Open access rheumatology : research and reviews · 2019
    Review
  9. Article
  10. Article
  11. 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

3 authors at 2 institutions in 1 country.

Halima MoncrieffeaDivision of Rheumatology and the Center for Autoimmune Disease Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio bDivision of Pediatric Rheumatology, Department of Pediatrics and Genetics,, Emory University School of Medicine, Atlanta, Georgia, USA.
Sampath Prahalad
Susan D Thompson
Cincinnati Children's Hospital Medical Center · USPediatrics and Genetics · US

Funding

Pediatric Rheumatology Tissue RepostoryP01AR048929 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2003 to 2015
$13.6M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
NIAMS NIH HHS P01 AR048929NIAMS NIH HHS P01AR048929NIAMS NIH HHS P30 AR047363NIAMS NIH HHS P30AR047363
6 · The paper itself

Abstract

purpose of reviewIn juvenile idiopathic arthritis (JIA), there are now more than 25 regions represented by single nucleotide polymorphisms that show strong genetic associations. The causal variants and corresponding functions have not yet been defined for the majority of these regions. Here, we review current JIA association findings and the recent progress in the annotation of noncoding portion of the human genome as well as the new technologies necessary to apply this knowledge to JIA association findings. RECENT

findingsAn international collaboration was able to amass sufficient numbers of JIA and control samples to identify significantly robust genetic associations for JIA. The Encyclopedia of DNA Elements project and the National Institutes of Health (NIH) Roadmap Epigenetics Program have now annotated more than 80% of the noncoding genome, important in understanding the impact of risk loci, the majority of which fall outside of protein coding regions. Recent technological advances in high throughput sequencing, chromatin structure determination, transcription factor and enhancer binding site mapping and genome editing will likely provide a basis for understanding JIA genetic risk. SUMMARY: Understanding the role of genetic variation in the cause of JIA will provide insight for disease mechanism and may explain disease heterogeneity between JIA subtypes and between autoimmune diseases in general.

Indexed as

Arthritis, JuvenileChildCRISPR-Cas SystemsGene ExpressionGenome-Wide Association StudyHLA-DRB1 ChainsHumansPolymorphism, Single NucleotideRisk FactorsRNA EditingRNA, UntranslatedHLA-DRB1 ChainsRNA, Untranslated

Identifiers

PMID25010442
PMCPMC4445412
OpenAlexW1996582669

What OpenQuestion holds

Textmetadata
LicenceTDM
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.