Evidence map›Paper›PMID 19323961›Full record

ReviewCurrent diabetes reports2009

Genome-wide association studies in type 1 diabetes.

Struan F A Grant, Hakon Hakonarson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Recent advances in childhood diabetes mellitus.Annals of Ibadan postgraduate medicine · 2008
    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

2 authors.

Struan F A GrantCenter for Applied Genomics, 1216E Abramson Research Center, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA.
Hakon Hakonarson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is a chronic disease that typically manifests itself in childhood through the autoimmune destruction of pancreatic beta cells, resulting in a lack of production of insulin. T1D is a multifactorial disease with a strong genetic component that is thought to interact with specific environmental triggers. Several genetic determinants of T1D were already established before the era of genome-wide association studies, primarily with the HLA class II genes, encoding highly polymorphic antigen-presenting proteins that account for almost 50% of the genetic risk for T1D. The recent development of high-throughput single nucleotide polymorphism genotyping array technologies has enabled investigators to perform high-density genome-wide association studies in search of the remaining T1D loci. Combined with the well-established genes known for many years, 16 loci have now been uncovered to date as being robustly associated with the pathogenesis of this phenotype.

Indexed as

Genome-Wide Association StudyDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HumansMajor Histocompatibility ComplexMeta-Analysis as TopicPolymorphism, Single Nucleotide

Identifiers

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.