Evidence map›Paper›PMID 30050001›Full record

ReviewGenes2018

High-Throughput Approaches onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes.

Anna Dziewulska, Aneta M Dobosz, Agnieszka Dobrzyn

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Pharmacogenetics of new classes of antidiabetic drugs.Bosnian journal of basic medical sciences · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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.

Anna DziewulskaLaboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland. a.dziewulska@nencki.gov.pl.
Aneta M DoboszLaboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland. a.dobosz@nencki.gov.pl.
Agnieszka DobrzynLaboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland. a.dobrzyn@nencki.gov.pl.
Polish Academy of Sciences · PLInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is a complex disorder that is caused by a combination of genetic, epigenetic, and environmental factors. High-throughput approaches have opened a new avenue toward a better understanding of the molecular bases of T2D. A genome-wide association studies (GWASs) identified a group of the most common susceptibility genes for T2D (i.e.,

Indexed as

beta-cell failureepigeneticsGWASinsulin resistanceNGStype 2 diabetes

Identifiers

PMID30050001
PMCPMC6115814
OpenAlexW2884798826

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.