Evidence map›Paper›PMID 22895852›Full record

ReviewCurrent diabetes reports2012

Influence of type 1 diabetes genes on disease progression: similarities and differences between countries.

Johanna Lempainen, Jorma Ilonen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Dynamics of Islet Autoantibodies During Prospective Follow-Up From Birth to Age 15 Years.The Journal of clinical endocrinology and metabolism · 2020
    Article
  3. 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 at 2 institutions in 1 country.

Johanna LempainenImmunogenetics Laboratory, University of Turku, Tykistökatu 6A, 20520, Turku, Finland. johanna.lempainen@utu.fi
Jorma Ilonen
Turku Centre for Biotechnology · FIUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease causing the destruction of pancreatic beta cells. The onset of clinical T1D is preceded by a time period called pre-diabetes, the duration of which varies widely. However, not all subjects developing beta-cell autoimmunity progress to clinical T1D. The inherited risk for T1D is determined by the human leukocyte antigen (HLA) class II genes, HLA class I genes, and several loci outside the HLA area. Although the role of the genetic risk variants in disease pathogenesis is not completely understood, some of the variants affecting disease risk are thought to influence the initiation of beta-cell autoimmunity whereas others seem to play a role during the later stages of the autoimmune process. In this review we describe the current knowledge on the genetic factors mediating the fate of already-established beta-cell autoimmunity and the rate of beta-cell destruction.

Indexed as

AnimalsDiabetes Mellitus, Type 1Disease ProgressionGenetic Predisposition to DiseaseHLA AntigensHumansProtein Tyrosine Phosphatase, Non-Receptor Type 22HLA AntigensProtein Tyrosine Phosphatase, Non-Receptor Type 22

Identifiers

PMID22895852
OpenAlexW2088200218

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.