Evidence map›Paper›PMID 27895620›Full record

ReviewFrontiers in endocrinology2016

Excessive Cytosolic DNA Fragments as a Potential Trigger of Graves' Disease: An Encrypted Message Sent by Animal Models.

Yuqian Luo, Aya Yoshihara, Kenzaburo Oda, Yuko Ishido, Koichi Suzuki

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. 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

5 authors at 1 institution in 1 country.

Yuqian LuoDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University , Tokyo , Japan.
Aya YoshiharaDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan; Department of Education Planning and Development, Faculty of Medicine, Toho University, Tokyo, Japan.
Kenzaburo OdaDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan; Department of Internal Medicine, Division of Diabetes, Metabolism and Endocrinology, Toho University, Tokyo, Japan.
Yuko IshidoDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University , Tokyo , Japan.
Koichi SuzukiDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University , Tokyo , Japan.
Teikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graves' hyperthyroidism is caused by autoantibodies directed against the thyroid-stimulating hormone receptor (TSHR) that mimic the action of TSH. The establishment of Graves' hyperthyroidism in experimental animals has proven to be an important approach to dissect the mechanisms of self-tolerance breakdown that lead to the production of thyroid-stimulating TSHR autoantibodies (TSAbs). "Shimojo's model" was the first successful Graves' animal model, wherein immunization with fibroblasts cells expressing TSHR and a major histocompatibility complex (MHC) class II molecule, but not either alone, induced TSAb production in AKR/N (H-2

Indexed as

experimental animal modelsgenomic DNAGraves’ diseasemajor histocompatibility complex class IIthyroid-stimulating hormone receptor

Identifiers

PMID27895620
PMCPMC5107990
OpenAlexW2556201396

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.