Evidence map›Paper›PMID 34177886›Full record

ArticleFrontiers in immunology2021

Milena Iwaszko, Joanna Wielińska, Jerzy Świerkot, Katarzyna Kolossa, Renata Sokolik, Bartosz Bugaj, Monika Chaszczewska-Markowska, Sławomir Jeka, Katarzyna Bogunia-Kubik

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

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  18. Impact ofJournal of personalized medicine · 2022
    Article
  19. Article
  20. Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 2022
    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

9 authors at 5 institutions in 1 country.

Milena IwaszkoLaboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Joanna WielińskaLaboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Jerzy ŚwierkotDepartment of Rheumatology and Internal Medicine, Wroclaw Medical University, Wrocław, Poland.
Katarzyna KolossaDepartment of Rheumatology and Connective Tissue Diseases, Jan Biziel University Hospital No. 2, Bydgoszcz, Poland.
Renata SokolikDepartment of Rheumatology and Internal Medicine, Wroclaw Medical University, Wrocław, Poland.
Bartosz BugajDepartment of Rheumatology and Internal Medicine, Wroclaw Medical University, Wrocław, Poland.
Monika Chaszczewska-MarkowskaLaboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Sławomir JekaDepartment of Rheumatology and Connective Tissue Diseases, Jan Biziel University Hospital No. 2, Bydgoszcz, Poland.
Katarzyna Bogunia-KubikLaboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
Polish Academy of Sciences · PLWroclaw Medical University · PLJan Biziel University Hospital No. 2 in BydgoszczLudwik Hirszfeld Institute of Immunology and Experimental Therapy · PLNicolaus Copernicus University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) belong to inflammatory rheumatic diseases, the group of conditions of unknown etiology. However, a strong genetic component in their pathogenesis has been well established. A dysregulation of cytokine networks plays an important role in the development of inflammatory arthritis. Interleukin 33 (IL-33) is a recently identified member of the IL-1 family. To date, the significance of IL-33 in inflammatory arthritis has been poorly studied. This research aimed to investigate the potential of Materials and Methods: In total, 735 patients diagnosed with RA, AS, and PsA and 229 healthy individuals were enrolled in the study. Genotyping for three single nucleotide polymorphisms (SNPs) within the Results: In the present study, the Conclusions: The obtained results suggest that

Indexed as

AdultAllelesAntirheumatic AgentsArthritis, PsoriaticArthritis, RheumatoidBiomarkersFemaleGenetic Predisposition to DiseaseGenotypeHumansInterleukin-33MaleMiddle AgedPolymorphism, Single NucleotideSpondylitis, AnkylosingTreatment OutcomeAntirheumatic AgentsBiomarkersIL33 protein, humanInterleukin-33Tumor Necrosis Factor Inhibitorsankylosing spondylitisanti-TNF therapyIL-33 gene polymorphismpsoriatic arthritisrheumatoid arthritisspondyloarthritisTNF inhibitors

Identifiers

PMID34177886
PMCPMC8226138
OpenAlexW3171880216

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.