Evidence map›Paper›PMID 15270852›Full record

ArticleClinical and experimental immunology2004

Environmental factors and not genotype influence the plasma level of interleukin-1 receptor antagonist in normal individuals.

H Cullup, P G Middleton, G Duggan, J S Conn, A M Dickinson

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

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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.

H CullupHaematological Sciences, School of Clinical Laboratory Sciences, University of Newcastle upon Tyne, Newcastle upon Tyne, UK. hannah.Cullup@ncl.ac.uk
P G Middleton
G Duggan
J S Conn
A M Dickinson
Newcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokine production may be regulated by both genotypic (single nucleotide or tandem repeat polymorphisms) and non-genotypic factors relating to the environment and inherent biology (i.e. gender). Interleukin (IL)-1 is one of the body's most highly proinflammatory cytokines and is implicated in the pathophysiology of numerous diseases, but also in the maintenance of homeostasis in a number of tissues. The cytokine IL-1 receptor antagonist (IL-1Ra) is the competitive inhibitor of the IL-1 agonists IL-1alpha and IL-1beta. In vivo IL-1Ra was measured in a cohort of 200 + blood donors and the effect of the IL-1 gene polymorphisms, environmental and biological factors assessed. In this study, we observed that possession of particular alleles of 5 IL-1 gene polymorphisms (IL1A-889, IL1Alpha VNTR, IL1B -511, IL1B +3953 and the IL1RN VNTR) did not correlate with higher plasma IL-1Ra levels. Environmental factors such as smoking and non-steroidal anti-inflammatory drug ingestion were associated with higher in vivo IL-1Ra levels (P = 0.015 and 0.022, respectively), but biological factors such as gender, age and menstruation status did not have any impact upon in vivo IL-1Ra levels. Genotypic associations of IL-1 gene family polymorphisms with disease features may reflect characteristics of stressed rather than normal control circuits for cytokine production.

Indexed as

AdolescentAdultAgedAnti-Inflammatory Agents, Non-SteroidalFemaleGene FrequencyGenotypeHaplotypesHumansInterleukin-1Interleukin 1 Receptor Antagonist ProteinLinkage DisequilibriumMaleMiddle AgedSialoglycoproteinsSmokingAnti-Inflammatory Agents, Non-SteroidalIL1RN protein, humanInterleukin-1Interleukin 1 Receptor Antagonist ProteinSialoglycoproteins

Identifiers

PMID15270852
PMCPMC1809100
OpenAlexW2090515941

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.