Evidence map›Paper›PMID 32153623›Full record

ArticleFrontiers in genetics2019

Transcript Analysis Reveals a Hypoxic Inflammatory Environment in Human Chronic Otitis Media With Effusion.

Mahmood F Bhutta, Jane Lambie, Lindsey Hobson, Debbie Williams, Hayley E Tyrer, George Nicholson, Steve D M Brown, Helen Brown, Chiara Piccinelli, Guillaume Devailly and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

10 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

12 authors at 8 institutions in 2 countries.

Mahmood F BhuttaDepartment of ENT, Brighton & Sussex University Hospitals NHS Trust, Brighton, United Kingdom.
Jane LambieNuffield Department of Surgical Sciences, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Lindsey HobsonDepartment of ENT, Oxford University Hospitals NHS Trust, John Radcliffe Hospital, Oxford, United Kingdom.
Debbie WilliamsMammalian Genetics Unit, MRC Harwell Institute, Harwell, United Kingdom.
Hayley E TyrerFaculty of Health and Wellbeing, University of Lancashire, Preston, United Kingdom.
George NicholsonDepartment of Statistics, University of Oxford, Oxford, United Kingdom.
Steve D M BrownMammalian Genetics Unit, MRC Harwell Institute, Harwell, United Kingdom.
Helen BrownThe Roslin Institute, University of Edinburgh, Midlothian, United Kingdom.
Chiara PiccinelliThe Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, United Kingdom.
Guillaume DevaillyGenPhySE, Université de Toulouse, INRA, ENVT, Castanet Tolosan, France.
James RamsdenDepartment of ENT, Oxford University Hospitals NHS Trust, John Radcliffe Hospital, Oxford, United Kingdom.
Michael T CheesemanThe Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, United Kingdom.
University of Edinburgh · GBJohn Radcliffe Hospital · GBMary Lyon Centre at MRC Harwell · GBGénétique Physiologie et Systèmes d'Elevage · FROxford University Hospitals NHS Trust · GBUniversity Hospitals Sussex NHS Foundation Trust · GBUniversity of Lancashire · GBUniversity of Oxford · GB

Funding

Medical Research Council MC_U142670371Medical Research Council MC_UP_1503/1Wellcome Trust
6 · The paper itself

Abstract

Chronic otitis media with effusion (COME) is the most common cause of childhood hearing loss in the developed world. Underlying pathophysiology is not well understood, and in particular the factors that lead to the transition from acute to chronic inflammation. Here we present the first genome-wide transcript analysis of white blood cells in the effusion of children with COME. Analysis of microarray data for enriched pathways reveals upregulation of hypoxia pathways, which is confirmed using real-time PCR and determining VEGF protein titres. Other pathways upregulated in both mucoid and serous effusions include Toll-like receptor signaling, complement, and RANK-RANKL. Cytology reveals neutrophils and macrophages predominated in both serous and mucoid effusions, however, serous samples had higher lymphocyte and eosinophil differential counts, while mucoid samples had higher neutrophil differential counts. Transcript analysis indicates serous fluids have CD4+ and CD8+ T-lymphocyte, and NK cell signatures. Overall, our findings suggest that inflammation and hypoxia pathways are important in the pathology of COME, and targets for potential therapeutic intervention, and that mucoid and serous COME may represent different immunological responses.

Indexed as

effusionhypoxiainflammationotitis mediatranscript

Identifiers

PMID32153623
PMCPMC7047850
OpenAlexW3007076480

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.