Evidence map›Paper›PMID 24268519›Full record

ReviewTrends in immunology2014

Lipid mediators in immune dysfunction after severe inflammation.

James N Fullerton, Alastair J O'Brien, Derek W Gilroy

Open access · hybridAbstract readReview
In one paragraph

Review in Trends in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Cell-cell interactions and bronchoconstrictor eicosanoid reduction with inhaled carbon monoxide and resolvin D1.American journal of physiology. Lung cellular and molecular physiology · 2014
    Trial
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Design, synthesis,Journal of enzyme inhibition and medicinal chemistry · 2024
    Article
  12. Article
  13. Occult hypoperfusion and changes of systemic lipid levels after severe trauma: an analysis in a standardized porcine polytrauma model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. NSAIDs and Cancer Resolution: New Paradigms beyond Cyclooxygenase.International journal of molecular sciences · 2022
    Review
  20. Review

1 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

James N FullertonCentre for Clinical Pharmacology, Division of Medicine, Rayne Institute, 5 University Street, University College London, London, WC1E 6JF, UK. Electronic address: james.fullerton@doctors.org.uk.
Alastair J O'BrienCentre for Clinical Pharmacology, Division of Medicine, Rayne Institute, 5 University Street, University College London, London, WC1E 6JF, UK.
Derek W GilroyCentre for Clinical Pharmacology, Division of Medicine, Rayne Institute, 5 University Street, University College London, London, WC1E 6JF, UK.
University College London · GB

Funding

Wellcome Trust 087520Wellcome Trust 099089
6 · The paper itself

Abstract

Sepsis, trauma, burns, and major surgical procedures activate common systemic inflammatory pathways. Nosocomial infection, organ failure, and mortality in this patient population are associated with a quantitatively different reprioritization of the circulating leukocyte transcriptome to the initial inflammatory insult, greater in both magnitude and duration, and secondary to multiple observed defects in innate and adaptive immune function. Dysregulation of inflammatory resolution processes and associated bioactive lipid mediators (LMs) mechanistically contribute to this phenotype. Recent data indicate the potential efficacy of therapeutic interventions that either reduce immunosuppressive prostaglandins (PGs) or increase specialized proresolving LMs. Here, we reassess the potential for pharmacological manipulation of these LMs as therapeutic approaches for the treatment of critical illness (CI).

Indexed as

AnimalsCritical IllnessHumansInflammationInflammation MediatorsLipid MetabolismSignal TransductionInflammation Mediatorscyclooxygenaseeicosanoidsimmunosuppressionprostaglandinsresolution of inflammationsepsis

Identifiers

PMID24268519
PMCPMC3884129
OpenAlexW2079478719

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.