Evidence map›Paper›PMID 17880845›Full record

ArticleCurrent infectious disease reports2007

Sepsis mediators.

François Philippart, Jean-Marc Cavaillon

Open access · bronzeAbstract read
In one paragraph

Article in Current infectious disease reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

2 authors at 1 institution in 1 country.

François PhilippartUnit Cytokines and Inflammation, Institut Pasteur, 28 rue Dr. Roux, 75015 Paris, France.
Jean-Marc Cavaillon
Institut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During sepsis, the plasma levels of numerous inflammatory markers are enhanced. Some of these markers are the mediators responsible for the syndromes observed during sepsis as well as for organ dysfunction and eventually death. Their role has been demonstrated in experimental models that employed either transgenic and gene-targeted animals or the use of neutralizing agents. Accordingly, anaphylatoxins generated after complement system activation, factors of coagulation and fibrinolysis, proinflammatory cytokines, chemokines, proteases, lipid mediators, nitric oxide, and cell markers of stress (eg, high mobility group box-1) have been shown to contribute to the deleterious events observed during sepsis. On the other hand, the counter-regulation of the inflammatory process, which involves mediators such as anti-inflammatory cytokines and some neuromediators, can jeopardize the immune status of the host and render the patients more sensitive to nosocomial infections.

Identifiers

PMID17880845
PMCPMC7102023
OpenAlexW3192185453

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.