Evidence map›Paper›PMID 29930815›Full record

ReviewAcute medicine & surgery2014

Neutrophil extracellular traps, damage-associated molecular patterns, and cell death during sepsis.

Toshiaki Iba, Miwa Murai, Isao Nagaoka, Yoko Tabe

Open access · bronzeAbstract readReview
In one paragraph

Review in Acute medicine & surgery, 2014. 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
0.1field-weighted citation impact, top 44% 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, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Detection of Neutrophil Activation by Automated Blood Cell Counter in Sepsis.Juntendo Iji zasshi = Juntendo medical journal · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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

4 authors at 1 institution in 1 country.

Toshiaki IbaDepartment of Emergency and Disaster Medine Graduate School of Medicine, Juntendo University Tokyo Japan.
Miwa MuraiDepartment of Emergency and Disaster Medine Graduate School of Medicine, Juntendo University Tokyo Japan.
Isao NagaokaDepartment of Host Defense and Biochemical Research Graduate School of Medicine, Juntendo University Tokyo Japan.
Yoko TabeDepartment of Clinical Laboratory Medicine Graduate School of Medicine, Juntendo University Tokyo Japan.
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to pathogen-associated molecular patterns from invasive microorganisms, alarmins, which are major components of host defense mechanisms, are involved in the pathophysiology of sepsis. In fact, the magnitude of the insult is defined according to the damage-associated molecular pattern (DAMP), which is composed of alarmins as well as pathogen-associated molecular patterns, such as those involving nucleosomes, histones, and DNA. Regarding the antimicrobial mechanism of neutrophils, an alternative non-phagocytic mechanism was first recognized as "NETosis" in 2004. In this mechanism, microorganisms are trapped and eliminated by neutrophil extracellular traps (NETs). These NETs are composed of histones and DNA that have been expelled from the nucleus as well as antimicrobial proteases, including elastase and myeloperoxidase. NETosis, a cell death pathway reported to be distinct from apoptosis, is an active area of research. As NETs are composed of deleterious substances, they are extremely harmful to the host cells once they are released into the circulating blood. Therefore, the meanings and putative roles of these components in sepsis have attracted much attention.

Indexed as

Alarminhistoneinnate immune systemnecrosisneutrophil

Identifiers

PMID29930815
PMCPMC5997206
OpenAlexW1502714351

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.