Evidence map›Paper›PMID 21349145›Full record

ArticleCritical care (London, England)2011

Platelets, endothelium and shear join forces to mislead neutrophils in sepsis.

Heitor A Paula Neto, Paul Kubes

Open access · goldAbstract readComment
In one paragraph

Article in Critical care (London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Heitor A Paula NetoImmunology Research Group, Department of Physiology and Pharmacology, Calvin, Phoebe & Joan Snyder Institute for Infection, Immunity & Inflammation, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, Canada T2N 4N1.
Paul Kubes
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are circulating leukocytes with great cytotoxic potential, responsible for the first combat against invading pathogens. Their accumulation in tissues must be highly controlled so that the number of neutrophils delivered to the affected site is sufficient to control infection with minimum injury to the surrounding healthy tissue. In sepsis, neutrophil migration is dysregulated - resulting in insufficient delivery of neutrophils to the infectious site and massive neutrophil accumulation in uninfected organs. This dysregulation has the potential to cause inappropriate tissue injury that may explain the multiple organ dysfunction observed in severe sepsis. A better understanding of the mechanisms that contribute to this process is fundamental to design therapeutic strategies to circumvent tissue injury and organ dysfunction in sepsis.

Indexed as

Endothelium, VascularHumansInflammation MediatorsLeukocytesSepsisShear StrengthInflammation Mediators

Identifiers

PMID21349145
PMCPMC3222017
OpenAlexW2131499742

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.