Evidence map›Paper›PMID 2040692›Full record

ArticleThe Journal of clinical investigation1991

Shape changes, exocytosis, and cytosolic free calcium changes in stimulated human eosinophils.

P Kernen, M P Wymann, V von Tscharner, D A Deranleau, P C Tai, C J Spry, C A Dahinden, M Baggiolini

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
  2. Article
  3. DisruptingMicroorganisms · 2020
    Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Cytokines in asthma.Thorax · 1999
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Binding to heparan sulfate or heparin enhances neutrophil responses to interleukin 8.Proceedings of the National Academy of Sciences of the United States of America · 1993
    Article
  16. Article
  17. Article
  18. 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

8 authors at 2 institutions in 3 countries.

P KernenTheodor-Kocher Institute, University of Bern, Switzerland.
M P Wymann
V von Tscharner
D A Deranleau
P C Tai
C J Spry
C A Dahinden
M Baggiolini
University of Bern · CHSt George's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Essentially pure preparations of normal density eosinophils obtained from patients with hypereosinophilic syndrome (HES) were stimulated with complement factor 5a (C5a), platelet-activating factor (PAF), FMLP and neutrophil-activating peptide (NAP-1/IL-8). Three responses were studied, the transient rise in cytosolic free calcium concentration ([Ca2+]i) (derived from indo-1 fluorescence), shape changes (measured by laser turbidimetry), and exocytosis of eosinophil peroxidase (EPO) (assessed by H2O2/luminol-dependent chemiluminescence). Responses were obtained with all four agonists, but C5a and PAF were by far more potent than FMLP and NAP-1/IL-8, which induced only minor effects. Pretreatment of the cells with pertussis toxin attenuated [Ca2+]i changes, EPO release and, to a lesser extent, shape changes, indicating that GTP-binding proteins of Gi-type are involved in receptor-dependent signal transduction processes leading to these responses. A clear dissociation was observed in the control of the shape change response and EPO exocytosis. The shape change was not affected by Ca2+ depletion or treatment with the protein kinase inhibitor staurosporine, but exocytosis was prevented by Ca2+ depletion and markedly enhanced by staurosporine. The activation of the contractile system, leading to shape changes and motility, thus appears to be independent of the classical signal transduction pathway involving phospholipase C, a [Ca2+]i rise and protein kinase C activation. Exocytosis is, as expected, Ca2+ dependent and appears to be under a negative control involving protein phosphorylations.

Indexed as

ExocytosisAlkaloidsCalciumComplement C5aEosinophilsHumansInterleukin-8N-Formylmethionine Leucyl-PhenylalaninePeroxidasesPertussis ToxinPlatelet Activating FactorStaurosporineTetradecanoylphorbol AcetateTime FactorsVirulence Factors, BordetellaAlkaloidsCalciumComplement C5aInterleukin-8N-Formylmethionine Leucyl-PhenylalaninePeroxidasesPertussis ToxinPlatelet Activating FactorStaurosporineTetradecanoylphorbol AcetateVirulence Factors, Bordetella

Identifiers

PMID2040692
PMCPMC296956
OpenAlexW2082456912

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.