Evidence map›Paper›PMID 21964405›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Airway tissue factor-dependent coagulation activity in response to sulfur mustard analog 2-chloroethyl ethyl sulfide.

Raymond C Rancourt, Livia A Veress, Xiaoling Guo, Tara N Jones, Tara B Hendry-Hofer, Carl W White

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Bronchiolitis Obliterans and Pulmonary Fibrosis after Sulfur Mustard Inhalation in Rats.American journal of respiratory cell and molecular biology · 2018
    Article
  10. Article
  11. From the Cover: Catalytic Antioxidant Rescue of Inhaled Sulfur Mustard Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2016
    Article
  12. Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 2016
    Review
  13. Review
  14. Emerging targets for treating sulfur mustard-induced injuries.Annals of the New York Academy of Sciences · 2016
    Review
  15. Article
  16. Airway tissue plasminogen activator prevents acute mortality due to lethal sulfur mustard inhalation.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Article
  17. Antifibrinolytic mechanisms in acute airway injury after sulfur mustard analog inhalation.American journal of respiratory cell and molecular biology · 2014
    Article
  18. Postexposure aerosolized heparin reduces lung injury in chlorine-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Raymond C RancourtDepartment of Pediatrics, National Jewish Health, Denver, Colorado 80206, USA.
Livia A Veress
Xiaoling Guo
Tara N Jones
Tara B Hendry-Hofer
Carl W White
University of Colorado Denver · USNational Jewish Health · US

Funding

Thiols in sulfur mustard toxicityU54ES015678 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI WHITE, CARL W · 2006 to 2015
$20.5M
NIEHS NIH HHS U54 ES015678
6 · The paper itself

Abstract

Acute lung injury is a principal cause of morbidity and mortality in response to mustard gas (SM) inhalation. Obstructive, fibrin-containing airway casts have recently been reported in a rat inhalation model employing the SM analog 2-chloroethyl ethyl sulfide (CEES). The present study was designed to identify the mechanism(s) causing activation of the coagulation cascade after CEES-induced airway injury. Here we report that CEES inhalation elevates tissue factor (TF) activity and numbers of detached epithelial cells present in lavage fluid (BALF) from rats after exposure (18 h). In vitro studies using 16HBE cells, or with rat BALF, indicated that detached epithelial cells could convert factor X (FX) to the active form FXa when incubated with factor VII and could elicit rapid clotting of plasma. In addition, immunocytochemical analysis demonstrated elevated cell surface (TF) expression on CEES-exposed 16HBE cells as a function of time. However, total cell TF expression did not increase. Since membrane surfaces bearing TF are important determinants of clot initiation, anticoagulants directed against these entities were tested for ability to limit plasma clotting or FX activation capacity of BALF or culture media. Addition of tifacogin, a TF pathway inhibitor, effectively blocked either activity, demonstrating that the procoagulant actions of CEES were TF pathway dependent. Lactadherin, a protein capable of competing with clotting factors for phospholipid-binding sites, was partially effective in limiting these procoagulant actions. These findings indicate that TF pathway inhibition could be an effective strategy to prevent airway obstruction after SM or CEES inhalation.

Indexed as

Airway ObstructionAnimalsAntigens, SurfaceBronchiBronchoalveolar Lavage FluidCell Line, TransformedChemical Warfare AgentsDisease Models, AnimalEpithelial CellsFactor VIIFactor XaHumansInhalation ExposureMaleMilk ProteinsMustard Gas2-chloroethyl ethyl sulfideAntigens, SurfaceChemical Warfare AgentsFactor VIIFactor XaMFGE8 protein, ratMilk ProteinsMustard GasProteinsThromboplastinTifacogin

Identifiers

PMID21964405
PMCPMC3349374
OpenAlexW2099950499

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.