Evidence map›Paper›PMID 24921658›Full record

ArticlePloS one2014

Comparative response of platelet fV and plasma fV to activated protein C and relevance to a model of acute traumatic coagulopathy.

James E Campbell, Michael Adam Meledeo, Andrew P Cap

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Plasmatic coagulation profile after major traumatic injury: a prospective observational study.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022
    Observational
  4. Article
  5. The roles of activated protein C in experimental trauma models.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018
    Review
  6. Review
  7. Review
  8. Hemorrhagic blood failure: Oxygen debt, coagulopathy, and endothelial damage.The journal of trauma and acute care surgery · 2017
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. 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

3 authors at 1 institution in 1 country.

James E CampbellUnited States Army Institute of Surgical Research, Coagulation and Blood Research Program, JBSA-FT Sam Houston, Houston, Texas, United States of America.
Michael Adam MeledeoUnited States Army Institute of Surgical Research, Coagulation and Blood Research Program, JBSA-FT Sam Houston, Houston, Texas, United States of America.
Andrew P CapUnited States Army Institute of Surgical Research, Coagulation and Blood Research Program, JBSA-FT Sam Houston, Houston, Texas, United States of America.
United States Army Institute of Surgical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute traumatic coagulopathy (ATC) has been linked to an increase in activated protein C (aPC) from 40 pM in healthy individuals to 175 pM. aPC exerts its activity primarily through cleavage of active coagulation factor Va (fVa). Platelets reportedly possess fVa which is more resistant to aPC cleavage than plasma fVa; this work examines the hypothesis that normal platelets are sufficient to maintain coagulation in the presence of elevated aPC.

methodsCoagulation responses of normal plasma, fV deficient plasma (fVdp), and isolated normal platelets in fVdp were conducted: prothrombin (PT) tests, turbidimetry, and thromboelastography (TEG), including the dose response of aPC on the samples.

resultsPT and turbidimetric assays demonstrate that normal plasma is resistant to aPC at doses much higher than those found in ATC. Additionally, an average physiological number of washed normal platelets (200,000 platelets/mm3) was sufficient to eliminate the anti-coagulant effects of aPC up to 10 nM, nearly two orders of magnitude above the ATC concentration and even the steady-state pharmacological concentration of human recombinant aPC, as measured by TEG. aPC also demonstrated no significant effect on clot lysis in normal plasma samples with or without platelets.

conclusionsAlthough platelet fVa shows slightly superior resistance to aPC's effects compared to plasma fVa in static models, neither fVa is sufficiently cleaved in simulations of ATC or pharmacologically-delivered aPC to diminish coagulation parameters. aPC is likely a correlative indicator of ATC or may play a cooperative role with other activity altering products generated in ATC.

Indexed as

Models, BiologicalAcute DiseaseAnticoagulantsAntigens, CDBlood Coagulation DisordersBlood PlateletsEndothelial Protein C ReceptorFactor VFactor VaFactor VIIIFibrinFibrinolysisHumansInternational Normalized RatioNephelometry and TurbidimetryPhospholipidsAnticoagulantsAntigens, CDEndothelial Protein C ReceptorFactor VFactor VaFactor VIIIFibrinPhospholipidsPROCR protein, humanProtein CReceptors, Cell SurfaceTissue Plasminogen Activator

Identifiers

PMID24921658
PMCPMC4055642
OpenAlexW2002353122

What OpenQuestion holds

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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.