Evidence map›Paper›PMID 31417909›Full record

ArticleFrontiers in cardiovascular medicine2019

Comparative Analysis of Microfluidics Thrombus Formation in Multiple Genetically Modified Mice: Link to Thrombosis and Hemostasis.

Magdolna Nagy, Johanna P van Geffen, David Stegner, David J Adams, Attila Braun, Susanne M de Witt, Margitta Elvers, Mitchell J Geer, Marijke J E Kuijpers, Karl Kunzelmann and 11 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
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  7. Platelet GPVI (Glycoprotein VI) and Thrombotic Complications in the Venous System.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Review
  8. Review
  9. Article
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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

21 authors at 11 institutions in 4 countries.

Magdolna NagyDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Johanna P van GeffenDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
David StegnerRudolf Virchow Center, Institute of Experimental Biomedicine, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
David J AdamsWellcome Trust Sanger Institute, Cambridge, United Kingdom.
Attila BraunRudolf Virchow Center, Institute of Experimental Biomedicine, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Susanne M de WittDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Margitta ElversDepartment of Vascular Surgery, Experimental Vascular Medicine, Heinrich Heine University, Düsseldorf, Germany.
Mitchell J GeerInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Marijke J E KuijpersDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Karl KunzelmannInstitute of Physiology, University of Regensburg, Regensburg, Germany.
Jun MoriInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Cécile OuryGIGA-Cardiovascular Sciences, University of Liège, Liège, Belgium.
Joachim PircherMedizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians-University, and DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Irina PleinesRudolf Virchow Center, Institute of Experimental Biomedicine, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Alastair W PooleDepartment of Physiology and Pharmacology, School of Medical Sciences, University of Bristol, Bristol, United Kingdom.
Yotis A SenisInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Remco VerdooldDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Christian WeberDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Bernhard NieswandtRudolf Virchow Center, Institute of Experimental Biomedicine, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Johan W M HeemskerkDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Constance C F M J BaatenDepartment of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
Maastricht University · NLUniversity of Würzburg · DEUniversity of Birmingham · GBGerman Centre for Cardiovascular Research · DEHeinrich Heine University Düsseldorf · DELudwig-Maximilians-Universität München · DEUniversitätsklinikum Aachen · DEUniversity of Bristol · GBUniversity of Liège · BEUniversity of Regensburg · DEWellcome Sanger Institute · GB

Funding

British Heart Foundation RG/15/13/31673
6 · The paper itself

Abstract

Genetically modified mice are indispensable for establishing the roles of platelets in arterial thrombosis and hemostasis. Microfluidics assays using anticoagulated whole blood are commonly used as integrative proxy tests for platelet function in mice. In the present study, we quantified the changes in collagen-dependent thrombus formation for 38 different strains of (genetically) modified mice, all measured with the same microfluidics chamber. The mice included were deficient in platelet receptors, protein kinases or phosphatases, small GTPases or other signaling or scaffold proteins. By standardized re-analysis of high-resolution microscopic images, detailed information was obtained on altered platelet adhesion, aggregation and/or activation. For a subset of 11 mouse strains, these platelet functions were further evaluated in rhodocytin- and laminin-dependent thrombus formation, thus allowing a comparison of glycoprotein VI (GPVI), C-type lectin-like receptor 2 (CLEC2) and integrin α

Indexed as

arterial thrombus formationbleedingcollagenglycoprotein VImicrofluidicsplatelets

Identifiers

PMID31417909
PMCPMC6682619
OpenAlexW2956603010

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.