Evidence map›Paper›PMID 26848552›Full record

ReviewJournal of thrombosis and haemostasis : JTH2016

Transport physics and biorheology in the setting of hemostasis and thrombosis.

L F Brass, S L Diamond

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 93 citations in OpenAlex.

  1. Mesoscale Simulations of Blood Coagulation in Flow and Quiescent Domains Using SDPD.International journal for numerical methods in biomedical engineering · 2026
    Article
  2. Article
  3. Fibrin as a Versatile Fibrous Biopolymer.Sub-cellular biochemistry · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Platelet Adhesion and Activation in an ECMO Thrombosis-on-a-Chip Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Fibrin clot properties and thrombus composition in cirrhosis.Research and practice in thrombosis and haemostasis · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. A multiscale model for multiple platelet aggregation in shear flow.Biomechanics and modeling in mechanobiology · 2021
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

L F BrassDepartments of Medicine and Systems Pharmacology, University of Pennsylvania, Philadelphia, PA, USA.
S L DiamondInstitute for Medicine and Engineering, Department of Chemical Engineering, Philadelphia, PA, USA.
University of Pennsylvania · US

Funding

Subcellular Mechanisms pf Platelet ActivationP01HL040387 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI PONCZ, MORTIMER · 1988 to 2018
$35.5M
Blood Systems BiologyR01HL103419 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DIAMOND, SCOTT L · 2010 to 2019
$7.4M
NHLBI NIH HHS P01 HL040387NHLBI NIH HHS R01 HL103419
6 · The paper itself

Abstract

The biophysics of blood flow can dictate the function of molecules and cells in the vasculature with consequent effects on hemostasis, thrombosis, embolism, and fibrinolysis. Flow and transport dynamics are distinct for (i) hemostasis vs. thrombosis and (ii) venous vs. arterial episodes. Intraclot transport changes dramatically the moment hemostasis is achieved or the moment a thrombus becomes fully occlusive. With platelet concentrations that are 50- to 200-fold greater than platelet-rich plasma, clots formed under flow have a different composition and structure compared with blood clotted statically in a tube. The platelet-rich, core/shell architecture is a prominent feature of self-limiting hemostatic clots formed under flow. Importantly, a critical threshold concentration of surface tissue factor is required for fibrin generation under flow. Once initiated by wall-derived tissue factor, thrombin generation and its spatial propagation within a clot can be modulated by γ'-fibrinogen incorporated into fibrin, engageability of activated factor (FIXa)/activated FVIIIa tenase within the clot, platelet-derived polyphosphate, transclot permeation, and reduction of porosity via platelet retraction. Fibrin imparts tremendous strength to a thrombus to resist embolism up to wall shear stresses of 2400 dyne cm(-2) . Extreme flows, as found in severe vessel stenosis or in mechanical assist devices, can cause von Willebrand factor self-association into massive fibers along with shear-induced platelet activation. Pathological von Willebrand factor fibers are A Disintegrin And Metalloprotease with ThromboSpondin-1 domain 13 resistant but are a substrate for fibrin generation due to FXIIa capture. Recently, microfluidic technologies have enhanced the ability to interrogate blood in the context of stenotic flows, acquired von Willebrand disease, hemophilia, traumatic bleeding, and drug action.

Indexed as

HemostasisRheologyAnimalsBlood CoagulationBlood Flow VelocityBlood PlateletsConstriction, PathologicDiffusionFactor IXaFactor VIIIaFibrinFibrinolysisHumansMicePlatelet ActivationPlatelet AdhesivenessFactor IXaFactor VIIIaFibrinPolyphosphatesThrombinThromboplastinvon Willebrand Factorfibrinhemodynamicsplateletshear stressthrombinvon Willebrand factor

Identifiers

PMID26848552
PMCPMC4870125
OpenAlexW2328847125

What OpenQuestion holds

Textmetadata
LicenceTDM
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.