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Persistence of platelet thrombus formation in arterioles of mice lacking both von Willebrand factor and fibrinogen

2000· article· en· 489 citations· W2126683943 on OpenAlex· 10.1172/jci9896

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A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.077
GPT teacher head0.339
Teacher spread
0.263 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

We used intravital microscopy to observe the formation of platelet plugs in ferric chloride-injured arterioles of live mice. With this model, we evaluated thrombus growth in mice lacking von Willebrand factor (vWF) and fibrinogen (Fg), the two key ligands known to mediate platelet adhesion and aggregation. In vWF(-/-) mice, despite the presence of arterial shear, delayed platelet adhesion occurred and stable thrombi formed. In many mice, a persisting high-shear channel never occluded. Abundant thrombi formed in Fg(-/-) mice, but they detached from the subendothelium, which ultimately caused downstream occlusion in all cases. Surprisingly, mice deficient in both vWF and Fg successfully formed thrombi with properties characteristic of both mutations, leading to vessel occlusion in the majority of vessels. Platelets of these doubly deficient mice specifically accumulated fibronectin in their alpha-granules, suggesting that fibronectin could be the ligand supporting the platelet aggregation.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Journal of Clinical Investigation
Topic
Platelet Disorders and Treatments
Field
Medicine
Canadian institutions
Funders
National Heart, Lung, and Blood InstituteNational Institutes of HealthHeart and Stroke Foundation of CanadaAmerican Heart Association
Keywords
PlateletVon Willebrand factorThrombusFibrinogenChemistryFibrinFibronectinIntravital microscopyCoagulationADAMTS13Platelet adhesivenessImmunologyInternal medicinePathologyCell biologyMedicineMicrocirculationBiologyBiochemistryPlatelet aggregationExtracellular matrix
Has abstract in OpenAlex
yes