Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
EDTA: Auxiliary Complexing Reagents01:26

EDTA: Auxiliary Complexing Reagents

EDTA titrations are usually carried out in highly basic conditions, where the fully deprotonated form of EDTA, Y4−, actively complexes with the free metal ions in the solution. Several metal ions precipitate as hydrous oxide (hydroxides, oxides, or oxyhydroxides) under these conditions, lowering the concentration of free metal ions in the solution. For this reason, auxiliary complexing agents or ligands such as ammonia, tartrate, citrate, or triethanolamine are used in EDTA titrations to...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pharmacokinetic modelling and validation of the half-life extension needed to reduce the burden of infusions compared with standard factor VIII.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Fifth Åland Island conference on von Willebrand disease.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Replacement therapy during surgery in von Willebrand disease needs personalization.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Defining extended half-life rFVIII-A critical review of the evidence.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Bleeding-related hospitalization in patients with von Willebrand disease and the impact of prophylaxis: Results from national registers in Sweden compared with normal controls and participants in the von Willebrand Disease Prophylaxis Network.

Haemophilia : the official journal of the World Federation of Hemophilia·2018
Same author

Immune tolerance induction: What have we learned over time?

Haemophilia : the official journal of the World Federation of Hemophilia·2018

Related Experiment Video

Updated: May 14, 2026

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
12:24

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes

Published on: June 3, 2014

Von Willebrand factor containing factor VIII concentrates.

E Berntorp1

  • 1Department for Coagulation Disorders, University of Lund, University Hospital, Malmö, Sweden. erik.berntorp@medforsk.mas.lu.se

Haemophilia : the Official Journal of the World Federation of Hemophilia
|February 13, 2013
PubMed
Summary

Plasma-derived von Willebrand factor (vWF) concentrates effectively raise Factor VIII levels for von Willebrand disease (vWD) treatment. However, normalizing bleeding times remains challenging, highlighting the need for improved vWF concentrate development.

More Related Videos

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice
08:13

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Published on: September 30, 2021

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

Related Experiment Videos

Last Updated: May 14, 2026

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
12:24

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes

Published on: June 3, 2014

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice
08:13

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Published on: September 30, 2021

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

Area of Science:

  • Hematology
  • Plasma Protein Therapeutics

Background:

  • Von Willebrand disease (vWD) is treated with plasma-derived concentrates containing von Willebrand factor (vWF) and Factor VIII (FVIII).
  • Current concentrates vary in their vWF multimer composition, impacting treatment efficacy.

Purpose of the Study:

  • To evaluate the effectiveness of plasma-derived vWF/FVIII concentrates in treating vWD.
  • To identify challenges in achieving normal bleeding times with existing concentrates.
  • To discuss future directions in vWF concentrate development.

Main Methods:

  • Review of existing literature on vWF/FVIII concentrates.
  • Analysis of postinfusion FVIII:C levels and bleeding time normalization.
  • Comparison of different concentrate compositions, including high molecular weight vWF multimers.

Main Results:

  • All evaluated concentrates effectively normalized postinfusion Factor VIII:C levels.
  • Achieving normal bleeding times was difficult, even with concentrates containing all vWF multimers.
  • Haemate P is considered a current gold standard concentrate.

Conclusions:

  • While vWF/FVIII concentrates are effective for FVIII:C normalization in vWD, bleeding time normalization remains a challenge.
  • Development of purified vWF concentrates lacking FVIII:C is a key future goal.
  • Further research is needed to optimize vWF concentrate composition for improved clinical outcomes.