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Coagulation01:06

Coagulation

1.6K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
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Coagulation01:09

Coagulation

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The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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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...
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Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Related Experiment Video

Updated: Mar 24, 2026

Rapid One-step Enzymatic Synthesis and All-aqueous Purification of Trehalose Analogues
09:27

Rapid One-step Enzymatic Synthesis and All-aqueous Purification of Trehalose Analogues

Published on: February 17, 2017

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Trehalose 6,6-Dimycolate from Mycobacterium tuberculosis Induces Hypercoagulation.

Elizabeth Donnachie1, Elena P Fedotova2, Shen-An Hwang3

  • 1Gulf States Hemophilia and Thrombophilia Center, Department of Pediatrics, University of Texas Medical School at Houston, Houston, Texas.

The American Journal of Pathology
|March 13, 2016
PubMed
Summary

Trehalose 6,6-dimycolate (TDM) can induce inflammation and hypercoagulopathy in a new mouse model. This study shows TDM alone is sufficient to cause the blood clotting issues seen in tuberculosis patients.

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Area of Science:

  • Immunology
  • Pathology
  • Hematology

Background:

  • Tuberculosis (TB) is a global health issue.
  • Trehalose 6,6-dimycolate (TDM) is implicated in TB pathogenesis, activating innate and chronic inflammation.
  • Existing noninfectious TB models using TDM emulsions replicate some patient pathologies.

Purpose of the Study:

  • To develop a novel, noninfectious mouse model using TDM to study TB-related inflammation and vascular pathology.
  • To investigate the role of TDM in promoting inflammatory lung findings, vascular occlusion, hemorrhage, and hypercoagulopathy.

Main Methods:

  • Mice (C57BL/6 and BALB/c) received intraperitoneal (i.p.) TDM followed by intravenous (i.v.) TDM (TDM-IPIV) or single i.p. or i.v. TDM injections.
  • Evaluated inflammatory responses, cytokine profiles (including IL-10 and GM-CSF), T-cell populations (CD4+), and coagulation parameters.
  • Assessed vascular changes using Masson's trichrome staining for collagen deposition.

Main Results:

  • The TDM-IPIV model induced significant inflammatory lung pathology and increased inflammatory and T-cell cytokines in both mouse strains.
  • The TDM-IPIV group exhibited enhanced IL-10 and granulocyte-macrophage colony-stimulating factor levels and increased CD4+ T cells in lung tissue.
  • Hypercoagulopathy was observed in the TDM-IPIV group, characterized by increased coagulation, reduced clot formation time, and increased clot firmness, with collagen deposition in occluded vasculature.
  • These TDM-induced effects on coagulation were independent of the observed inflammation.

Conclusions:

  • The novel TDM-IPIV mouse model effectively replicates key inflammatory and vascular pathologies seen in TB.
  • TDM is sufficient to induce a state of hypercoagulopathy, suggesting a direct role in the coagulation abnormalities observed in TB patients.
  • This model provides a valuable tool for studying TB pathogenesis and developing targeted therapies for associated complications.