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Hansen2019 - Nine species reduced model of blood coagulation

ABSTRACT: its a nine species reduced model of Hockin 2002. Model uses different level of reduction (5,7,9,11) and testing the best alignment with Hockin model results

SUBMITTER: Krishna Kumar Tiwari

PROVIDER: BIOMD0000000755 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000755?filename=Hansen2019-biopax2.owl	Owl
	BIOMD0000000755?filename=Hansen2019-biopax3.owl	Owl
	BIOMD0000000755?filename=Hansen2019-matlab.m	Other
	BIOMD0000000755?filename=Hansen2019-octave.m	Other
	BIOMD0000000755?filename=Hansen2019.cps	Other

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Publications

Automated reduction of blood coagulation models.

Hansen Kirk B KB Shadden Shawn C SC

International journal for numerical methods in biomedical engineering 20190829 10

Mathematical modeling of thrombosis typically involves modeling the coagulation cascade. Models of coagulation generally involve the reaction kinetics for dozens of proteins. The resulting system of equations is difficult to parameterize, and its numerical solution is challenging when coupled to blood flow or other physics important to clotting. Prior research suggests that essential aspects of coagulation may be reproduced by simpler models. This evidence motivates a systematic approach to mode ...[more]

PMID: 31161687

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Lo2005 - Stochastic Modeling of Blood Coagulation Initiation

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Inhibition of caspase-1-mediated inflammasome activation reduced blood coagulation in cerebrospinal fluid after subarachnoid haemorrhage.

Project description:BackgroundNeuroinflammation and blood coagulation responses in cerebrospinal fluid (CSF) contribute to the poor outcome associated with subarachnoid haemorrhage (SAH). We explored the role of caspase-1-mediated inflammasome activation on extrinsic blood coagulation in CSF after SAH.MethodsPost-SAH proteomic changes and correlation between caspase-1 with extrinsic coagulation factors in human CSF after SAH were analysed. Time course and cell localisation of brain inflammasome and extrinsic coagulation proteins after SAH were explored in a rat SAH model. Pharmacological inhibition of caspase-1 via VX-765 was used to explore the role of caspase-1 in blood clearance and CSF circulation after SAH in rats. Primary astrocytes were used to evaluate the role of caspase-1 in haemoglobin-induced pyroptosis and tissue factor (TF) production/release.FindingsNeuroinflammation and blood coagulation activated after SAH in human CSF. The caspase-1 levels significantly correlated with the extrinsic coagulation factors. The activated caspase-1 and extrinsic coagulation initiator TF was increased on astrocytes after SAH in rats. VX-765 attenuated neurological deficits by accelerating CSF circulation and blood clearance through inhibiting pyroptotic neuroinflammation and TF-induced fibrin deposition in the short-term, and improved learning and memory capacity by preventing hippocampal neuronal loss and hydrocephalus in the long-term after SAH in rats. VX-765 reduced haemoglobin-induced pyroptosis and TF production/release in primary astrocytes.InterpretationInhibition of caspase-1 by VX-765 appears to be a potential treatment against neuroinflammation and blood coagulation in CSF after SAH.FundingThis study was supported by National Institutes of Health of United States of America, and National Natural Science Foundation of China.

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