A model for the formation, growth, and lysis of clots in quiescent plasma. A comparison between the effects of antithrombin III deficiency and protein C deficiency
A mathematical model comprised of 23 reaction–diffusion equations is used to simulate the biochemical changes and transport of various reactants involved in coagulation and fibrinolysis in quiescent plasma. The growth and lysis of a thrombus, as portrayed by the model equations, is governed by bound...
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Veröffentlicht in: | Journal of theoretical biology 2008-08, Vol.253 (4), p.725-738 |
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creator | Anand, M. Rajagopal, K. Rajagopal, K.R. |
description | A mathematical model comprised of 23 reaction–diffusion equations is used to simulate the biochemical changes and transport of various reactants involved in coagulation and fibrinolysis in quiescent plasma. The growth and lysis of a thrombus, as portrayed by the model equations, is governed by boundary conditions that include the surface concentration of TF–VIIa, the generation of XIa by contact activation (in vitro), and the secretion of tPA due to endothelial activation. We apply the model to two clinically relevant hypercoagulable states, caused by deficiency of either antithrombin III or protein C. These predictions are compared with published experimental data which validate the utility of the developed model under the special case of static conditions. The incorporation of varying hemodynamic conditions in to the current fluid static model remains to be performed. |
doi_str_mv | 10.1016/j.jtbi.2008.04.015 |
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These predictions are compared with published experimental data which validate the utility of the developed model under the special case of static conditions. 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A comparison between the effects of antithrombin III deficiency and protein C deficiency</title><title>Journal of theoretical biology</title><addtitle>J Theor Biol</addtitle><description>A mathematical model comprised of 23 reaction–diffusion equations is used to simulate the biochemical changes and transport of various reactants involved in coagulation and fibrinolysis in quiescent plasma. The growth and lysis of a thrombus, as portrayed by the model equations, is governed by boundary conditions that include the surface concentration of TF–VIIa, the generation of XIa by contact activation (in vitro), and the secretion of tPA due to endothelial activation. We apply the model to two clinically relevant hypercoagulable states, caused by deficiency of either antithrombin III or protein C. These predictions are compared with published experimental data which validate the utility of the developed model under the special case of static conditions. The incorporation of varying hemodynamic conditions in to the current fluid static model remains to be performed.</description><subject>Antithrombin III</subject><subject>Antithrombin III Deficiency - metabolism</subject><subject>Blood Coagulation - physiology</subject><subject>Blood Coagulation Factors - metabolism</subject><subject>Fibrinolysis - physiology</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>Hypercoagulable state</subject><subject>Mathematical model</subject><subject>Models, Biological</subject><subject>Plasma - metabolism</subject><subject>Protein C</subject><subject>Protein C Deficiency - metabolism</subject><issn>0022-5193</issn><issn>1095-8541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcuOEzEQtBCIzQZ-gAPyidPO4Md4ZEtcomiBSCtxgbPlsdvE0cw4azus8j37ozgPCU6gPvShq6q7qxB6R0lLCe0_7tpdGULLCJEt6VpCxQu0oESJRoqOvkQLQhhrBFX8Bt3mvCOEqI73r9ENlYIrTugCPa_wFB2M2MeEyxZOfTIlxPkO_0zxqWzvsJkdHo85ZBw9tmMsGYcZPx4CZAtzwfvR5Mm0eIVtnPYmhRxnPEB5ApjPmuA92HKmm7mEsk1xGqrEZrPBDnywAWZ7PO_Zp1igjtZ_Dd6gV96MGd5e-xL9-Hz_ff21efj2ZbNePTSWS1Ea3rFa0PeDckxwKx0bFGOG9lxa5okQggnofSeFc6IDLpRysmOGG6CdGfgSfbjo1iMeD5CLnkL9cBzNDPGQda-45ILw_wIZkRVab1gidgHaFHNO4PU-hcmko6ZEnzLUO33KUJ8y1KTTNcNKen9VPwwTuD-Ua2gV8OkCgGrGrwBJ57NR4EKqPmsXw7_0fwNBXK6A</recordid><startdate>20080821</startdate><enddate>20080821</enddate><creator>Anand, M.</creator><creator>Rajagopal, K.</creator><creator>Rajagopal, K.R.</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080821</creationdate><title>A model for the formation, growth, and lysis of clots in quiescent plasma. 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A comparison between the effects of antithrombin III deficiency and protein C deficiency</atitle><jtitle>Journal of theoretical biology</jtitle><addtitle>J Theor Biol</addtitle><date>2008-08-21</date><risdate>2008</risdate><volume>253</volume><issue>4</issue><spage>725</spage><epage>738</epage><pages>725-738</pages><issn>0022-5193</issn><eissn>1095-8541</eissn><abstract>A mathematical model comprised of 23 reaction–diffusion equations is used to simulate the biochemical changes and transport of various reactants involved in coagulation and fibrinolysis in quiescent plasma. The growth and lysis of a thrombus, as portrayed by the model equations, is governed by boundary conditions that include the surface concentration of TF–VIIa, the generation of XIa by contact activation (in vitro), and the secretion of tPA due to endothelial activation. We apply the model to two clinically relevant hypercoagulable states, caused by deficiency of either antithrombin III or protein C. These predictions are compared with published experimental data which validate the utility of the developed model under the special case of static conditions. The incorporation of varying hemodynamic conditions in to the current fluid static model remains to be performed.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>18539301</pmid><doi>10.1016/j.jtbi.2008.04.015</doi><tpages>14</tpages></addata></record> |
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subjects | Antithrombin III Antithrombin III Deficiency - metabolism Blood Coagulation - physiology Blood Coagulation Factors - metabolism Fibrinolysis - physiology Hemostasis Humans Hypercoagulable state Mathematical model Models, Biological Plasma - metabolism Protein C Protein C Deficiency - metabolism |
title | A model for the formation, growth, and lysis of clots in quiescent plasma. A comparison between the effects of antithrombin III deficiency and protein C deficiency |
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