Reaction–diffusion model of atherosclerosis development
Atherosclerosis begins as an inflammation in blood vessel walls (intima). The inflammatory response of the organism leads to the recruitment of monocytes. Trapped in the intima, they differentiate into macrophages and foam cells leading to the production of inflammatory cytokines and further recruit...
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2012
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| Online Access: | http://hdl.handle.net/10725/2355 http://dx.doi.org/10.1007/s00285-011-0461-1 http://link.springer.com/article/10.1007/s00285-011-0461-1 |
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| _version_ | 1864513457959731200 |
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| author | El Khatib, N. |
| author2 | Génieys, S. Kazmierczak, B. Volpert, V. |
| author2_role | author author author |
| author_facet | El Khatib, N. Génieys, S. Kazmierczak, B. Volpert, V. |
| author_role | author |
| dc.creator.none.fl_str_mv | El Khatib, N. Génieys, S. Kazmierczak, B. Volpert, V. |
| dc.date.none.fl_str_mv | 2012-08-21 2015-10-27T12:50:42Z 2015-10-27T12:50:42Z 2015-10-27 |
| dc.identifier.none.fl_str_mv | 0303-6812 http://hdl.handle.net/10725/2355 http://dx.doi.org/10.1007/s00285-011-0461-1 El Khatib, N., Génieys, S., Kazmierczak, B., & Volpert, V. (2012). Reaction–diffusion model of atherosclerosis development. Journal of mathematical biology, 65(2), 349-374. http://link.springer.com/article/10.1007/s00285-011-0461-1 |
| dc.language.none.fl_str_mv | en |
| dc.relation.none.fl_str_mv | Journal of Mathematical Biology |
| dc.rights.*.fl_str_mv | info:eu-repo/semantics/openAccess |
| dc.title.none.fl_str_mv | Reaction–diffusion model of atherosclerosis development |
| dc.type.none.fl_str_mv | Article info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/article |
| description | Atherosclerosis begins as an inflammation in blood vessel walls (intima). The inflammatory response of the organism leads to the recruitment of monocytes. Trapped in the intima, they differentiate into macrophages and foam cells leading to the production of inflammatory cytokines and further recruitment of white blood cells. This self-accelerating process, strongly influenced by low-density lipoproteins (cholesterol), results in a dramatic increase of the width of blood vessel walls, formation of an atherosclerotic plaque and, possibly, of its rupture. We suggest a 2D mathematical model of the initiation and development of atherosclerosis which takes into account the concentration of blood cells inside the intima and of pro- and anti-inflammatory cytokines. The model represents a reaction–diffusion system in a strip with nonlinear boundary conditions which describe the recruitment of monocytes as a function of the concentration of inflammatory cytokines. We prove the existence of travelling waves described by this system and confirm our previous results which suggest that atherosclerosis develops as a reaction–diffusion wave. The theoretical results are confirmed by the results of numerical simulations. |
| eu_rights_str_mv | openAccess |
| format | article |
| id | LAURepo_30604cb8f6fe3aa17b1104c20f024f05 |
| identifier_str_mv | 0303-6812 El Khatib, N., Génieys, S., Kazmierczak, B., & Volpert, V. (2012). Reaction–diffusion model of atherosclerosis development. Journal of mathematical biology, 65(2), 349-374. |
| language_invalid_str_mv | en |
| network_acronym_str | LAURepo |
| network_name_str | Lebanese American University repository |
| oai_identifier_str | oai:laur.lau.edu.lb:10725/2355 |
| publishDate | 2012 |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| spelling | Reaction–diffusion model of atherosclerosis developmentEl Khatib, N.Génieys, S.Kazmierczak, B.Volpert, V.Atherosclerosis begins as an inflammation in blood vessel walls (intima). The inflammatory response of the organism leads to the recruitment of monocytes. Trapped in the intima, they differentiate into macrophages and foam cells leading to the production of inflammatory cytokines and further recruitment of white blood cells. This self-accelerating process, strongly influenced by low-density lipoproteins (cholesterol), results in a dramatic increase of the width of blood vessel walls, formation of an atherosclerotic plaque and, possibly, of its rupture. We suggest a 2D mathematical model of the initiation and development of atherosclerosis which takes into account the concentration of blood cells inside the intima and of pro- and anti-inflammatory cytokines. The model represents a reaction–diffusion system in a strip with nonlinear boundary conditions which describe the recruitment of monocytes as a function of the concentration of inflammatory cytokines. We prove the existence of travelling waves described by this system and confirm our previous results which suggest that atherosclerosis develops as a reaction–diffusion wave. The theoretical results are confirmed by the results of numerical simulations.PublishedN/A2015-10-27T12:50:42Z2015-10-27T12:50:42Z2012-08-212015-10-27Articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article0303-6812http://hdl.handle.net/10725/2355http://dx.doi.org/10.1007/s00285-011-0461-1El Khatib, N., Génieys, S., Kazmierczak, B., & Volpert, V. (2012). Reaction–diffusion model of atherosclerosis development. Journal of mathematical biology, 65(2), 349-374.http://link.springer.com/article/10.1007/s00285-011-0461-1enJournal of Mathematical Biologyinfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/23552016-08-02T11:05:50Z |
| spellingShingle | Reaction–diffusion model of atherosclerosis development El Khatib, N. |
| status_str | publishedVersion |
| title | Reaction–diffusion model of atherosclerosis development |
| title_full | Reaction–diffusion model of atherosclerosis development |
| title_fullStr | Reaction–diffusion model of atherosclerosis development |
| title_full_unstemmed | Reaction–diffusion model of atherosclerosis development |
| title_short | Reaction–diffusion model of atherosclerosis development |
| title_sort | Reaction–diffusion model of atherosclerosis development |
| url | http://hdl.handle.net/10725/2355 http://dx.doi.org/10.1007/s00285-011-0461-1 http://link.springer.com/article/10.1007/s00285-011-0461-1 |