A model of cardiovascular disease giving a plausible mechanism for the effect of fractionated low-dose ionizing radiation exposure

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dc.contributor.authorLittle, M. P.en
dc.contributor.authorGola, A.en
dc.contributor.authorTzoulaki, I.en
dc.date.accessioned2015-11-24T19:40:16Z
dc.date.available2015-11-24T19:40:16Z
dc.identifier.issn1553-7358-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24324
dc.rightsDefault Licence-
dc.subjectAlgorithmsen
dc.subjectAtherosclerosis/*etiology/metabolismen
dc.subjectChemokine CCL2/metabolismen
dc.subjectCholesterol, LDL/metabolismen
dc.subjectDose-Response Relationship, Radiationen
dc.subjectEndothelial Cells/metabolism/radiation effectsen
dc.subjectHumansen
dc.subjectLinear Modelsen
dc.subject*Models, Cardiovascularen
dc.subjectMonocytes/metabolism/radiation effectsen
dc.subjectOccupational Exposure/adverse effectsen
dc.subjectRadiation Injuries/*metabolismen
dc.subjectRadiation, Ionizingen
dc.subjectTime Factorsen
dc.titleA model of cardiovascular disease giving a plausible mechanism for the effect of fractionated low-dose ionizing radiation exposureen
heal.abstractAtherosclerosis is the main cause of coronary heart disease and stroke, the two major causes of death in developed society. There is emerging evidence of excess risk of cardiovascular disease at low radiation doses in various occupationally exposed groups receiving small daily radiation doses. Assuming that they are causal, the mechanisms for effects of chronic fractionated radiation exposures on cardiovascular disease are unclear. We outline a spatial reaction-diffusion model for atherosclerosis and perform stability analysis, based wherever possible on human data. We show that a predicted consequence of multiple small radiation doses is to cause mean chemo-attractant (MCP-1) concentration to increase linearly with cumulative dose. The main driver for the increase in MCP-1 is monocyte death, and consequent reduction in MCP-1 degradation. The radiation-induced risks predicted by the model are quantitatively consistent with those observed in a number of occupationally-exposed groups. The changes in equilibrium MCP-1 concentrations with low density lipoprotein cholesterol concentration are also consistent with experimental and epidemiologic data. This proposed mechanism would be experimentally testable. If true, it also has substantive implications for radiological protection, which at present does not take cardiovascular disease into account. The Japanese A-bomb survivor data implies that cardiovascular disease and cancer mortality contribute similarly to radiogenic risk. The major uncertainty in assessing the low-dose risk of cardiovascular disease is the shape of the dose response relationship, which is unclear in the Japanese data. The analysis of the present paper suggests that linear extrapolation would be appropriate for this endpoint.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1371/journal.pcbi.1000539-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/19851450-
heal.identifier.secondaryhttp://www.ploscompbiol.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pcbi.1000539&representation=PDF-
heal.journalNamePLoS Comput Biolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2009-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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