A biomathematical model of lymphopoiesis is described and used to analyze the lymphocyte changes observed in the blood of exposed victims in radiation accidents. The coarse-grained architecture of cellular replication and production and implicit cellular regulation mechanisms used in this model make it straightforward to incorporate various radiation conditions. Model simulations with reported absorbed doses as inputs are shown to qualitatively and quantitatively describe a wide range of accidental data in vastly different scenarios. In addition, the absolute lymphocyte counts and the depletion rate constants calculated by this model show good correlation with two widely recognized empirical methods for early dose assessment. This demonstrates the potential to use the biophysical model as an alternative method for the assessment of radiation injury in the case of large-scale radiation disaster. The physiological assumptions underlying the model are also discussed, which may provide a putative mechanism for some biodosimetric tools that use the peripheral blood cell counts as markers of radiation impairment.
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http://dx.doi.org/10.1097/HP.0b013e318240593d | DOI Listing |
PLoS Comput Biol
January 2025
Genesupport, Avenue de Sévelin 18, Lausanne, Switzerland.
Catalysis and specifically autocatalysis are the quintessential building blocks of life. Yet, although autocatalytic networks are necessary, they are not sufficient for the emergence of life-like properties, such as replication and adaptation. The ultimate and potentially fatal threat faced by molecular replicators is parasitism; if the polymerase error rate exceeds a critical threshold, even the fittest molecular species will disappear.
View Article and Find Full Text PDFSci Rep
December 2024
Institute for Medical Informatics, Statistics and Epidemiology (IMISE), University of Leipzig, 04107, Leipzig, Germany.
When infected with SARS-CoV-2, Syrian hamsters (Mesocricetus auratus) develop moderate disease severity presenting key features of human COVID-19. We here develop a biomathematical model of the disease course by translating known biological mechanisms of virus-host interactions and immune responses into ordinary differential equations. We explicitly describe the dynamics of virus population, affected alveolar epithelial cells, and involved relevant immune cells comprising for example CD4+ T cells, CD8+ T cells, macrophages, natural killer cells and B cells.
View Article and Find Full Text PDFPLoS One
December 2024
Facultad de Ingeniería, Universidad de San Buenaventura, Cali, Colombia.
The Covid-19 pandemic has challenged both the scientific community and government authorities in Colombia. Both sectors are collaborating to understand the transmission and spread of the virus and to establish control strategies. This study proposes a biomathematical model with difference equations to analyze the transmission of Covid-19 in Santiago de Cali from March 2020 to June 2022.
View Article and Find Full Text PDFClin Transl Med
October 2024
Cardiovascular Research Unit, Department of Precision Health, Luxembourg Institute of Health, Strassen, Luxembourg.
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