scholarly journals A mathematical model for lactate transport to red blood cells

2010 ◽  
Vol 61 (2) ◽  
pp. 93-102 ◽  
Author(s):  
Patrick Wahl ◽  
Zengyuan Yue ◽  
Christoph Zinner ◽  
Wilhelm Bloch ◽  
Joachim Mester
1995 ◽  
Vol 03 (02) ◽  
pp. 447-455
Author(s):  
FORTUNATA SOLIMANO

A mathematical model for the drug delivery to macrophages of the tissues by using a preassigned cohort of red blood cells loaded with a drug is presented. This model is a system of three nonlinear differential equations, with a discrete time delay and an input depending on the time. The input should be controlled in order to obtain the longest duration of the therapeutic effect.


2018 ◽  
Author(s):  
Ronan Duchesne ◽  
Anissa Guillemin ◽  
Fabien Crauste ◽  
Olivier Gandrillon

AbstractThe in vivo erythropoiesis, which is the generation of mature red blood cells in the bone marrow of whole organisms, has been described by a variety of mathematical models in the past decades. However, the in vitro erythropoiesis, which produces red blood cells in cultures, has received much less attention from the modelling community. In this paper, we propose the first mathematical model of in vitro erythropoiesis. We start by formulating different models and select the best one at fitting experimental data of in vitro erythropoietic differentiation. It is based on a set of linear ODE, describing 3 hypothetical populations of cells at different stages of differentiation. We then compute confidence intervals for all of its parameters estimates, and conclude that our model is fully identifiable. Finally, we use this model to compute the effect of a chemical drug called Rapamycin, which affects all states of differentiation in the culture, and relate these effects to specific parameter variations. We provide the first model for the kinetics of in vitro cellular differentiation which is proven to be identifiable. It will serve as a basis for a model which will better account for the variability which is inherent to experimental protocol used for the model calibration.


1995 ◽  
Author(s):  
Nikolaos K. Uzunoglou ◽  
Georgios Stamatakos ◽  
Dimitrios Koutsouris ◽  
Dido M. Yova-Loukas

2002 ◽  
Vol 34 (S34) ◽  
pp. 555-559 ◽  
Author(s):  
N. M. KOHO ◽  
L. K. VÄIHKÖNEN ◽  
A. R. PÖSÖ

2008 ◽  
Vol 69 (8) ◽  
pp. 1091-1096 ◽  
Author(s):  
Ninna M. Koho ◽  
Marja Raekallio ◽  
Erja Kuusela ◽  
Jaana Vuolle ◽  
A. Reeta Pösö

Author(s):  
Titus Okello Orwa ◽  
Rachel Waema Mbogo ◽  
Livingstone Serwadda Luboobi

Human malaria remains a major killer disease worldwide, with nearly half (3.2 billion) of the world’s population at risk of malaria infection. The infectious protozoan disease is endemic in tropical and subtropical regions, with an estimated 212 million new cases and 429,000 malaria-related deaths in 2015. An in-host mathematical model ofPlasmodium falciparummalaria that describes the dynamics and interactions of malaria parasites with the host’s liver cells (hepatocytic stage), the red blood cells (erythrocytic stage), and macrophages is reformulated. By a theoretical analysis, an in-host basic reproduction numberR0is derived. The disease-free equilibrium is shown to be locally and globally asymptotically stable. Sensitivity analysis reveals that the erythrocyte invasion rateβr, the average number of merozoites released per bursting infected erythrocyteK, and the proportion of merozoites that cause secondary invasions at the blood phaseζare the most influential parameters in determining the malaria infection outcomes. Numerical results show that macrophages have a considerable impact in clearing infected red blood cells through phagocytosis. Moreover, the density of infected erythrocytes and hence the severity of malaria are shown to increase with increasing density of merozoites in the blood. Concurrent use of antimalarial drugs and a potential erythrocyte invasion-avoidance vaccine would minimize the density of infected erythrocytes and hence malaria disease severity.


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