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A characteristic of ecosystems is the existence of manifold of independencies which are highly complex. Various mathematical models have made considerable contributions in gaining a better understanding of the predator–prey interactions. The main components of any predator–prey models are, firstly, how the different population classes grow and secondly, how the prey and predator interacts. In this paper, the two populations’ growth rates obey the logistic law and the carrying capacity of the predator depends on the available number of prey are considered. Our aim is to clarify the relationship between models and Holling types functional and numerical responses in order to gain insights into predator interferences and to answer an important question how competition is carried out. We consider a predator–prey model and a two-predator one-prey model to explain the idea. The novel approach is explained for the mechanism measurement of predator interference through depending on numerical response. Our approach gives good correspondence between an important real data and computer simulations. [ABSTRACT FROM AUTHOR]

Mathematical models have shed light on the dynamics of HIV- 1 infection in vivo. In this paper, we generalize continuous mathematical models of drug therapy for HIV-1 by Perelson et al. (Science 271:1582–1586, 1996) and Perelson and Nelson (SIAM Rev 41:3–44, 1999) on time scales, i.e., a nonempty closed subset of real numbers in order to derive new discrete models that predict the total concentration of plasma virus as a function of time. One of our main goals is to compare discrete mathematical models with the continuous model in Perelson et al. (1996) where HIV infected patients were given protease inhibitors and sampled frequently thereafter. For the comparison, we use experimental data collected in Perelson et al. (1996) and estimate the parameters such as the virion clearance rate and the rate of loss of infected cells by fitting the total concentration of plasma virus to this data set. Our results show that discrete systems describe the best fit. In the previous models of this study, the efficacy of protease inhibitor is assumed to be perfect. Motivated by Perelson and Nelson (1999), we end the paper with a mathematical model of imperfect protease inhibitor and reverse transcriptase (RT) inhibitor combination therapy of HIV-1 infection on time scales with its stability analysis. [ABSTRACT FROM AUTHOR]

The focus of this paper is to develop a new partial differential equation model for the pattern formation of the human pathogen Staphylococcus aureus, starting from a newly developed model of selected gene regulation mechanisms. In our model, we do not only account for the bacteria densities and nutrient concentrations, but also for the quorum sensing and biofilm components, since they enable bacteria to coordinate their behavior and provide the environment in which the colony grows. To this end, we model the relevant gene regulation systems using ordinary differential equations and therefrom derive our evolution equations for quorum sensing and biofilm environment by time-scale arguments. Furthermore, we compare and validate our model and the corresponding simulation results with biological real data observations of Staphylococcus aureus mutant colony growth in the laboratory. We show that we are able to adequately display the qualitative biological features of pattern formation in selected mutants, using the parameter changes indicated by the gene regulation mechanisms. [ABSTRACT FROM AUTHOR]

Recent years have seen the introduction of non-local interactions in various fields. A typical example of a non-local interaction is where the convolution kernel incorporates short-range activation and long-range inhibition. This paper presents the relationship between non-local interactions and reaction-diffusion systems in the following sense: (a) the relationship between the instability induced by non-local interaction and diffusion-driven instability; (b) the realization of non-local interactions by reaction-diffusion systems. More precisely, it is shown that the non-local interaction of a Mexican-hat kernel destabilizes the stable homogeneous state and that this instability is related to diffusion-driven instability. Furthermore, a reaction-diffusion system that approximates the non-local interaction system with any even convolution kernel is shown to exist. [ABSTRACT FROM AUTHOR]

Although diseases such as influenza, tuberculosis and SARS are transmitted through an environmentally mediated mechanism, most modeling work on these topics is based on the concepts of infectious contact and direct transmission. In this paper we use a paradigm model to show that environmental transmission appears like direct transmission in the case where the pathogen persists little time in the environment. Furthermore, we formulate conditions for the validity of this modeling approximation and we illustrate them numerically for the cases of cholera and influenza. According to our results based on recently published parameter estimates, the direct transmission approximation fails for both cholera and influenza. While environmental transmission is typically chosen over direct transmission in modeling cholera, this is not the case for influenza. [ABSTRACT FROM AUTHOR]

Systems Biology is the science that aims to understand how biological function absent from macromolecules in isolation, arises when they are components of their system. Dedicated to the memory of Reinhart Heinrich, this paper discusses the origin and evolution of the new part of systems biology that relates to metabolic and signal-transduction pathways and extends mathematical biology so as to address postgenomic experimental reality. Various approaches to modeling the dynamics generated by metabolic and signal-transduction pathways are compared. The silicon cell approach aims to describe the intracellular network of interest precisely, by numerically integrating the precise rate equations that characterize the ways macromolecules’ interact with each other. The non-equilibrium thermodynamic or ‘lin–log’ approach approximates the enzyme rate equations in terms of linear functions of the logarithms of the concentrations. Biochemical Systems Analysis approximates in terms of power laws. Importantly all these approaches link system behavior to molecular interaction properties. The latter two do this less precisely but enable analytical solutions. By limiting the questions asked, to optimal flux patterns, or to control of fluxes and concentrations around the (patho)physiological state, Flux Balance Analysis and Metabolic/Hierarchical Control Analysis again enable analytical solutions. Both the silicon cell approach and Metabolic/Hierarchical Control Analysis are able to highlight where and how system function derives from molecular interactions. The latter approach has also discovered a set of fundamental principles underlying the control of biological systems. The new law that relates concentration control to control by time is illustrated for an important signal transduction pathway, i.e. nuclear hormone receptor signaling such as relevant to bone formation. It is envisaged that there is much more Mathematical Biology to be discovered in the area between molecules and Life. [ABSTRACT FROM AUTHOR]

A mathematical model for infectious disease epidemics with behaviour change and treatment is formulated and analysed. It is indicated that behaviour modification by the population has a significant impact on the dynamics of the disease. Moreover, an optimal control theory is applied to propose the best possible combination of efforts in controlling a disease. It is shown that it may not be necessary to continuously apply treatment at a full rate to eradicate the disease, if the effort is supported by effective behaviour modification strategies. [ABSTRACT FROM AUTHOR]

Dynamics on networks is considered from the perspective of Markov stochastic processes. We partially describe the state of the system through network motifs and infer any missing data using the available information. This versatile approach is especially well adapted for modelling spreading processes and/or population dynamics. In particular, the generality of our framework and the fact that its assumptions are explicitly stated suggests that it could be used as a common ground for comparing existing epidemics models too complex for direct comparison, such as agent-based computer simulations. We provide many examples for the special cases of susceptible-infectious-susceptible and susceptible-infectious-removed dynamics ( e.g., epidemics propagation) and we observe multiple situations where accurate results may be obtained at low computational cost. Our perspective reveals a subtle balance between the complex requirements of a realistic model and its basic assumptions. [ABSTRACT FROM AUTHOR]

Mathematical models have long been used for prediction of dynamics in biological systems. Recently, several efforts have been made to render these models patient specific. One way to do so is to employ techniques to estimate parameters that enable model based prediction of observed quantities. Knowledge of variation in parameters within and between groups of subjects have potential to provide insight into biological function. Often it is not possible to estimate all parameters in a given model, in particular if the model is complex and the data is sparse. However, it may be possible to estimate a subset of model parameters reducing the complexity of the problem. In this study, we compare three methods that allow identification of parameter subsets that can be estimated given a model and a set of data. These methods will be used to estimate patient specific parameters in a model predicting baroreceptor feedback regulation of heart rate during head-up tilt. The three methods include: structured analysis of the correlation matrix, analysis via singular value decomposition followed by QR factorization, and identification of the subspace closest to the one spanned by eigenvectors of the model Hessian. Results showed that all three methods facilitate identification of a parameter subset. The 'best' subset was obtained using the structured correlation method, though this method was also the most computationally intensive. Subsets obtained using the other two methods were easier to compute, but analysis revealed that the final subsets contained correlated parameters. In conclusion, to avoid lengthy computations, these three methods may be combined for efficient identification of parameter subsets. [ABSTRACT FROM AUTHOR]

Systems biology aims at building computational models of biological pathways in order to study in silico their behaviour and to verify biological hypotheses. Modelling can become a new powerful method in molecular biology, if correctly used. Here we present step-by-step the derivation and identification of the dynamical model of a biological pathway using a novel synthetic network recently constructed in the yeast Saccharomyces cerevisiae for In-vivo Reverse-Engineering and Modelling Assessment. This network consists of five genes regulating each other transcription. Moreover, it includes one protein-protein interaction, and its genes can be switched on by addition of galactose to the medium. In order to describe the network dynamics, we adopted a deterministic modelling approach based on non-linear differential equations. We show how, through iteration between experiments and modelling, it is possible to derive a semi-quantitative prediction of network behaviour and to better understand the biology of the pathway of interest. [ABSTRACT FROM AUTHOR]

A stochastic model is proposed to explain one possible underlying mechanism of the postantibiotic effect (PAE). This phenomenon, of continued inhibition of bacterial growth after removal of the antibiotic drug, is of high relevance in the context of optimizing dosing regimens. One clinical implication of long PAE lies in the possibility of increasing intervals between drug administrations. The model describes the dynamics of synthesis, saturation and removal of penicillin binding proteins (PBPs). High fractions of saturated PBPs are in the model associated with a lower growth capacity of bacteria. An analytical solution for the bivariate probability of saturated and unsaturated PBPs is used as a basis to explore optimal antibiotic dosing regimens. Our finding that longer PAEs do not necessarily promote for increased intervals between doses, might help for our understanding of data provided from earlier PAE studies and for the determination of the clinical relevance of PAE in future studies. [ABSTRACT FROM AUTHOR]