Theory in Biosciences最新文献

This paper addresses the relationship between information and structure of the genetic code. The code has two puzzling anomalies: First, when viewed as 64 sub-cubes of a [Formula: see text] cube, the codons for serine (S) are not contiguous, and there are amino acid codons with zero redundancy, which goes counter to the objective of error correction. To make sense of this, the paper shows that the genetic code must be viewed not only on stereochemical, co-evolution, and error-correction considerations, but also on two additional factors of significance to natural systems, that of an information-theoretic dimensionality of the code data, and the principle of maximum entropy. One implication of non-integer dimensionality associated with data dimensions is self-similarity to different scales, and it is shown that the genetic code does satisfy this property, and it is further shown that the maximum entropy principle operates through the scrambling of the elements in the sense of maximum algorithmic information complexity, generated by an appropriate exponentiation mapping. It is shown that the new considerations and the use of maximum entropy transformation create new constraints that are likely the reasons for the non-uniform codon groups and codons with no redundancy.

This work concerns a many-body deterministic model that displays life-like properties such as emergence, complexity, self-organization, self-regulation, excitability and spontaneous compartmentalization. The model portraits the dynamics of an ensemble of locally coupled polar phase oscillators, moving in a two-dimensional space, that under certain conditions exhibit emergent superstructures. Those superstructures are self-organized dynamic networks, resulting from a synchronization process of many units, over length scales much greater than the interaction range. Such networks compartmentalize the two-dimensional space with no a priori constraints, due to the formation of porous transport walls, and represent a highly complex and novel non-linear behavior. The analysis is numerically carried out as a function of a control parameter showing distinct regimes: static pattern formation, dynamic excitable networks formation, intermittency and chaos. A statistical analysis is drawn to determine the control parameter ranges for the various behaviors to appear. The model and the results shown in this work are expected to contribute to the field of artificial life.

In this work, we analyse the dynamics of a five-dimensional hepatitis C virus infection mathematical model including the spatial mobility of hepatitis C virus particles, the transmission of hepatitis C virus infection by mitosis process of infected hepatocytes with logistic growth, time delays, antibody response and cytotoxic T lymphocyte (CTL) immune response with general incidence functions for both modes of infection transmission, namely virus-to-cell as well as cell-to-cell. Firstly, we prove rigorously the existence, the uniqueness, the positivity and the boundedness of the solution of the initial value and boundary problem associated with the new constructed model. Secondly, we found that the basic reproductive number is the sum of the basic reproduction number determined by cell-free virus infection, determined by cell-to-cell infection and determined by proliferation of infected cells. It is proved the existence of five spatially homogeneous equilibria known as infection-free, immune-free, antibody response, CTL response and antibody and CTL responses. By using the linearization methods, the local stability of the latter is established under some rigorous conditions. Finally, we proved the existence of periodic solutions by highlighting the occurrence of a Hopf bifurcation for a certain threshold value of one delay.

Advancement of new technologies such as laser, focused ultrasound, microwave and radio frequency for thermal therapy of skin tissue has increased numerous challenging situations in medical treatment. In this article, a new meticulous bio-heat transfer model based on memory-dependent derivative with dual-phase-lag has been developed under different thermal conditions such as thermal shock and harmonic-type heating. Laplace transform method is acquired to perceive the analytical consequences. Quantitative results are evaluated for displacement, strain and temperature along with stress distributions in time domain by adopting the technique of inverse Laplace transform. Impacts of the constituents of memory-dependent derivatives-kernel functions along with time-delay parameter are analysed on the studied fields (temperature, displacement, strain and stress) for both thermal conditions separately using computational results. It has been found that the insertion of the memory effect proves itself a unified model, and therefore, this model can better predict temperature field data for thermal treatment processes.

In this work, we formulate the following question: How the distribution of aminoacyl-tRNA synthetases (aaRSs) went from an ancestral bidirectional gene (mirror symmetry) to the symmetrical distribution of aaRSs in a six-dimensional hypercube of the Standard Genetic Code (SGC)? We assume a primeval RNY code, two Extended Genetic RNA codes type 1 and 2, and the SGC. We outline the types of symmetries of the distribution of aaRSs in each code. The symmetry groups of aaRSs in each code are described, until the symmetries of the SGC display a mirror symmetry. Considering both Extended RNA codes the 20 aaRSs were already present before the Last Universal Ancestor. These findings reveal intricacies in the diversification of aaRSs accompanied by the evolution of the genetic code.

We consider a modified SIR model with a four-dimensional system of ordinary differential equations to consider the influence of a limited isolation capacity on the final epidemic size defined as the total number of individuals who experienced the disease at the end of an epidemic season. We derive the necessary and sufficient condition that the isolation reaches the capacity in a finite time on the way of the epidemic process, and show that the final epidemic size is monotonically decreasing in terms of the isolation capacity. We find further that the final epidemic size could have a discontinuous change at the critical value of isolation capacity below which the isolation reaches the capacity in a finite time. Our results imply that the breakdown of isolation with a limited capacity would cause a drastic increase of the epidemic size. Insufficient capacity of the isolation could lead to an unexpectedly severe epidemic situation, while such a severity would be avoidable with the sufficient isolation capacity.

In this paper a Feynman-type path integral control approach is used for a recursive formulation of a health objective function subject to a fatigue dynamics, a forward-looking stochastic multi-risk susceptible-infective-recovered (SIR) model with risk-group's Bayesian opinion dynamics toward vaccination against COVID-19. My main interest lies in solving a minimization of a policy-maker's social cost which depends on some deterministic weight. I obtain an optimal lock-down intensity from a Wick-rotated Schrödinger-type equation which is analogous to a Hamiltonian-Jacobi-Bellman (HJB) equation. My formulation is based on path integral control and dynamic programming tools facilitates the analysis and permits the application of algorithm to obtain numerical solution for pandemic control model.

In this article, we study the dynamical properties of susceptible-vaccinated-infected-susceptible (SVIS) epidemic system with saturated incidence rate and vaccination strategies. By constructing the suitable Lyapunov function, we examine the existence and uniqueness of the stochastic system. With the help of Khas'minskii theory, we set up a critical value [Formula: see text] with respect to the basic reproduction number [Formula: see text] of the deterministic system. A unique ergodic stationary distribution is investigated under the condition of [Formula: see text]. In the epidemiological study, the ergodic stationary distribution represents that the disease will persist for long-term behavior. We focus for developing the general three-dimensional Fokker-Planck equation using appropriate solving theories. Around the quasi-endemic equilibrium, the probability density function of the stochastic system is analyzed which is the main theme of our study. Under [Formula: see text], both the existence of ergodic stationary distribution and density function can elicit all the dynamical behavior of the disease persistence. The condition of disease extinction of the system is derived. For supporting theoretical study, we discuss the numerical results and the sensitivities of the biological parameters. Results and conclusions are highlighted.

Autosomal dominant diseases typically have an age-related onset. Here, I focus on genetic prion disease (gPrD), caused by various mutations in the PRNP gene. While gPrD typically occurs at or after middle age, there can be considerable variability in the specific age of onset. This variability can occur among patients with the same PRNP mutation; in some cases, these differences occur not only between families but even within the same family. It is not known why gPrD onset is typically delayed for decades when the causative mutation is present from birth. Mouse models of gPrD manifest disease; however, unlike human gPrD, which typically takes decades to manifest, mouse models exhibit disease within months. Therefore, the time to onset of prion disease is proportional to species lifespan; however, it is not known why this is the case. I hypothesize that the initiation of gPrD is strongly influenced by the process of aging; therefore, disease onset is related to proportional functional age (e.g., mice vs. humans). I propose approaches to test this hypothesis and discuss its significance with respect to delaying prion disease through suppression of aging.

In this study, we proposed a biological model explaining the progress of autoimmune activation along different stages of systemic lupus erythematosus (SLE). For any upcoming stage of SLE, any new component is introduced, when it is added to the model. Particularly, the interaction of mesenchymal stem cells, with the components of the model, is specified in a way that both the inflammatory and anti-inflammatory functions of these cells would be covered. The biological model is then recapitulated to a model with less complexity that explains the main features of the problem. Later, a 7th-order mathematical model for SLE is proposed, based on this simplified model. Finally, the range of validity of the proposed mathematical model was assessed. For this purpose, we simulated the model and analyzed the simulation results in case of some known behaviors of the disease, such as tolerance breach, the appearance of systemic inflammation, development of clinical signs, and occurrence of flares and improvements. The model was able to reproduce these events, qualitatively.