Acta Biotheoretica最新文献

Natural selection of specific protobiomonomers during abiogenic development of the prototype genetic code is hindered by the diversity of structural, spatial, and rotational isomers that have identical elemental composition and molecular mass (M), but can vary significantly in their physicochemical characteristics, such as the melting temperature T_m, the T_m:M ratio, and the solubility in water, due to different positions of atoms in the molecule. These parameters differ between cis- and trans-isomers of dicarboxylic acids, spatial monosaccharide isomers, and structural isomers of α-, β-, and γ-amino acids. The stable planar heterocyclic molecules of the major nucleobases comprise four (C, H, N, O) or three (C, H, N) elements and contain a single –C=C bond and two nitrogen atoms in each heterocycle involved in C–N and C=N bonds. They exist as isomeric resonance hybrids of single and double bonds and as a mixture of tautomer forms due to the presence of –C=O and/or –NH₂ side groups. They are thermostable, insoluble in water, and exhibit solid-state stability, which is of central importance for DNA molecules as carriers of genetic information. In M–T_m diagrams, proteinogenic amino acids and the corresponding codons are distributed fairly regularly relative to the distinct clusters of purine and pyrimidine bases, reflecting the correspondence between codons and amino acids that was established in different periods of genetic code development. The body of data on the evolution of the genetic code system indicates that the elemental composition and molecular structure of protobiomonomers, and their M, T_m, photostability, and aqueous solubility determined their selection in the emergence of the standard genetic code.

The concept of causal specificity is drawing considerable attention from philosophers of biology. It became the rationale for rejecting (and occasionally, accepting) a thesis of causal parity of developmental factors. This literature assumes that attributing specificity to causal relations is at least in principle a straightforward (if not systematic) task. However, the parity debate in philosophy of biology seems to be stuck at a point where it is not the biological details that will help move forward. In this paper, I take a step back to reexamine the very idea of causal specificity and its intended role in the parity dispute in philosophy of biology. I contend that the idea of causal specificity across variations as currently discussed in the literature is irreducibly twofold in nature: it is about two independent components that are not mutually entailed. I show this to be the source of prior complications with the notion of specificity itself that ultimately affect the purposes for which it is often invoked, notably to settle the parity dispute.

To mitigate the spread of schistosomiasis, a deterministic human-bovine mathematical model of its transmission dynamics accounting for contaminated water reservoirs, including treatment of bovines and humans and mollusciciding is formulated and theoretically analyzed. The disease-free equilibrium is locally and globally asymptotically stable whenever the basic reproduction number (R_0<1), while global stability of the endemic equilibrium is investigated by constructing a suitable Lyapunov function. To support the analytical results, parameter values from published literature are used for numerical simulations and where applicable, uncertainty analysis on the non-dimensional system parameters is performed using the Latin Hypercube Sampling and Partial Rank Correlation Coefficient techniques. Sensitivity analysis to determine the relative importance of model parameters to disease transmission shows that the environment-related parameters namely, (varepsilon _s) (snails shedding rate of cercariae), (p_s) (probability that cercariae shed by snails survive), c (fraction of the contaminated environment sprayed by molluscicides) and (mu _c) (mortality rate of cercariae) are the most significant to mitigate the spread of schistosomiasis. Mollusciciding, which directly impacts the contaminated environment as a single control strategy is more effective compared to treatment. However, concurrently applying mollusciciding and treatment will yield a better outcome.

Radial growth has long been a subject of interest in tree biology research. Recent studies have brought a significant change in the understanding of some basic processes characteristic to the vascular cambium, a meristem that produces secondary vascular tissues (phloem and xylem) in woody plants. A new hypothesis regarding the mechanism of intrusive growth of the cambial initials, which has been ratified by studies of the arrangement of cambial cells, negates the influence of this apical cell growth on the expansion of the cambial circumference. Instead, it suggests that the tip of the elongating cambial initial intrudes between the tangential (periclinal) walls, rather than the radial (anticlinal) walls, of the initial(s) and its(their) derivative(s) lying ahead of the elongating cell tip. The new concept also explains the hitherto obscure mechanism of the cell event called ‘elimination of initials’. This article evaluates these new concepts of the cambial cell dynamics and offers a new interpretation for some curious events occurring in the cambial meristem in relation to the radial growth in woody plants.

The proliferation of mitochondrial DNA (mtDNA) with deletion mutations has been linked to aging and age related neurodegenerative conditions. In this study we model the effect of mtDNA half-life on mtDNA competition and selection. It has been proposed that mutation deletions ((text {mtDNA}_{del})) have a replicative advantage over wild-type ((text {mtDNA}_{wild})) and that this is detrimental to the host cell, especially in post-mitotic cells. An individual cell can be viewed as forming a closed ecosystem containing a large population of independently replicating mtDNA. Within this enclosed environment a selfishly replicating (text {mtDNA}_{del}) would compete with the (text {mtDNA}_{wild}) for space and resources to the detriment of the host cell. In this paper, we use a computer simulation to model cell survival in an environment where (text {mtDNA}_{wild}) compete with (text {mtDNA}_{del}) such that the cell expires upon (text {mtDNA}_{wild}) extinction. We focus on the survival time for long lived post-mitotic cells, such as neurons. We confirm previous observations that (text {mtDNA}_{del}) do have a replicative advantage over (text {mtDNA}_{wild}). As expected, cell survival times diminished with increased mutation probabilities, however, the relationship between survival time and mutation rate was non-linear, that is, a ten-fold increase in mutation probability only halved the survival time. The results of our model also showed that a modest increase in half-life had a profound affect on extending cell survival time, thereby, mitigating the replicative advantage of (text {mtDNA}_{del}). Given the relevance of mitochondrial dysfunction to various neurodegenerative conditions, we propose that therapies to increase mtDNA half-life could significantly delay their onset.

Ion channels are transport proteins present in the lipid bilayers of biological membranes. They are involved in many physiological processes, such as the generation of nerve impulses, hormonal secretion, and heartbeat. Conformational changes in the ion channel-forming protein allow the opening or closing of pores to control the ionic flux through the cell membranes. The opening and closing of the ion channel have been classically treated as a random kinetic process, known as a Markov process. Here the time the channel remains in a given state is assumed to be independent of the condition it had in the previous state. More recently, however, several studies have shown that this process is not random but a deterministic one, where both the open and closed dwell-times and the ionic current flowing through the channel are history-dependent. This property is called long memory or long-range correlation. However, there is still much controversy regarding how this memory originates, which region of the channel is responsible for this property, and which models could best reproduce the memory effect. In this article, we provide a review of what is, where it is, its possible origin, and the mathematical methods used to analyze the long-term memory present in the kinetic process of ion channels.

We propose a mathematical model for a class of predator–prey systems more complex than the usual one, involving a commensalism effect consisting in an influence of the predator on the sustainability of the prey. This effect induces interesting new features, including bi-stability (two attractors with disjoint attraction basins). The question of the possibility of reaching a certain attractor starting from initial conditions with a small population of predators, which presents an interest from the vewpoint of the onset of the predator in evolution, is addressed. We propose two possibilities: the classical one involving adapted conditions in the far past and a new (up to our knowledge) one using biodiversity, specifically the presence of another predator which operates as a starter, being displaced in the sequel.

Three competing ‘methods’ have been endorsed for inferring phylogenetic hypotheses: parsimony, likelihood, and Bayesianism. The latter two have been claimed superior because they take into account rates of sequence substitution. Can rates of substitution be justified on its own accord in inferences of explanatory hypotheses? Answering this question requires addressing four issues: (1) the aim of scientific inquiry, (2) the nature of why-questions, (3) explanatory hypotheses as answers to why-questions, and (4) acknowledging that neither parsimony, likelihood, nor Bayesianism are inferential actions leading to explanatory hypotheses. The aim of scientific inquiry is to acquire causal understanding of effects. Observation statements of organismal characters lead to implicit or explicit why-questions. Those questions, conveyed in data matrices, assume the truth of observation statements, which is contrary to subsequently invoking substitution rates within inferences to phylogenetic hypotheses. Inferences of explanatory hypotheses are abductive in form, such that some version of an evolutionary theory(ies) is/are included or implied. If rates of sequence evolution are to be considered, it must be done prior to, rather than within abduction, which requires renaming those putatively-shared nucleotides subject to substitution rates. There are, however, no epistemic grounds for renaming characters to accommodate rates, calling into question the legitimacy of causally accounting for sequence data.

Tuberculosis has continued to retain its title as “the captain among these men of death”. This is evident as it is the leading cause of death globally from a single infectious agent. TB as it is fondly called has become a major threat to the achievement of the sustainable development goals (SDG) and hence require inputs from different research disciplines. This work presents a mathematical model of tuberculosis. A compartmental model of seven classes was used in the model formulation comprising of the susceptible S, vaccinated V, exposed E, undiagnosed infectious I₁, diagnosed infectious I₂, treated T and recovered R. The stability analysis of the model was established as well as the condition for the model to undergo backward bifurcation. With the existence of backward bifurcation, keeping the basic reproduction number less than unity (({R_{0}}<1)) is no more sufficient to keep TB out of the community. Hence, it is shown by the analysis that vaccination program, diagnosis and treatment helps to control the TB dynamics. In furtherance to that, it is shown that preference should be given to diagnosis over treatment as diagnosis precedes treatment. It is as well shown that at lower vaccination rate (0–20%), TB would still be endemic in the population. As such, high vaccination rate is required to send TB out of the community.