Biomedical subjects

J F Fontanari

Publications and source records attributed to J F Fontanari.

6 recordsLinked to original sources

PubMed2002

Nonequilibrium phase transitions in a model for the origin of life.

The requisites for the persistence of small colonies of self-replicating molecules living in a two-dimensional lattice are investigated analytically in the infinite diffusion or mean-field limit and through Monte Carlo simulations in the position-fixed or contact process limit. The molecules are modeled by hypercyclic replicators A that are capable of replicating via binary fission A+E-->2A with production rate s, as well as via catalytically assisted replication 2A+E-->3A with rate c. In addition, a molecule can degrade into its source materials E with rate gamma. In the asymptotic regime, the system can be characterized by the presence (active phase) and the absence (empty phase) of replicators in the lattice. In both diffusion regimes, we find that for small values of the ratio c/gamma these phases are separated by a second-order phase transition that is in the universality class of the directed percolation, while for small values of s/gamma the phase transition is of first order. Furthermore, we show the suitability of the dynamic Monte Carlo method, which is based on the analysis of the spreading behavior of a few active cells in the center of an otherwise infinite empty lattice, to address the problem of the emergence of replicators. Rather surprisingly, we show that this method allows an unambiguous identification of the order of the nonequilibrium phase transition.

Biophysical Phenomena↗

PubMed2001

Soluble model for the accumulation of mutations in asexual populations.

Finite asexual populations can accumulate an increasing number of deleterious mutations by a process known as Muller's ratchet, which consists of successive losses of the fittest or least-loaded classes of individuals in the population. We present here a simplified theoretical framework to describe the serial bottleneck passages setup used in experiments to demonstrate the decrease of the population mean fitness due to the operation of ratchet. In particular, we calculate the expected time between consecutive clicks of the ratchet and derive expressions relating the moments of the mean fitness distribution to the mutation and selection parameters.

Models, Genetic↗

PubMed2001

Extinctions in the random replicator model.

The statistical properties of an ecosystem composed of species interacting via pairwise, random interactions and deterministic, concentration limiting self-interactions are studied analytically with tools of equilibrium statistical mechanics of disordered systems. Emphasis is given to the effects of externally induced extinction of a fixed fraction of species at the outset of the evolutionary process. The manner the ecosystem copes with the initial extinction event depends on the degree of competition among the species as well as on the strength of that event. For instance, in the regime of high competition the ecosystem diversity, given by the fraction of surviving species, is practically insensitive to the strength of the initial extinction provided it is not too large, while in the less competitive regime the diversity decreases linearly with the size of the event. In the case of large extinction events we find that no further biotic extinctions take place and, furthermore, that rare species become very unlikely to be found in the ecosystem at equilibrium. In addition, we show that the reciprocal of the Edwards-Anderson order parameter yields a good measure of the diversity of the model ecosystem.

Animals↗

PubMed2001

Phase transitions in a model for the formation of herpes simplex ulcers.

The critical properties of a cellular automaton model describing the spreading of infection of the herpes simplex virus in corneal tissue are investigated through the dynamic Monte Carlo method. The model takes into account different cell susceptibilities to the viral infection, as suggested by experimental findings. In a two-dimensional square lattice the sites are associated with two distinct types of cells, namely, permissive and resistant to the infection. While a permissive cell becomes infected in the presence of a single infected cell in its neighborhood, a resistant cell needs to be surrounded by at least R>1 infected or dead cells in order to become infected. The infection is followed by the death of the cells resulting in ulcers whose forms may be dendritic (self-limited clusters) or amoeboid (percolating clusters) depending on the degree of resistance R of the resistant cells as well as on the density of permissive cells in the healthy tissue. We show that a phase transition between these two regimes occurs only for R>/=5 and, in addition, that the phase transition is in the universality class of the ordinary percolation.

Ganglia↗

PubMed2000

Group selection models in prebiotic evolution.

The evolution of enzyme production is studied analytically using ideas of the group selection theory for the evolution of altruistic behavior. In particular, we argue that the mathematical formulation of Wilson's structured deme model [The Evolution of Populations and Communities (Benjamin-Cumings, Menlo Park, 1980)] is a mean-field approach in which the actual environment that a particular individual experiences is replaced by an average environment. That formalism is further developed so as to avoid the mean-field approximation and then applied to the problem of enzyme production in the prebiotic context, where the enzyme producer molecules play the altruists role while the molecules that benefit from the catalyst without paying its production cost play the nonaltruists role. The effects of synergism (i.e., division of labor) as well as of mutations are also considered and the results of the equilibrium analysis are summarized in phase diagrams showing the regions of the space of parameters where the altruistic, nonaltruistic, and the coexistence regimes are stable. In general, those regions are delimitated by discontinuous transition lines which end at critical points.

Enzymes↗

PubMed2000

Error propagation in the hypercycle.

We study analytically the steady-state regime of a network of n error-prone self-replicating templates forming an asymmetric hypercycle and its error tail. We show that the existence of a master template with a higher noncatalyzed self-replicative productivity a than the error tail ensures the stability of chains in which m < n-1 templates coexist with the master species. The stability of these chains against the error tail is guaranteed for catalytic coupling strengths K on the order of a. We find that the hypercycle becomes more stable than the chains only if K is on the order of a2. Furthermore, we show that the minimal replication accuracy per template needed to maintain the hypercycle, the so-called error threshold, vanishes as square root of n/K for large K and N < or = 4.

DNA Replication↗