Biomedical subjects

Zhilan Feng

Publications and source records attributed to Zhilan Feng.

8 recordsLinked to original sources

PubMed2006

A schistosomiasis model with an age-structure in human hosts and its application to treatment strategies.

We study a system of partial differential equations which models the disease transmission dynamics of schistosomiasis. The model incorporates both the definitive human hosts and the intermediate snail hosts. The human hosts have an age-dependent infection rate and the snail hosts have an infection-age-dependent cercaria releasing rate. The parasite reproduction number R is computed and is shown to determine the disease dynamics. Stability results are obtained via both analytic and numerical studies. Results of the model are used to discuss age-targeted drug treatment strategies for humans. Sensitivity and uncertainty analysis is conducted to determine the role of various parameters on the variation of R. The effects of various drug treatment programs on disease control are compared in terms of both R and the mean parasite load within the human hosts.

Age Factors↗

PubMed2006

On the role of schistosome mating structure in the maintenance of drug-resistant strains.

The effects of drug treatment of human hosts on a population of schistosome parasites depends on a variety of factors. Previous models have shown that multiple strains of drug-resistant parasites are likely to be favored as the treatment rate increases. However, such models have neglected to account for the complex nature of schistosome mating biology. To more accurately account for the biology of these parasites, a simple mating structure is included in a multi-strain schistosome model, with parasites under the influence of drug treatment of their human hosts. Parasites are assumed to pay a cost for drug resistance in terms of reduced reproduction and transmission. The dynamics of the parasite population are described by a system of homogeneous differential equations, and the existence and stability of the exponential solutions for this system are used to infer the impact of drug treatment on the maintenance of schistosome genetic diversity.

Algorithms↗

PubMed2005

A spatially structured metapopulation model with patch dynamics.

Metapopulation models that incorporate both spatial and temporal structure are studied in this paper. The existence and stability of equilibria are provided, and an extinction threshold condition is derived which depends on patch dynamics (patch destruction and creation) and metapopulation dynamics (patch colonization and extinction). These results refine threshold conditions given by previous metapopulation models. By comparing landscapes with different spatial heterogeneities with respect to weighted long-term patch occupancies, we conclude that the pattern of a landscape is of overwhelming importance in determining metapopulation persistence and patch occupancy. We show that the same conclusion holds when a rescue effect is considered. We also derive a stochastic differential equations (SDE) model of the Itô type based on our deterministic model. Our simulations reveal good agreement between the deterministic model and the SDE model.

Animals↗

PubMed2005

Merging spatial and temporal structure within a metapopulation model.

Current research recognizes that both the spatial and temporal structure of the landscape influence species persistence. Patch models that incorporate the spatial structure of the landscape have been used to investigate static habitat destruction by comparing persistence results within nested landscapes. Other researchers have incorporated temporal structure into their models by making habitat suitability a dynamic feature of the landscape. In this article, we present a spatially realistic patch model that allows patches to be in one of three states: uninhabitable, habitable, or occupied. The model is analytically tractable and allows us to explore the interactions between the spatial and temporal structure of the landscape as perceived by the target species. Extinction thresholds are derived that depend on habitat suitability, mean lifetime of a patch, and metapopulation capacity. We find that a species is able to tolerate more ephemeral destruction, provided that the rate of the destruction does not exceed the scale of its own metapopulation dynamics, which is dictated by natural history characteristics and the spatial structure of the landscape. This model allows for an expansion of the classic definition of a patch and should prove useful when considering species inhabiting complex dynamic landscapes, for example, agricultural landscapes.

Ecosystem↗

PubMed2005

Cats protecting birds revisited.

In this paper, we revisit the dynamical interaction among prey (bird), mesopredator (rat), and superpredator (cat) discussed in [Courchamp, F., Langlais, M., Sugihara, G., 1999. Cats protecting birds: modelling the mesopredator release effect. Journal of Animal Ecology 68, 282-292]. First, we develop a prey-mesopredator-superpredator (i.e., bird-rat-cat, briefly, BRC) model, where the predator's functional responses are derived based on the classical Holling's time budget arguments. Our BRC model overcomes several model construction problems in Courchamp et al. (1999), and admits richer, reasonable and realistic dynamics. We explore the possible control strategies to save or restore the bird by controlling or eliminating the rat or the cat when the bird is endangered. We establish the existence of two types of mesopredator release phenomena: severe mesopredator release, where once superpredators are suppressed, a burst of mesopredators follows which leads their shared prey to extinction; and mild mesopredator release, where the mesopredator release could assert more negative impact on the endemic prey but does not lead the endemic prey to extinction. A sharp sufficient criterion is established for the occurrence of severe mesopredator release. We also show that, in a prey-mesopredator-superpredator trophic food web, eradication of introduced superpredators such as feral domestic cats in the BRC model, is not always the best solution to protect endemic insular prey. The presence of a superpredator may have a beneficial effect in such systems.

Algorithms↗

PubMed2005

On the role of schistosome mating structure in the maintenance of drug resistant strains.

The effects of drug treatment of human hosts upon a population of schistosome parasites depend upon a variety of factors. Previous models have shown that multiple strains of drug-resistant parasites are likely to be favored as the treatment rate increases. However, such models have neglected to account for the complex nature of schistosome mating biology. To more accurately account for the biology of these parasites, a simple mating structure is included in a multi-strain schistosome model, with parasites under the influence of drug treatment of their human hosts. Parasites are assumed to pay a cost for drug resistance in terms of reduced reproduction and transmission. The dynamics of the parasite population are described by a system of homogeneous differential equations, and the existence and stability of the exponential solutions for this system are used to infer the impact of drug treatment on the maintenance of schistosome genetic diversity.

Animals↗

PubMed2004

Coupling ecology and evolution: malaria and the S-gene across time scales.

Malaria has long been a scourge to humans. The exceptionally high mortality in some regions has led to strong selection for resistance, even at the cost of increased risk of potentially fatal red blood cell deformities in some offspring. In particular, genes that confers resistance to malaria when they appear in heterozygous individuals are known to lead to sickle-cell anemia, or other blood diseases, when they appear in homozygous form. Thus, there is balancing selection against the evolution of resistance, with the strength of that selection dependent upon malaria prevalence. Over longer time scales, the increased frequency of resistance in a population might be expected to decrease the frequency of malaria and reduce selection for resistance. However, possession of the sickle-cell gene leads to longer-lasting parasitaemia in heterozygote individuals, and therefore the presence of resistance may actually increase infection prevalence. In this paper, we explore the interplay among these processes, operating over very different time scales. In particular, we show that on the fast time scale of malarial dynamics, the disease level reaches an equilibrium; on the slower, evolutionary time scale, this equilibrium tracks gene frequency. We analyze the slow time scale dynamics to investigate the impact of malaria on the evolution of resistance.

Algorithms↗

PubMedDate not supplied

Schistosomiasis models with density dependence and age of infection in snail dynamics.

New models for schistosomiasis are developed. These models incorporate several realistic features including drug treatment for human hosts, an infection age in snail hosts, density-dependent birth rate of snails, distribution of schistosomes within human hosts, and disease-induced mortality in both human and snail hosts. The qualitative and quantitative mathematical properties of the models are studied, their biological consequences and some control strategies are discussed, and the results of the new models are compared with those of simpler models. It is shown that the new model may have a bifurcation at which the unique endemic equilibrium changes the stability and stable periodic solutions exist. This is quite different from the simpler models. Explicit thresholds of treatment rate are established above which the infection will be controlled under certain levels. Evaluations of cost-effectiveness are also discussed by analyzing the sensitivity of the mean number of parasites per person to changes of other parameters.

Animals↗