Using models to advance medicine: mathematical modeling of post-myocardial infarction left ventricular remodeling.

The heart is an organ with limited capacity for regeneration and repair. The irreversible cell death and corresponding diminished ability of the heart to repair after myocardial infarction (MI), is a leading cause of morbidity and mortality worldwide. In this paper, a new mathematical model is presented to study the left ventricular (LV) remodeling and associated events after MI.

A simple model of immune and muscle cell crosstalk during muscle regeneration.

Muscle injury during aging predisposes skeletal muscles to increased damage due to reduced regenerative capacity. Some of the common causes of muscle injury are strains, while other causes are more complex muscle myopathies and other illnesses, and even excessive exercise can lead to muscle damage. We develop a new mathematical model based on ordinary differential equations of muscle regeneration.

Transit times and mean ages for nonautonomous and autonomous compartmental systems.

We develop a theory for transit times and mean ages for nonautonomous compartmental systems. Using the McKendrick-von Förster equation, we show that the mean ages of mass in a compartmental system satisfy a linear nonautonomous ordinary differential equation that is exponentially stable. We then define a nonautonomous version of transit time as the mean age of mass leaving the compartmental system at a particular time and show that our nonautonomous theory generalises the autonomous case.

Modeling Chagas Disease at Population Level to Explain Venezuela's Real Data.

Objectives: In this paper we present an age-structured epidemiological model for Chagas disease. This model includes the interactions between human and vector populations that transmit Chagas disease.

Methods: The human population is divided into age groups since the proportion of infected individuals in this population changes with age as shown by real prevalence data.