| Description |
We use mathematical models to explore two physiological systems. Adipocytes, or fat cells, are responsible for limiting the exposure of other tissues to lipid accumulation by sequestering and storing lipids during feeding and providing energy by releasing lipids during fasting. Fat tissue expands by increasing the size of adipocytes, (hypertrophic expansion), and/or the number of adipocytes, (hyperplasic expansion). We develop a size-structured model of adipocyte dynamics to study fat tissue expansion. The model can produce steady-state size distributions qualitatively matching measured size distributions. Using a method of moments, we approximate the size-structured model with a one-size model. Chronic inflammation is associated with obesity and linked to the development of insulin resistance and other metabolic disorders. We extend the adipocyte dynamics model to include macrophages to enable the future study of the coordinated development of obesity and associated chronic inflammation. The amount of mRNA in a cell depends on the balance between production through transcription from DNA and removal via decay. Maximum likelihood estimation is used to estimate the decay rate for each transcript in an extensive data set of the Arabidopsis transcriptome. A model comparison and estimated decay rates are used to study the contribution of three pathways of mRNA decay. A suite of simple mechanistic models of mRNA decay are developed to extend this analysis. |
