scispace - formally typeset
D

Denise E. Kirschner

Researcher at University of Michigan

Publications -  183
Citations -  13318

Denise E. Kirschner is an academic researcher from University of Michigan. The author has contributed to research in topics: Tuberculosis & Immune system. The author has an hindex of 56, co-authored 175 publications receiving 11744 citations. Previous affiliations of Denise E. Kirschner include University of Pittsburgh & Albert Einstein College of Medicine.

Papers
More filters
Journal ArticleDOI

A Methodology For Performing Global Uncertainty And Sensitivity Analysis In Systems Biology

TL;DR: This work develops methods for applying existing analytical tools to perform analyses on a variety of mathematical and computer models and provides a complete methodology for performing these analyses, in both deterministic and stochastic settings, and proposes novel techniques to handle problems encountered during these types of analyses.
Journal ArticleDOI

Dynamics of HIV infection of CD4+ T cells

TL;DR: A model for the interaction of HIV with CD4+ T cells that considers four populations, characterized by generating differing numbers of infective virions within infected T cells, can cause different amounts of T-cell depletion and generate depletion at different rates.
Journal ArticleDOI

Modeling immunotherapy of the tumor-immune interaction.

TL;DR: The dynamics between tumor cells, immune-effector cells, and IL-2 are illustrated through mathematical modeling and the effects of adoptive cellular immunotherapy are explored to explain both short tumor oscillations in tumor sizes as well as long-term tumor relapse.
Journal ArticleDOI

Optimal control of the chemotherapy of HIV.

TL;DR: Using an existing ordinary differential equation model, chemotherapy is introduced in an early treatment setting through a dynamic treatment and then solved for an optimal chemotherapy strategy based on a combination of maximizing benefit based on T cell counts and minimizing the systemic cost of chemotherapy.
Journal ArticleDOI

Identifying control mechanisms of granuloma formation during M. tuberculosis infection using an agent-based model.

TL;DR: This model combines continuous representations of chemokines with discrete agent representations of macrophages and T cells in a cellular automata-like environment and indicates that key host elements involved in granuloma formation are chemokine diffusion, prevention ofmacrophage overcrowding within the granulomas, arrival time, location and number of T cells within thegranuloma, and an overall host ability to activate macrophage.