A mathematical model of neuroinflammation in severe clinical traumatic brain injury.

ABSTRACT:

Background

Understanding the interdependencies among inflammatory mediators of tissue damage following traumatic brain injury (TBI) is essential in providing effective, patient-specific care. Activated microglia and elevated concentrations of inflammatory signaling molecules reflect the complex cascades associated with acute neuroinflammation and are predictive of recovery after TBI. However, clinical TBI studies to date have not focused on modeling the dynamic temporal patterns of simultaneously evolving inflammatory mediators, which has potential in guiding the design of future immunomodulation intervention studies.

Methods

We derived a mathematical model consisting of ordinary differential equations (ODE) to represent interactions between pro- and anti-inflammatory cytoki

SUBMITTER: Vaughan LE 

PROVIDER: S-EPMC6299616 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature