I am an Associate Professor of Medicine at the University of Kansas. I am an intensivist - I care for patients who are critically ill (near death) from a variety of causes. My research is centered on a condition called severe sepsis, which is a total body inflammatory response to overwhelming infection. I've investigated cellular and molecular mechanisms of sepsis, and I've also been heavily involved in clinical research in many trials of interventional agents in severe sepsis. I helped to describe and develop treatment for a particular form of sepsis, the hantavirus pulmonary syndrome. While we know a great deal about the molecular mechanisms of severe sepsis, we are faced in the clinical arena with making treatment decisions that are not based on molecular cues but instead on very basic physiological information that can be obtained at the bedside. I suspect that the derangements we see in these basic parameters may actually represent a loss of physiological complexity, when compared with normal homeostasis, and that the organism may be driven down a particular path to destruction in a deterministic way. My research questions are: a) when analyzed as time series, do the basic vital signs in severe sepsis interact in a more or less complex fashion than in the normal homeostatic state? b) can this gain or loss in complexity or change in dynamic characteristics be detected early in the clinical course of patients at risk for sepsis and be predictive of developing severe sepsis? c) can intervention much earlier in the clinical course avert the development of severe sepsis and improve mortality?