Education
1954 B.A., Rutgers University , NCAS, Newark, New Jersey
1955 M.Sc., University of Iowa, Iowa City, Iowa
1957 Ph.D., University of Iowa, Iowa City, Iowa
Research Interest
For almost 35 years, our lab has been principally engaged in elucidating the mechanisms that underlie the febrile response to infection. The focus of our research has been on the interactions between the immune and nervous systems that initiate this response.
Fever is one among an array of non-specific innate immune, endocrine, metabolic, behavioral, and other responses to the entry into the body of infectious microorganisms or their products, designed to defend the afflicted host from the deleterious effects of the invading pathogens. These responses are collectively termed the acute-phase reaction (APR). The APR is thus a physiological, not a pathological, response. In its simplest terms, the febrile response per se is characterized by a rise of the body core temperature (Tc). It is, thus, a thermoregulatory response that involves a complete, prototypic reflex arc ? sensory signaling, central integration, and effector mechanisms.
Over the years, we have, in turn, described the ontogeny of fever and the change in effector mechanisms that occurs over the first month of post-natal life, localized the several brain sites that mediate the febrile response, and eventually characterized the complete loop of fever production, from the moment the pyrogenic material enters the body until the febrile response is initiated. In more recent years, our efforts have been concentrated most heavily on resolving this latter issue. Thus, we have identified various endogenous factors liberated in immediate response to the presence of a pyrogen and the neural and humoral pathways activated that ultimately communicate these signals to the brain. In the course of these studies, we have uncovered several fever-triggering processes and delineated the trajectories of their pathways from the periphery to the brain. We have also described the neurochemical processes in the brain for febrigenesis, and developed a conceptual model of the afferent and central mechanisms involved. These are depicted in the diagram below.