The public defence will be held as a video conference over Zoom.
The digital defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Click here to participate in the public defence
Digital trial lecture - time and place
Adjudication committee
- First opponent: Chief Quality Officer Richard P. Dutton, US Anesthesia Partners, Dallas, USA
- Second opponent: Associate Professor Peder Olofsson, Karolinska Institutet, Stockholm, Sweden
- Third member and chair of the evaluation committee: Professor II Ingebjørg Seljeflot, Institute of Clinical Medicine, University of Oslo
Chair of defence
Professor Torgeir Bruun Wyller, Institute of Clinical Medicine, University of Oslo
Principal supervisor
Professor II Torsten Eken, Institute of Clinical Medicine, University of Oslo
Summary
Victims of major trauma run a considerable risk of death even if they arrive in hospital alive. In part this mortality is due to detrimental systemic inflammation leading to fail-ure of organs not initially injured. Unbridled inflammation is the result of innate im-mune system activation, incited by proteins referred to as “alarmins” being passively released from mechanically damaged cells, or secreted from activated immune cells. Alarmins are constitutively expressed and harbor important housekeeping functions. However, once released to the extracellular space, alarmins acquire a new identity to serve as powerful mediators of inflammation.
The main goal of this research was to obtain high-resolution data on the release pattern of two alarmins, HMGB1 and IL-33, after trauma, and to explore their statistical rela-tionship with patient outcome in terms of remote organ failure.
HMGB1 and IL-33 kinetics in individual patients were explored in 1094 blood samples from 136 patients with a broad spectrum of injuries and outcomes. We coupled this in-formation to data from the Oslo University Hospital Trauma Registry and we found that a biphasic release of HMGB1 after trauma was strongly associated with unfavorable out-come. IL-33 was undetectable in the majority of patients, although a rapid and transient release of IL-33 was observed in a subset of critically injured patients. Our findings pro-vide new insights regarding proximal mediators of inflammation in the aftermath of trauma and shock, hopefully paving the way for identification of therapeutic targets.
Additional information
contact the Research Support staff