Prøveforelesning og disputas Ina Isabella Høiland
Disputas – master i biomedisin Ina Isabella Høiland
Master i biomedisin Ina Isabella Høiland disputerer for ph.d.-graden i helsevitenskap og vil offentlig forsvare avhandlingen:
“ Role of the Complement System in the Pathogenesis of Venous Thromboembolism”
Kort sammendrag av avhandlingen:
Venous thromboembolism (VTE) is a common disease with serious short- and long-term complications. VTE is a collective term for deep vein thrombosis (DVT) and pulmonary embolism (PE) and is the third most common cardiovascular disease, causing significant morbidity and mortality. Despite preventive strategies, the incidence of VTE has been stable or increasing slightly during the last decades, affecting 1-2 per 1000 individuals each year. Identifying new biomarkers and underlying mechanisms might ease the health burden of VTE. The complement system is an important part of our immune defense system, and is a cascade system similar to the coagulation system. These two systems have a high degree of crosstalk and are activated together in many conditions, such as fighting infections. Short-Chained (SC)-PolyPs are secreted from platelets when they are stimulated and there linear polymers, are reported to inhibit the complement- and to activate the coagulation system. This indicates that SC-polyP might modulate the possible link between the two systems, and play a role in the formation of a VTE.
The main goals of this thesis were to assess the association between complement activation and VTE risk, and to investigate the role of SC-polyPs in the activation of these two systems. We found that individuals that had a potential of a high activity of one part of the complement system, and individuals with deficiency in another part of the complement system had higher risk for VTE. In addition, we found that high degree of complement activation was associated with increased risk of VTE. We also showed that SC-polyPs had the ability to activate the coagulation system through the pathway associated with thrombus formation, whereas it did not inhibit the complement system. Our findings suggest that complement activation is involved in the pathogenesis of VTE, and that SC-polyP, might initiate coagulation activation without affect complement activation.
Hovedveileder professor John-Bjarne Hansen
Biveileder professor Tom Eirik Mollnes
1. opponent professor Thomas Renné, University Medical Center Hamburg, Tyskland
2. opponent seniorforsker Nina Iversen, Oslo universitetssykehus, Norge
Leder av komite professor Trond Flægstad, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, UiT – Norges arktiske universitet
førsteamanuensis Åshild Bjørnerem, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, Universitetet i Tromsø – Norges arktiske universitet
Prøveforelesning over oppgitt emne holdes kl. 10.15, samme sted: “The role of intrinsic coagulation pathway in inflammation and cancer: possible implications”