Public Defence: Terje Ricardo Selnes Kolstad

MSc Terje Ricardo Selnes Kolstad at Institute of Clinical Medicine will be defending the thesis “Cardiac myocyte structure and function in development, adulthood and disease” for the degree of PhD (Philosophiae Doctor).

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Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.

Trial Lecture – time and place

See Trial Lecture.

Adjudication committee

  • First opponent: Associate Professor Benjamin Prosser, Perelman School of Medicine, University of Pennsylvania, USA
  • Second opponent: Associate Professor Neoma Boardman, Department of Medical Biology, UiT - The Arctic University of Norway
  • Third member and chair of the evaluation committee: Associate Professor Kjetil Wessel Andressen, University of Oslo

Chair of the Defence

Associate Professor Tor Erik Rusten, University of Oslo

Principal Supervisor

Professor William E. Louch, University of Oslo


The failing heart cells have a structure and a function that is reminiscent of cells in early development rather than healthy, fully developed cells.

Despite intensive research over the previous decades, we still lack understanding of the basic mechanisms for human heart failure (HF). Due to an aging population, we will likely have to commit large resources to managing this disease in the future. 

In his doctoral thesis, Terje R Selnes Kolstad has, by means of super-resolution microscopy, looked at structural and functional alterations in heart cells during development, adulthood and disease.

The main finding in article I was that during HF, the internal heart structure that normally ensures a swift and synchronous release of calcium is re-organized. The ensuing alteration to calcium balance is a plausible mechanism for a reduced contractility of the heart. Specifically slow and dyssynchronous release of calcium could lead to a slow and dyssynchronous heartbeat.

In article II they found that a chemical modification to the calcium release channel (Ryanodine receptor, RyR) was both sufficient and necessary for this alteration in calcium balance to occur.

In the third article, the candidate investigated stem cells generated from human embryos that were treated to become heart muscle cells. Despite several indication of maturity of these cells, their internal structures were more reminiscent of cells during early development rather than mature and healthy cells.

The most important finding from this body of work is that the calcium release channel undergoes dynamic and reversible dispersion during heart failure. This has important implications for the hearts’ calcium balance, its contractility and rhythm.          

Additional information

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Published May 4, 2022 3:42 PM - Last modified May 18, 2022 12:48 PM