My name is Coen and I was born in ‘s Hertogenbosch, the Netherlands in December 1980 (36). I currently live and work in Utrecht, the Netherlands, where I try to study and fix clinical problems in the laboratories of the Utrecht University Medical Center. I started working on blood plasma proteins in 2002, whereafter I did my PhD from 2004-2008. This field that is mainly related to thrombosis; the formation of blood clots where they really shouldn’t be. After that, my interests expanded to vascular biology and innate immunity.
Main scientific interest
At present, I am working on the concept that the endothelial cells that line the blood vessel wall together form a smart and independently operating tissue that can ‘sense and destroy’ nearby threats or exchange signals from the outside to the inside of the vessel. This signaling controls the localized release of cells and proteins to repair damaged or infected tissues. We have seen that defects in this system are related to mysterious and deadly diseases such as thrombotic thrombocytopenic purpura (too little ‘destroy‘ activity), (hereditary) angioedema or anaphylactic shock (too much vessel leakage). During our studies, we are identifying treatment strategies that are sometimes already available in hospital pharmacies around the world. Because of this, I believe that it is not always needed to develop completely new drugs to solve serious medical problems!
It sometimes appears as if available technology is a rate limiting factor for high quality scientific output. I believe that this is not always the case. Although it is veryÂ motivating to generate new tools for the interrogation of pathological mechanisms, I aim to use existing biochemical techniques where I can. Why would I put my efforts into inventing alternatives for the wheel (which is a great invention)? In stead, I prefer to use available technologies and biochemical techniques that have proven themselves in the past. I expect that they will continue to show their value in the present and in the future. In my opinion, research is not only limited by technological power, it is also limited by the capacity to ask the right questions and outline the right research strategy. What’s the point of buying a million euro microscope without a good feeling of what to study with it? Because the pictures look better? For our research we can still get by fine with a microscope that costs >20x less and still make groundbreaking progress. However, if anyone has an awesome new piece of equipment for sharing – we never mind trying!
My strategy: lessons from rare diseases can carry broad impact
Rare dangerous diseases are rewarding to investigate – it is exciting work. In these conditions, I believe that there is much room for research that directly makes a benefit to the patient. In itself, this is very rewarding: we try to generate diagnostic tools and identify therapeutic targets and -strategies. I like to think that we are making promising progress.
Priority for medical research funding is often guided by the numbers of patients that have a disease. The use of collective terms like “cardiovascular disease”, amplifies this effect. Other driving factors are, whether companies think there is money to be made, or whether a medical problem is strongly presented in the (social) media. As a result, biomedical research appears to become increasingly sensitive to ‘hypes’. I believe that this is a somewhat unwanted phenomenon. Yes, the relevance of research should be demonstrable where possible, but I think that seeing possibilities where others have not (yet) is the unique and artistic skill of a good researcher (and hopefully not easily matched by the general Facebook user). This skill should be one of the essential driving factors for science innovation. Becoming an independent researcher takes effort, experience and, admittedly, luck. At present, less prevalently occurring conditions receive less scientific attention – the attention simply goes where the money is.
I believe that by overlooking rare conditions, we are missing out on great opportunities. Important mechanistic lessons can be learned from them that can be implicated in prevalent multifactorial diseases, such as stroke, sepsis, atherosclerosis, diabetes, and Alzheimer’s disease.
I sometimes compare diseases with “Murder Mysteries”: the light goes out in the hotel lobby and when it is turned on, a murder victim is on the floor. With 80 persons in the lobby (multifactorial diseases), the detective will have a hard time to find the killer. However, had there only been three persons in the lobby (rare diseases), the case would have been a lot easier to crack. The molecular players that are central in rare diseases (i.e. von Willebrand Factor in TTP or bradykinin in hereditary angioedema) are also well-known to contribute to prevalent multifactorial conditions. I am convinced that through understanding them in rare conditions, we will be able to unlock a full understanding on these factors in general. I hope that in the future, there will still be room for researchers to determine what course to take and what subjects to study. Of course, always in good dialogue with society.
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