Three ACS researchers received a Dekker grant from the Dutch Heart Foundation.
Dr. Kak Khee Yeung, vascular surgeon of Amsterdam UMC - location VUmc, has been awarded last week with the prestigious Dekker Fellowship Senior Clinical Scientist for her project “The key role of smooth muscle cell function (SMC) in aortic aneurysms”. In her earlier studies she found that SMC function is crucial for a healthy aorta and that a disturbed SMC function promotes development of aortic aneurysms. Her studies were supported by the ACS, by an ICaR-AIO and MD-PhD grant and further by ACS-postdoc grant to investigate a new involved gene family. Now, she will continue her research by studying aortic remodelling in relation with gender, environmental stress factors like smoking, aging, aneurysm causing genes, hormones, glucose disbalance and aortic wall stress. Her project aims to provide detailed understanding of the pathophysiology of aortic aneurysms and dissections in order to predict its behavior with biophysiological smooth muscle cell specific analysis. Her passion is to perform research and bring basic science in the field of vascular surgery.
Dr. Rik Olde Engberink (Internal Medicine – Nephrology, AMC) has been awarded a clinical scientist Dekkerbeurs from the Dutch Heart Foundation. He receives 210,000 euros to investigate a new treatment target for heart failure: nonosmotic sodium storage. Heart failure patients have been shown to accumulate large amounts of sodium under their skin without concurrent water retention in addition to the systemic sodium and water overload. He will examine whether sodium and water overload in heart failure patients can be reduced by making use of nonosmotic sodium storage.
Dr. Marit Wiersma, researcher in the Physiology department at the Amsterdam UMC - location VUmc, received the Dekker Postdoc grant for her project on how a mutation in the desmin and lamin protein can lead to the development of atrial fibrillation (AF). During this project she studies whether a disturbed protein balance is present in a specific group of familial AF patients. In the Netherlands, several families have been identified with mutations in the proteins desmin (DES) or lamin A/C (LMNA), proteins that are important for the structure and contraction of the heart cell. These mutations not only led to familial AF, but also to the development of dilating cardiomyopathy (DCM, heart muscle disease). She will investigate whether a disruption in protein management plays an important role and she already has important indications that these mutations lead to mitochondrial and contractile dysfunction. In addition, extra attention will be paid to differences between men and women with a mutation and the development of atrial fibrillation.