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Research Cardiologie Experimental Cardiology
University Medical Center Groningen

Information for master students

We have frequently openings for master student projects. Current projects for master students are listed below, together with the contact person.

Role of galectin-3 in cardiac remodeling

Rudolf de Boer


Cardiac remodeling is the answer of the heart to increased stress, for instance after myocardial infarction, due to pressure overload or volume overload, and is characterized by increased production of extracellular proteins, leading to interstitial fibrosis (fibrogenesis).

The protein galectin-3 exerts important effects in the fibrotic process.  In various organs galectin-3 was implicated in the fibrotic response in answer to tissue damage. We recently conducted various studies showing that galectin-3 is also an important protein in cardiac fibrogenesis and remodeling. Galectin-3 is also secreted in the circulation and its plasma levels reflect the severity of heart failure. As such, galectin-3 has been FDA approved as a novel heart failure biomarker.

Currently, we conduct studies into the role of galectin-3 in cardiac fibrosis. We look for an enthusiast student who is interested in translational research. The experiments will involve cell culture studies to test the role of galectin-3 in the development of fibrosis, measuring galectin-3 levels and activity in cells and fibrotic heart tissue and galectin-3 levels with the use of galectin-3 ELISA.

Role of antidiabetic agents to prevent cardiac remodeling

Rudolf de Boer


Diabetes is an important risk factor for the development of heart failure. Examples of oral antidiabetic agents are metformin, SU derivatives, TZDs and DPP-4 inhibitors. Although current guidelines recommend metformin as first line choice treatment, relative few data have been published to support this, or to provide data what agent should be given to what particular patient..

The student will do a literature search into oral antidiabetic agents and heart failure. The aim is to review and summarize data, and write a scientific publication. This could be a starting point for further mechnistic studies.

Functional analysis of novel heart failure associated proteins

Herman Silljé

Email: h.h.w.sillje

Although heart failure account for the highest mortality and morbidity rates in Western society, there is still a considerable lack in our knowledge of genes that contribute to cardiac (dys)function. We have conducted gene array analysis on rat hearts from animals with and without heart failure and moreover, used in vitro heart failure models to identify cardiomyocyte specific changes. This resulted in the identification of several novel genes that are differentially regulated.

In this project we aim to uncover the function of the proteins encoded by these novel genes and investigate their potential role in heart failure. This includes cloning of the genes and their expression in several cell systems, including beating cardiomyocytes. Vice versa we will specific downregulate the expression of these genes by siRNA-based approaches. In addition specific antibodies will be generated to investigate changes in protein levels in heart tissue. Moreover, these antibodies will allow us to determine the dynamic localization of the proteins in the cell using confocal immunofluorescence microscopy. Together, this should clarify the function and role in heart failure of these hitherto unknown proteins.

Atrial fibrilation

Isabelle can Gelder or Alexander Maass

Emails: i.c.van.gelder or a.h.maass

Atrial fibrillation (AF) is the most common cardiac arrhythmia. It is expected that by 2050 over 1 million people in The Netherlands will suffer from AF. AF poses an important clinical problem, being responsible for substantial economic costs, morbidity and mortality.
AF underlying diseases often induce stretch. We investigate the effects of stretch on atrial cardiomyocytes. In addition, we study the mechanisms of these effects and we try to inhibit stretch-induced effects.
In the near future a project will start in which mice are subjected to atrial and ventricular pressure overload. Atrial structural remodeling as well as AF vulnerability will be investigated in this in vivo model.
For additional information see this poster.

Chipping away at the genetics of cardiovascular disease

Pim van der Harst

E-mail: p.van.der.harst

There is an urgent need to better understand the basic biology and pathophysiology of fundamental aspects of cardiovascular disease. Using cutting edge technology and pulling together the expertise from Centres of Excellence across the Europe and the United States we aim to discover novel genes essential to progress the cardiovascular field. Specific work packages will focus on: (1.) cardiac hypertrophy and heart failure, (2.) cardiac conduction, (3.) cardio-renal aspects, and (4.) cardiovascular risk factors. All work packages are embedded in the cardiovascular center of the CVC Groningen (GUIDE) and all include extensive international collaboration. Each work package can accommodate the participation of one Master Student. Our department offers a unique opportunity for a limited number of young ambitious students to explore their affinity with basic molecular science in combination with large human datasets (involving up to 80,000 subjects) and also to combine wet-lab work with using dedicated and advanced software to analyze and visualize data.

Predictors of Heart Failure in the general population.

Wiek van Gilst

Email: w.h.van.gilst

Heart Failure (HF) is an increasing burden on patients and their families, but also on society, through enormous use of health care resources. Overall population prevalence increases dramatically with age and following first hospital admission for HF, patients have a 5-year mortality of 75% - a survival rate worse than that for most forms of cancer. Little is known about the incidence of HF and its possible prognostic markers.

The Prevention of Renal and Vascular End stage Disease (PREVEND) study (n=8592) started in 1997, assessing the impact of (micro)albuminuria on renal and cardiovascular disease. We are currently collecting data of HF incidence and prevalence in PREVEND. Your task will be to identify subjects with new-incidence HF during the entire follow-up period of PREVEND. You will perform statistical analyses to determine population characteristics and possible prognostic factors for HF. Identified risk factors or targets can prospectively tested in other cohorts or experimental models.We aim to design a multi-marker model, including both clinical and biochemical markers, to predict new-incidence HF.

Laatst gewijzigd:24 juni 2014 11:24