Education
Biomea strives to provide educational support to current biomedical science students at Hasselt University and to achieve this goal, it collaborates closely with the Faculty of Medicine and Life Sciences.
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Biomea supports various educational activities, such as seminars, student internships and lectures, to help students deepen their knowledge and skills. Moreover, Biomea shares and promotes the high-impact research publications of its alumni, providing valuable insights into the current state of research in the field. Through these efforts, Biomea aims to enhance its members' academic and professional success.
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Biomea is constantly looking for enthusiastic members who are eager to contribute to education and share their knowledge with the upcoming generation.
Therefore, kindly inform us if you are willing to lend a hand.
"Education is the most powerful weapon which you can use to change the world."
Nelson Mandela
Enhancing Knowledge and Skills in Biomedical Sciences
Biomea understands that theoretical knowledge alone is not enough for students to excel in their careers. To bridge this gap, the organization strives to establish a connection between alumni and current students through lectures and social events. These events are conducted by alumni experts who bring their knowledge and experience to the students. The topics discussed range from fundamental skills such as CV coaching and career path exploration to advanced subjects such as nanotechnology.
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By participating in these activities, students have the opportunity to enhance their academic and professional growth by gaining insights into the latest developments in the field, learning new techniques and approaches, and connecting with peers and professionals. Biomea is also dedicated to creating a network that offers non-academic student internships in various life sciences companies. This network can be shared with biomedical science students at Hasselt University.
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Through these initiatives, Biomea is creating a supportive community of individuals who share a passion for biomedical sciences and are dedicated to each other's success.
Publications by Alumni
Oncostatin M triggers brain inflammation by compromising blood-brain barrier integrity
Author: Doryssa Hermans et. al.
Journal: Acta Neuropathologica
Abstract: Oncostatin M (OSM) is an IL-6 family member which exerts neuroprotective and remyelination-promoting effects after damage to the central nervous system (CNS). However, the role of OSM in neuro-inflammation is poorly understood. Here, we investigated OSM's role in pathological events important for the neuro-inflammatory disorder multiple sclerosis (MS). We show that OSM receptor (OSMRβ) expression is increased on circulating lymphocytes of MS patients, indicating their elevated responsiveness to OSM signalling. In addition, OSM production by activated myeloid cells and astrocytes is increased in MS brain lesions. In experimental autoimmune encephalomyelitis (EAE), a preclinical model of MS, OSMRβ-deficient mice exhibit milder clinical symptoms, accompanied by diminished T helper 17 (Th17) cell infiltration into the CNS and reduced BBB leakage. In vitro, OSM reduces BBB integrity by downregulating the junctional molecules claudin-5 and VE-cadherin, while promoting secretion of the Th17-attracting chemokine CCL20 by inflamed BBB-endothelial cells and reactive astrocytes. Using flow cytometric fluorescence resonance energy transfer (FRET) quantification, we found that OSM-induced endothelial CCL20 promotes activation of lymphocyte function-associated antigen 1 (LFA-1) on Th17 cells. Moreover, CCL20 enhances Th17 cell adhesion to OSM-treated inflamed endothelial cells, which is at least in part ICAM-1 mediated. Together, these data identify an OSM-CCL20 axis, in which OSM contributes significantly to BBB impairment during neuro-inflammation by inducing permeability while recruiting Th17 cells via enhanced endothelial CCL20 secretion and integrin activation. Therefore, care should be taken when considering OSM as a therapeutic agent for treatment of neuro-inflammatory diseases such as MS.
Glycolaldehyde-modified proteins cause adverse functional and structural aortic remodeling leading to cardiac pressure overload
Author: Sibren Haesen et. al.
Journal: Scientific Reports
Abstract: Growing evidence supports the role of advanced glycation end products (AGEs) in the development of diabetic vascular complications and cardiovascular diseases (CVDs). We have shown that high-molecular-weight AGEs (HMW-AGEs), present in our Western diet, impair cardiac function. Whether HMW-AGEs affect vascular function remains unknown. In this study, we aimed to investigate the impact of chronic HMW-AGEs exposure on vascular function and structure. Adult male Sprague Dawley rats were daily injected with HMW-AGEs or control solution for 6 weeks. HMW-AGEs animals showed intracardiac pressure overload, characterized by increased systolic and mean pressures. The contraction response to PE was increased in aortic rings from the HMW-AGEs group. Relaxation in response to ACh, but not SNP, was impaired by HMW-AGEs. This was associated with reduced plasma cyclic GMP levels. SOD restored ACh-induced relaxation of HMW-AGEs animals to control levels, accompanied by a reduced half-maximal effective dose (EC50). Finally, collagen deposition and intima-media thickness of the aortic vessel wall were increased with HMW-AGEs. Our data demonstrate that chronic HMW-AGEs exposure causes adverse vascular remodelling. This is characterised by disturbed vasomotor function due to increased oxidative stress and structural changes in the aorta, suggesting an important contribution of HMW-AGEs in the development of CVDs.
Phosphodiesterase (PDE) 4 inhibition boosts Schwann cell myelination in a 3D regeneration model
Author: Melissa Schepers et. al.
Journal: European Journal of Pharmaceutical Sciences
Abstract: Phosphodiesterase 4 (PDE4) inhibitors have been extensively researched for their anti-inflammatory and neuroregenerative properties. Despite the known neuroplastic and myelin regenerative properties of nonselective PDE4 inhibitors on the central nervous system, the direct impact on peripheral remyelination and subsequent neuroregeneration has not yet been investigated. Therefore, to examine the possible therapeutic effect of PDE4 inhibition on peripheral glia, we assessed the differentiation of primary rat Schwann cells exposed in vitro to the PDE4 inhibitor roflumilast. To further investigate the differentiation promoting effects of roflumilast, we developed a 3D model of rat Schwann cell myelination that closely resembles the in vivo situation. Using these in vitro models, we demonstrated that pan-PDE4 inhibition using roflumilast significantly promoted differentiation of Schwann cells towards a myelinating phenotype, as indicated by the upregulation of myelin proteins, including MBP and MAG. Additionally, we created a unique regenerative model comprised of a 3D co-culture of rat Schwann cells and human iPSC-derived neurons. Schwann cells treated with roflumilast enhanced axonal outgrowth of iPSC-derived nociceptive neurons, which was accompanied by an accelerated myelination speed, thereby showing not only phenotypic but also functional changes of roflumilast-treated Schwann cells. Taken together, the PDE4 inhibitor roflumilast possesses a therapeutic benefit to stimulate Schwann cell differentiation and, subsequently myelination, as demonstrated in the biologically relevant in vitro platform used in this study. These results can aid in the development of novel PDE4 inhibition-based therapies in the advancement of peripheral regenerative medicine.