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151. A mutation update on the LDS-associated genesTGFB2/3andSMAD2/3

Author

Schepers, Dorien, primary, Tortora, Giada, additional, Morisaki, Hiroko, additional, MacCarrick, Gretchen, additional, Lindsay, Mark, additional, Liang, David, additional, Mehta, Sarju G., additional, Hague, Jennifer, additional, Verhagen, Judith, additional, van de Laar, Ingrid, additional, Wessels, Marja, additional, Detisch, Yvonne, additional, van Haelst, Mieke, additional, Baas, Annette, additional, Lichtenbelt, Klaske, additional, Braun, Kees, additional, van der Linde, Denise, additional, Roos-Hesselink, Jolien, additional, McGillivray, George, additional, Meester, Josephina, additional, Maystadt, Isabelle, additional, Coucke, Paul, additional, El-Khoury, Elie, additional, Parkash, Sandhya, additional, Diness, Birgitte, additional, Risom, Lotte, additional, Scurr, Ingrid, additional, Hilhorst-Hofstee, Yvonne, additional, Morisaki, Takayuki, additional, Richer, Julie, additional, Désir, Julie, additional, Kempers, Marlies, additional, Rideout, Andrea L., additional, Horne, Gabrielle, additional, Bennett, Chris, additional, Rahikkala, Elisa, additional, Vandeweyer, Geert, additional, Alaerts, Maaike, additional, Verstraeten, Aline, additional, Dietz, Hal, additional, Van Laer, Lut, additional, and Loeys, Bart, additional

Published
2018
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152. MicroCT-Based Phenomics in the Zebrafish Skeleton Reveals Virtues of Deep Phenotyping in a Distributed Organ System

Author

Hur, Matthew, primary, Gistelinck, Charlotte A., additional, Huber, Philippe, additional, Lee, Jane, additional, Thompson, Marjorie H., additional, Monstad-Rios, Adrian T., additional, Watson, Claire J., additional, McMenamin, Sarah K., additional, Willaert, Andy, additional, Parichy, David M., additional, Coucke, Paul, additional, and Kwon, Ronald Y., additional

Published
2018
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153. Zebrafish type I collagen mutants faithfully recapitulate human type I collagenopathies

Author

Gistelinck, Charlotte, primary, Kwon, Ronald Y, additional, Malfait, Fransiska, additional, Symoens, Sofie, additional, Harris, Matthew P., additional, Henke, Katrin, additional, Fisher, Shannon, additional, Sips, Patrick, additional, Guillemyn, Brecht, additional, Bek, Jan Willem, additional, Vermassen, Petra, additional, De Saffel, Hanna, additional, Weis, MaryAnn, additional, De Paepe, Anne, additional, Eyre, David R, additional, Willaert, Andy, additional, and Coucke, Paul J, additional

Published
2018
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158. Reassessment of causality of ABCC6missense variants associated with pseudoxanthoma elasticum based on Sherloc

Author

Verschuere, Shana, Navassiolava, Nastassia, Martin, Ludovic, Nevalainen, Pasi I., Coucke, Paul J., and Vanakker, Olivier M.

Abstract

Pseudoxanthoma elasticum (PXE) is a heritable disorder affecting elastic fibers in the skin, eyes, and cardiovascular system. It is caused by biallelic pathogenic variants in the ABCC6gene. To date, over 300 ABCC6variants are associated with PXE, more than half being missense variants. Correct variant interpretation is essential for establishing a direct link between the variant and the patient’s phenotype and has important implications for diagnosis and treatment.

Published
2021
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159. Mutations in the ABCC6 gene are associated with an increased risk for ischaemic stroke

Author

De Reuck Jacques, De Vilder Eva, Hemelsoet Dimitri, Hosen Mohammad, Vanakker Olivier, Cardoen Stefanie, and Coucke Paul

Subjects
Aging, medicine.medical_specialty, biology, business.industry, Cognitive Neuroscience, ABCC6, Increased risk, Internal medicine, Ischaemic stroke, Cardiology, medicine, biology.protein, business, Gene
Published
2016

160. Association Between Kniest Dysplasia and Chondrosarcoma in a Child

Author

Hochart, Audrey, Dieux, Anne, Coucke, Paul, Fron, Damien, Fayoux, Pierre, Labalette, Pierre, Boutry, Nathalie, Escande, Fabienne, Aubert, Sébastien, Renaud, Florence, Rocourt, Nathalie, Vinchon, Matthieu, Leblond, Pierre, Centre Régional de Lutte contre le Cancer Oscar Lambret [Lille] (UNICANCER/Lille), Université Lille Nord de France (COMUE)-UNICANCER, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Ghent University Hospital, Université de Lille-UNICANCER, and Université de Lille, LillOA

Subjects
Male, musculoskeletal diseases, chondrosarcoma, Hyaline Membrane Disease, [SDV]Life Sciences [q-bio], COL2A1 gene, Collagen Diseases, Infant, Newborn, Bone Neoplasms, Dwarfism, Osteochondrodysplasias, Prognosis, musculoskeletal system, Cleft Palate, [SDV] Life Sciences [q-bio], pediatric, Face, Mutation, Humans, Kniest dysplasia, Collagen Type II
Abstract

International audience; Constitutive COL2A1 mutations are associated with a wide variety of clinical manifestations known as type II collagenopathies. Among them is Kniest dysplasia, which is phenotypically variable and includes both skeletal (short trunk and limbs, kyphoscoliosis, prominent joints, and osteoarthritis) and craniofacial characteristics. Kniest dysplasia mutations primarily arise in the triple-helicoidal region of the alpha 1 (II) chain in COL2A1 between exons 12 and 24. Somatic COL2A1 mutations have been identified in chondrosarcoma, a rare cartilage forming neoplasm, with a hypermutability of the gene reported in 37% of cases. However, to the best of our knowledge, there is no reported increase in predisposition to chondrosarcoma in human collagenopathies, and no reported clinical association between these congenital diseases and cartilaginous tumors. In the case study presented here, we report the first description of an association between these two rare diseases involving COL2A1, in a child presenting with Kniest dysplasia and a grade I sphenoethmoidal chondrosarcoma. We also describe a new constitutive mutation in COL2A1.

Published
2015

161. MicroCT-based phenomics in the zebrafish skeleton reveals virtues of deep phenotyping in a distributed organ system

Author

Hur, Matthew, primary, Gistelinck, Charlotte A, additional, Huber, Philippe, additional, Lee, Jane, additional, Thompson, Marjorie H, additional, Monstad-Rios, Adrian T, additional, Watson, Claire J, additional, McMenamin, Sarah K, additional, Willaert, Andy, additional, Parichy, David M, additional, Coucke, Paul, additional, and Kwon, Ronald Y, additional

Published
2017
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162. GLUT10—Lacking in Arterial Tortuosity Syndrome—Is Localized to the Endoplasmic Reticulum of Human Fibroblasts

Author

Gamberucci, Alessandra, primary, Marcolongo, Paola, additional, Németh, Csilla, additional, Zoppi, Nicoletta, additional, Szarka, András, additional, Chiarelli, Nicola, additional, Hegedűs, Tamás, additional, Ritelli, Marco, additional, Carini, Giulia, additional, Willaert, Andy, additional, Callewaert, Bert, additional, Coucke, Paul, additional, Benedetti, Angiolo, additional, Margittai, Éva, additional, Fulceri, Rosella, additional, Bánhegyi, Gábor, additional, and Colombi, Marina, additional

Published
2017
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163. Author response: MicroCT-based phenomics in the zebrafish skeleton reveals virtues of deep phenotyping in a distributed organ system

Author

Hur, Matthew, primary, Gistelinck, Charlotte A, additional, Huber, Philippe, additional, Lee, Jane, additional, Thompson, Marjorie H, additional, Monstad-Rios, Adrian T, additional, Watson, Claire J, additional, McMenamin, Sarah K, additional, Willaert, Andy, additional, Parichy, David M, additional, Coucke, Paul, additional, and Kwon, Ronald Y, additional

Published
2017
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166. Mutations in ATP6V1E1 or ATP6V1A Cause Autosomal-Recessive Cutis Laxa

Author

Van Damme, Tim, primary, Gardeitchik, Thatjana, additional, Mohamed, Miski, additional, Guerrero-Castillo, Sergio, additional, Freisinger, Peter, additional, Guillemyn, Brecht, additional, Kariminejad, Ariana, additional, Dalloyaux, Daisy, additional, van Kraaij, Sanne, additional, Lefeber, Dirk J., additional, Syx, Delfien, additional, Steyaert, Wouter, additional, De Rycke, Riet, additional, Hoischen, Alexander, additional, Kamsteeg, Erik-Jan, additional, Wong, Sunnie Y., additional, van Scherpenzeel, Monique, additional, Jamali, Payman, additional, Brandt, Ulrich, additional, Nijtmans, Leo, additional, Korenke, G. Christoph, additional, Chung, Brian H.Y., additional, Mak, Christopher C.Y., additional, Hausser, Ingrid, additional, Kornak, Uwe, additional, Fischer-Zirnsak, Björn, additional, Strom, Tim M., additional, Meitinger, Thomas, additional, Alanay, Yasemin, additional, Utine, Gulen E., additional, Leung, Peter K.C., additional, Ghaderi-Sohi, Siavash, additional, Coucke, Paul, additional, Symoens, Sofie, additional, De Paepe, Anne, additional, Thiel, Christian, additional, Haack, Tobias B., additional, Malfait, Fransiska, additional, Morava, Eva, additional, Callewaert, Bert, additional, and Wevers, Ron A., additional

Published
2017
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168. Loss of Type I Collagen Telopeptide Lysyl Hydroxylation Causes Musculoskeletal Abnormalities in a Zebrafish Model of Bruck Syndrome

Author

Gistelinck, Charlotte, primary, Witten, Paul Eckhard, additional, Huysseune, Ann, additional, Symoens, Sofie, additional, Malfait, Fransiska, additional, Larionova, Daria, additional, Simoens, Pascal, additional, Dierick, Manuel, additional, Van Hoorebeke, Luc, additional, De Paepe, Anne, additional, Kwon, Ronald Y, additional, Weis, MaryAnn, additional, Eyre, David R, additional, Willaert, Andy, additional, and Coucke, Paul J, additional

Published
2016
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171. A Second Gene for Otosclerosis, OTSC2, Maps to Chromosome 7q34-36

Author

Van Den Bogaert, Kris, Govaerts, Paul J., Schatteman, Isabelle, Brown, Matthew R., Caethoven, Goele, Offeciers, F. Erwin, Somers, Thomas, Declau, Frank, Coucke, Paul, Van de Heyning, Paul, Smith, Richard J. H., and Van Camp, Guy

Subjects
Genetic research -- Analysis, Otosclerosis -- Genetic aspects, Biological sciences
Published
2001

173. Glucose transporter type 10-lacking in arterial tortuosity syndrome-facilitates dehydroascorbic acid transport

Author

Németh, Csilla E., primary, Marcolongo, Paola, additional, Gamberucci, Alessandra, additional, Fulceri, Rosella, additional, Benedetti, Angiolo, additional, Zoppi, Nicoletta, additional, Ritelli, Marco, additional, Chiarelli, Nicola, additional, Colombi, Marina, additional, Willaert, Andy, additional, Callewaert, Bert L., additional, Coucke, Paul J., additional, Gróf, Pál, additional, Nagy, Szilvia K., additional, Mészáros, Tamás, additional, Bánhegyi, Gábor, additional, and Margittai, Éva, additional

Published
2016
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174. DNA Diagnostics of Hereditary Hearing Loss: A Targeted Resequencing Approach Combined with a Mutation Classification System

Author

Sommen, Manou, primary, Schrauwen, Isabelle, additional, Vandeweyer, Geert, additional, Boeckx, Nele, additional, Corneveaux, Jason J., additional, van den Ende, Jenneke, additional, Boudewyns, An, additional, De Leenheer, Els, additional, Janssens, Sandra, additional, Claes, Kathleen, additional, Verstreken, Margriet, additional, Strenzke, Nicola, additional, Predöhl, Friederike, additional, Wuyts, Wim, additional, Mortier, Geert, additional, Bitner-Glindzicz, Maria, additional, Moser, Tobias, additional, Coucke, Paul, additional, Huentelman, Matthew J., additional, and Van Camp, Guy, additional

Published
2016
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175. Loss of type I collagen telopeptide lysyl hydroxylation causes musculoskeletal abnormalities in a zebrafish model of Bruck syndrome

Author

Willaert, Andy, primary, Ghistelinck, Charlotte, additional, Witten, P Eckhard, additional, Huysseune, Ann, additional, Simoens, Pascal, additional, Symoens, Sofie, additional, Malfait, Fransiska, additional, De, Muynck Amelie, additional, De, Paepe Anne, additional, Kwon, Ronald Y, additional, Weiss, Mary Ann, additional, Eyre, David E, additional, and Coucke, Paul, additional

Published
2016
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176. Genetic Defects in TAPT1 Disrupt Ciliogenesis and Cause a Complex Lethal Osteochondrodysplasia

Author

Symoens, Sofie, primary, Barnes, Aileen M., additional, Gistelinck, Charlotte, additional, Malfait, Fransiska, additional, Guillemyn, Brecht, additional, Steyaert, Wouter, additional, Syx, Delfien, additional, D’hondt, Sanne, additional, Biervliet, Martine, additional, De Backer, Julie, additional, Witten, Eckhard P., additional, Leikin, Sergey, additional, Makareeva, Elena, additional, Gillessen-Kaesbach, Gabriele, additional, Huysseune, Ann, additional, Vleminckx, Kris, additional, Willaert, Andy, additional, De Paepe, Anne, additional, Marini, Joan C., additional, and Coucke, Paul J., additional

Published
2015
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177. Novel MYH11 and ACTA2 mutations reveal a role for enhanced TGFβ signaling in FTAAD

Author

Renard, M., Callewaert, B, Baetens, Machteld, Fryns, J.p., Bonduelle, Mary-Louise, Coucke, Paul, Loeys, B., De Paepe, A., De Backer, J., Coats, Andrew J. S., Department of Embryology and Genetics, and Reproduction and Genetics

Subjects
Thoracic aortic aneurysm, MYH11, genetics, ACTA2
Abstract

BACKGROUND: Thoracic aortic aneurysm/dissection (TAAD) is a common phenotype that may occur as an isolated manifestation or within the constellation of a defined syndrome. In contrast to syndromic TAAD, the elucidation of the genetic basis of isolated TAAD has only recently started. To date, defects have been found in genes encoding extracellular matrix proteins (fibrillin-1, FBN1; collagen type III alpha 1, COL3A1), proteins involved in transforming growth factor beta (TGF?) signaling (TGF? receptor 1 and 2, TGFBR1/2; and SMAD3) or proteins that build up the contractile apparatus of aortic smooth muscle cells (myosin heavy chain 11, MYH11; smooth muscle actin alpha 2, ACTA2; and MYLK). METHODS AND RESULT: In 110 non-syndromic TAAD patients that previously tested negative for FBN1 or TGFBR1/2 mutations, we identified 7 ACTA2 mutations in a cohort of 43 familial TAAD patients, including 2 premature truncating mutations. Sequencing of MYH11 revealed an in frame splice-site alteration in one out of two probands with TAA(D) associated with PDA but none in the series of 22 probands from the cohort of 110 patients with non-syndromic TAAD. Interestingly, immunohistochemical staining of aortic biopsies of a patient and a family member with MYH11 and patients with ACTA2 missense mutations showed upregulation of the TGF? signaling pathway. CONCLUSIONS: MYH11 mutations are rare and typically identified in patients with TAAD associated with PDA. ACTA2 mutations were identified in 16% of a cohort presenting familial TAAD. Different molecular defects in TAAD may account for a different pathogenic mechanism of enhanced TGF? signaling.

Published
2013

178. Genetic analysis of osteogenesis imperfecta in the Palestinian population: molecular screening of 49 affected families.

Author

Essawi, Osama, Symoens, Sofie, Fannana, Maha, Darwish, Mohammad, Farraj, Mohammad, Willaert, Andy, Essawi, Tamer, Callewaert, Bert, De Paepe, Anne, Malfait, Fransiska, and Coucke, Paul J.

Subjects
OSTEOGENESIS imperfecta, GENETIC testing, COLLAGEN, PALESTINIANS, BONE injuries
Abstract

Abstract: Background: Osteogenesis imperfecta (OI) is a heterogeneous hereditary connective tissue disorder clinically hallmarked by increased susceptibility to bone fractures. Methods: We analyzed a cohort of 77 diagnosed OI patients from 49 unrelated Palestinian families. Next‐generation sequencing technology was used to screen a panel of known OI genes. Results: In 41 probands, we identified 28 different disease‐causing variants of 9 different known OI genes. Eleven of the variants are novel. Ten of the 28 variants are located in COL1A1, five in COL1A2, three in BMP1, three in FKBP10, two in TMEM38B, two in P3H1, and one each in CRTAP, SERPINF1, and SERPINH1. The absence of disease‐causing variants in the remaining eight probands suggests further genetic heterogeneity in OI. In general, most OI patients (90%) harbor mainly variants in type I collagen resulting in an autosomal dominant inheritance pattern. However, in our cohort almost 61% (25/41) were affected with autosomal recessive OI. Moreover, we document a 21‐kb genomic deletion in the TMEM38B gene identified in 29% (12/41) of the tested probands, making it the most frequent OI‐causing variant in the Palestinian population. Conclusion: This is the first genetic screening of an OI cohort from the Palestinian population. Our data are important for genetic counseling of OI patients and families in highly consanguineous populations. [ABSTRACT FROM AUTHOR]

Published
2018
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179. Comprehensive characterization of LEDGF/p75 in a HIV-1-infected patient cohort

Author

Messiaen, Peter, De Spiegelaere, Ward, Verhofstede, Chris, Coucke, Paul, Van Acker, Petra, Vlummens, Philip, VERVISCH, KAREN, Vogelaers, Dirk, Poppe, Bruce, Alcami, Jose, and Vandekerckhove, Linos

Subjects
Biology and Life Sciences, HIV, LEDGF
Abstract

BACKGROUND: Lens epithelium derived growth factor/transcriptional co-activator p75 (LEDGF/p75) is an important cellular co-factor for the HIV enzyme integrase. In the present study, we evaluated if genetic variation in the LEDGF/p75 gene and mRNA expression levels might explain differences in HIV disease progression. METHODS: Samples were derived from a therapy-naïve patient cohort from the Ghent University Hospital and from the long-term-non-progressor patient Spanish RIS cohort. A comprehensive genomic scan of the coding region and 3’UTR of LEDGF/p75 was performed using high resolution melting curve analysis and Sanger sequencing to identify single nucleotide polymorphisms (SNPS). In addition, LEDGF/p75 mRNA expression levels were determined from patient PBMCs using RT-qPCR with validated reference genes for normalization. RESULTS: In total 325 patient samples were investigated, of which 291 (90%) of Caucasian and 34 (10%) of African origin, and among which a large group of Elite controllers (n=49) and Viremic controllers (n=62). In these samples, 24 SNPs were analyzed, including 5 in the coding region (2 synonymous and 3 non-synonymous), 17 in the flanking non-coding regions and in the 3’UTR, and two additional tagSNPs as described by Madlala et al. (Aids, 2011) in two South African cohorts. One SNP in the 3’UTR region (rs2737835, n=46) had a higher representation in Caucasian Elite controllers and was correlated with lower LEDGF/p75 mRNA levels (P=0.047) and with a slower CD4 decline (P= 0.042). rs2737828 (n=13) was under-represented in Caucasian HIV patients and linked to lower LEDGF/p75 expression (P=0.013). The presence of intron SNP (rs16933270, n=6) was associated with a slower CD4 decline in African patients (P=0.017), and this CD4 decline was comparable with that of African slow disease progressors. Interestingly, the presence of one tagSNP (rs12339417, n=95) was significantly correlated with a decreased viral load, but in contrast to the results of Madlala et al. (Aids, 2011), this SNP was not correlated with the CD4 slope and neither with LEDGF/p75 mRNA levels. CONCLUSIONS: Although the data of the present investigation was not entirely comparable with the results of Madlala et al. (Aids, 2011), our data supports their hypothesis that host factors influence HIV disease progression. The observed differences between the European and South African cohorts may be of ethnical origin, or due to different infection phases. In the investigated cohorts, two SNPs were associated with lower LEDGF/p75 mRNA expression in Caucasians, and one SNP was associated with slower disease progression in Africans. The significant correlation with the tagSNP (rs12339417) and the decreased viral load is surprising as this was not correlated with a delayed CD4 decline, nor with LEDGF/p75 expression. This might indicate that either conformational changes or factors upstream of mRNA transcription might influence the action of LEDGF/p75 in these HIV patients.

Published
2011

182. Altered cytoskeletal organization characterized lethal but not surviving Brtl+/−mice: insight on phenotypic variability in osteogenesis imperfecta

Author

Bianchi, Laura, primary, Gagliardi, Assunta, additional, Maruelli, Silvia, additional, Besio, Roberta, additional, Landi, Claudia, additional, Gioia, Roberta, additional, Kozloff, Kenneth M., additional, Khoury, Basma M., additional, Coucke, Paul J., additional, Symoens, Sofie, additional, Marini, Joan C., additional, Rossi, Antonio, additional, Bini, Luca, additional, and Forlino, Antonella, additional

Published
2015
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184. Refinement of the critical 2p25.3 deletion region: the role of MYT1L in intellectual disability and obesity

Author

De Rocker, Nina, primary, Vergult, Sarah, additional, Koolen, David, additional, Jacobs, Eva, additional, Hoischen, Alexander, additional, Zeesman, Susan, additional, Bang, Birgitte, additional, Béna, Frédérique, additional, Bockaert, Nele, additional, Bongers, Ernie M., additional, de Ravel, Thomy, additional, Devriendt, Koenraad, additional, Giglio, Sabrina, additional, Faivre, Laurence, additional, Joss, Shelagh, additional, Maas, Saskia, additional, Marle, Nathalie, additional, Novara, Francesca, additional, Nowaczyk, Malgorzata J.M., additional, Peeters, Hilde, additional, Polstra, Abeltje, additional, Roelens, Filip, additional, Rosenberg, Carla, additional, Thevenon, Julien, additional, Tümer, Zeynep, additional, Vanhauwaert, Suzanne, additional, Varvagiannis, Konstantinos, additional, Willaert, Andy, additional, Willemsen, Marjolein, additional, Willems, Marjolaine, additional, Zuffardi, Orsetta, additional, Coucke, Paul, additional, Speleman, Frank, additional, Eichler, Evan E., additional, Kleefstra, Tjitske, additional, and Menten, Björn, additional

Published
2015
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185. Defective Proteolytic Processing of Fibrillar Procollagens and Prodecorin Due to BiallelicBMP1Mutations Results in a Severe, Progressive Form of Osteogenesis Imperfecta

Author

Syx, Delfien, primary, Guillemyn, Brecht, additional, Symoens, Sofie, additional, Sousa, Ana Berta, additional, Medeira, Ana, additional, Whiteford, Margo, additional, Hermanns-Lê, Trinh, additional, Coucke, Paul J, additional, De Paepe, Anne, additional, and Malfait, Fransiska, additional

Published
2015
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186. Comparison of Methods for In-House Screening of HLA-B*57:01 to Prevent Abacavir Hypersensitivity in HIV-1 Care

Author

De Spiegelaere, Ward, primary, Philippé, Jan, additional, Vervisch, Karen, additional, Verhofstede, Chris, additional, Malatinkova, Eva, additional, Kiselinova, Maja, additional, Trypsteen, Wim, additional, Bonczkowski, Pawel, additional, Vogelaers, Dirk, additional, Callens, Steven, additional, Ruelle, Jean, additional, Kabeya, Kabamba, additional, De Wit, Stephane, additional, Van Acker, Petra, additional, Van Sandt, Vicky, additional, Emonds, Marie-Paule, additional, Coucke, Paul, additional, Sermijn, Erica, additional, and Vandekerckhove, Linos, additional

Published
2015
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196. Severe congenital cutis laxa with cardiovascular manifestations due to homozygous deletions in ALDH18A1

Author

Fischer, Björn, primary, Callewaert, Bert, additional, Schröter, Phillipe, additional, Coucke, Paul J., additional, Schlack, Claire, additional, Ott, Claus-Eric, additional, Morroni, Manrico, additional, Homann, Wolfgang, additional, Mundlos, Stefan, additional, Morava, Eva, additional, Ficcadenti, Anna, additional, and Kornak, Uwe, additional

Published
2014
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200. Absence of Cardiovascular Manifestations in a Haploinsufficient Tgfbr1 Mouse Model

Author

Renard, Marjolijn, primary, Trachet, Bram, additional, Casteleyn, Christophe, additional, Campens, Laurence, additional, Cornillie, Pieter, additional, Callewaert, Bert, additional, Deleye, Steven, additional, Vandeghinste, Bert, additional, van Heijningen, Paula M., additional, Dietz, Harry, additional, De Vos, Filip, additional, Essers, Jeroen, additional, Staelens, Steven, additional, Segers, Patrick, additional, Loeys, Bart, additional, Coucke, Paul, additional, De Paepe, Anne, additional, and De Backer, Julie, additional

Published
2014
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