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3. Correction to: Assessment of gene–disease associations and recommendations for genetic testing for somatic variants in vascular anomalies by VASCERN-VASCA

Author

Revencu, Nicole, Eijkelenboom, Astrid, Bracquemart, Claire, Alhopuro, Pia, Armstrong, Judith, Baselga, Eulalia, Cesario, Claudia, Dentici, Maria Lisa, Eyries, Melanie, Frisk, Sofia, Karstensen, Helena Gásdal, Gene‑Olaciregui, Nagore, Kivirikko, Sirpa, Lavarino, Cinzia, Mero, Inger‑Lise, Michiels, Rodolphe, Pisaneschi, Elisa, Schönewolf‑Greulich, Bitten, Wieland, Ilse, Zenker, Martin, and Vikkula, Miikka

Published
2024
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4. Assessment of gene–disease associations and recommendations for genetic testing for somatic variants in vascular anomalies by VASCERN-VASCA

Author

Revencu, Nicole, Eijkelenboom, Astrid, Bracquemart, Claire, Alhopuro, Pia, Armstrong, Judith, Baselga, Eulalia, Cesario, Claudia, Dentici, Maria Lisa, Eyries, Melanie, Frisk, Sofia, Karstensen, Helena Gásdal, Gene-Olaciregui, Nagore, Kivirikko, Sirpa, Lavarino, Cinzia, Mero, Inger-Lise, Michiels, Rodolphe, Pisaneschi, Elisa, Schönewolf-Greulich, Bitten, Wieland, Ilse, Zenker, Martin, and Vikkula, Miikka

Published
2024
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7. Transcriptional drifts associated with environmental changes in endothelial cells

Author

Afshar, Yalda, Ma, Feyiang, Quach, Austin, Jeong, Anhyo, Sunshine, Hannah L, Freitas, Vanessa, Jami-Alahmadi, Yasaman, Helaers, Raphael, Li, Xinmin, Pellegrini, Matteo, Wohlschlegel, James A, Romanoski, Casey E, Vikkula, Miikka, and Iruela-Arispe, M Luisa

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Human Genome, Biotechnology, Genetics, 2.1 Biological and endogenous factors, Humans, Endothelial Cells, Endothelium, Gene Expression Profiling, Cells, Cultured, Coculture Techniques, endothelial cell, vascular biology, molecular biology, Human, cell biology, developmental biology, human, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Environmental cues, such as physical forces and heterotypic cell interactions play a critical role in cell function, yet their collective contributions to transcriptional changes are unclear. Focusing on human endothelial cells, we performed broad individual sample analysis to identify transcriptional drifts associated with environmental changes that were independent of genetic background. Global gene expression profiling by RNA sequencing and protein expression by liquid chromatography-mass spectrometry directed proteomics distinguished endothelial cells in vivo from genetically matched culture (in vitro) samples. Over 43% of the transcriptome was significantly changed by the in vitro environment. Subjecting cultured cells to long-term shear stress significantly rescued the expression of approximately 17% of genes. Inclusion of heterotypic interactions by co-culture of endothelial cells with smooth muscle cells normalized approximately 9% of the original in vivo signature. We also identified novel flow dependent genes, as well as genes that necessitate heterotypic cell interactions to mimic the in vivo transcriptome. Our findings highlight specific genes and pathways that rely on contextual information for adequate expression from those that are agnostic of such environmental cues.

Published
2023

11. Loss-of-function mutations of the TIE1 receptor tyrosine kinase cause late-onset primary lymphedema

Author

Brouillard, Pascal, Murtomaki, Aino, Leppanen, Veli-Matti, Hyytiainen, Marko, Mestre, Sandrine, Potier, Lucas, Boon, Laurence M., Revencu, Nicole, Greene, Arin, Anisimov, Andrey, Salo, Miia H., Hinttala, Reetta, Eklund, Lauri, Quere, Isabelle, Alitalo, Kari, and Vikkula, Miikka

Subjects
Development and progression, Genetic aspects, Research, Causes of, Health aspects, Protein-tyrosine kinase -- Genetic aspects -- Health aspects, Lymphedema -- Genetic aspects -- Development and progression -- Causes of, Gene mutation -- Research, Medical research, Gene mutations -- Research, Medicine, Experimental, Protein tyrosine kinase -- Genetic aspects -- Health aspects
Abstract

Introduction The pathogenesis of primary lymphedema (PL) results from defective development and/or function of the lymphatic system (ref. 1; reviewed in refs. 2-5). PL is characterized by accumulation of interstitial [...], Primary lymphedema (PL), characterized by tissue swelling, fat accumulation, and fibrosis, results from defects in lymphatic vessels or valves caused by mutations in genes involved in development, maturation, and function of the lymphatic vascular system. Pathogenic variants in various genes have been identified in about 30% of PL cases. By screening of a cohort of 755 individuals with PL, we identified two TIE1 (tyrosine kinase with immunoglobulin- and epidermal growth factor-like domains 1) missense variants and one truncating variant, all predicted to be pathogenic by bioinformatic algorithms. The TIE1 receptor, in complex with TIE2, binds angiopoietins to regulate the formation and remodeling of blood and lymphatic vessels. The premature stop codon mutant encoded an inactive truncated extracellular TIE1 fragment with decreased mRNA stability, and the amino acid substitutions led to decreased TIE1 signaling activity. By reproducing the two missense variants in mouse Tie1 via CRISPR/Cas9, we showed that both cause edema and are lethal in homozygous mice. Thus, our results indicate that TIE1 loss-of-function variants can cause lymphatic dysfunction in patients. Together with our earlier demonstration that ANGPT2 loss-of-function mutations can also cause PL, our results emphasize the important role of the ANGPT2/TIE1 pathway in lymphatic function.

Published
2024
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16. Splenectomy improves erythrocyte functionality in spherocytosis based on septin abundance, but not maturation defects

Author

Cloos, Anne-Sophie, Pollet, Hélène, Stommen, Amaury, Maja, Mauriane, Lingurski, Maxime, Brichard, Bénédicte, Lambert, Catherine, Henriet, Patrick, Pierreux, Christophe, Pyr dit Ruys, Sébastien, Van Der Smissen, Patrick, Vikkula, Miikka, Gatto, Laurent, Martin, Manon, Brouillard, Pascal, Vertommen, Didier, and Tyteca, Donatienne

Published
2023
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19. First International Conference on RASopathies and Neurofibromatoses in Asia: Identification and advances of new therapeutics

Author

Rauen, Katherine A, Alsaegh, Abeer, Ben‐Shachar, Shay, Berman, Yemima, Blakeley, Jaishri, Cordeiro, Isabel, Elgersma, Ype, Evans, D Gareth, Fisher, Michael J, Frayling, Ian M, George, Joshi, Huson, Susan M, Kerr, Bronwyn, Khire, Uday, Korf, Bruce, Legius, Eric, Messiaen, Ludwine, van Minkelen, Rick, Nampoothiri, Sheela, Ngeow, Joanne, Parada, Luis F, Phadke, Shubha, Pillai, Ashok, Plotkin, Scott R, Puri, Ratna, Raji, Anup, Ramesh, Vijaya, Ratner, Nancy, Shankar, Suma P, Sharda, Sheetal, Tambe, Anant, Vikkula, Miikka, Widemann, Brigitte C, Wolkenstein, Pierre, and Upadhyaya, Meena

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Neurofibromatosis, Neurosciences, Brain Disorders, Intellectual and Developmental Disabilities (IDD), Rare Diseases, Pediatric, Congenital, Biomarkers, Disease Management, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Mitogen-Activated Protein Kinases, Molecular Diagnostic Techniques, Molecular Targeted Therapy, Neurofibromatoses, Signal Transduction, Translational Research, Biomedical, ras Proteins, clinical trial, neurofibromatoses, RASopathy, signal transduction pathway, therapy, Clinical Sciences, Clinical sciences
Abstract

The neurofibromatoses, which include neurofibromatosis type I (NF1), neurofibromatosis type II (NF2), and schwannomatosis, are a group of syndromes characterized by tumor growth in the nervous system. The RASopathies are a group of syndromes caused by germline mutations in genes that encode components of the RAS/mitogen-activated protein kinase (MAPK) pathway. The RASopathies include NF1, Noonan syndrome, Noonan syndrome with multiple lentigines, Costello syndrome, cardio-facio-cutaneous syndrome, Legius syndrome, capillary malformation arterio-venous malformation syndrome, and SYNGAP1 autism. Due to their common underlying pathogenetic etiology, all these syndromes have significant phenotypic overlap of which one common feature include a predisposition to tumors, which may be benign or malignant. Together as a group, they represent one of the most common multiple congenital anomaly syndromes estimating to affect approximately one in 1000 individuals worldwide. The subcontinent of India represents one of the largest populations in the world, yet remains underserved from an aspect of clinical genetics services. In an effort to bridge this gap, the First International Conference on RASopathies and Neurofibromatoses in Asia: Identification and Advances of New Therapeutics was held in Kochi, Kerala, India. These proceedings chronicle this timely and topical international symposium directed at discussing the best practices and therapies for individuals with neurofibromatoses and RASopathies.

Published
2019

22. The VASCERN-VASCA working group diagnostic and management pathways for severe and/or rare infantile hemangiomas

Author

Diociaiuti, Andrea, Baselga, Eulalia, Boon, Laurence M., Dompmartin, Anne, Dvorakova, Veronika, El Hachem, May, Gasparella, Paolo, Haxhija, Emir, Ghaffarpour, Nader, Kyrklund, Kristiina, Irvine, Alan D., Kapp, Friedrich G., Rößler, Jochen, Salminen, Päivi, van den Bosch, Caroline, van der Vleuten, Carine, Kool, Leo Schultze, and Vikkula, Miikka

Published
2022
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23. Non‐Hotspot PIK3CA Variants Have Higher Variant Allele Frequency and are More Common in Syndromic Vascular Malformations.

Author

Andreoti, Themis‐Areti A., Maiolo, Massimo, Tuleja, Aleksandra, Döring, Yvonne, Schaller, André, Vassella, Erik, Boon, Laurence M., Baumgartner, Iris, Bernhard, Sarah M., Zweier, Christiane, Vikkula, Miikka, and Rössler, Jochen

Abstract

PIK3CA variants are known to cause vascular malformations. We were interested in studying the phenotypic spectrum, the location within the PIK3CA gene, and the variant allele frequency (VAF) of somatic PI3KCA variants in vascular malformations. Clinical data of consecutive patients with extracranial/extraspinal vascular malformations were collected in the context of the VASCOM cohort (2008–2022, n = 558). Starting October 2020, biopsy samples were tested with the TSO500 gene panel (Illumina). All consenting patients with PIK3CA variants were included in this study. Eighty‐nine patients had available genetic results by June 2022. PIK3CA variants (n = 25) were found in 16 simple/combined (nonsyndromic) vascular malformations and in nine vascular malformations associated with other anomalies (syndromic). Four hotspot variants in exons 9 and 20 (c.1624G>A, c.1633G>A, c.3140A>G, c.3140A>T) were identified in 16/25 patients (VAF 0.9%–9.7%). Six non‐hotspot variants (c.328_330del, c.323_337del, c.353G>A, c.1258T>C, c.3132T>A, c.3195_3203delinsT) were detected in nine patients (VAF 3.6%–31.7%). Non‐hotspot variants were more frequent in syndromic than nonsyndromic vascular malformations (p = 0.0034) and exhibited a higher VAF than hotspot variants (p = 0.0253). Our study contributes to the growing body of knowledge of the genetic background in vascular malformations. Further studies will enrich the ever‐growing list of pathogenic PIK3CA variants associated with vascular malformations. [ABSTRACT FROM AUTHOR]

Published
2025
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24. Author Correction: Genetic investigation of fibromuscular dysplasia identifies risk loci and shared genetics with common cardiovascular diseases

Author

Georges, Adrien, Yang, Min-Lee, Berrandou, Takiy-Eddine, Bakker, Mark K., Dikilitas, Ozan, Kiando, Soto Romuald, Ma, Lijiang, Satterfield, Benjamin A., Sengupta, Sebanti, Yu, Mengyao, Deleuze, Jean-François, Dupré, Delia, Hunker, Kristina L., Kyryachenko, Sergiy, Liu, Lu, Sayoud-Sadeg, Ines, Amar, Laurence, Brummett, Chad M., Coleman, Dawn M., d’Escamard, Valentina, de Leeuw, Peter, Fendrikova-Mahlay, Natalia, Kadian-Dodov, Daniella, Li, Jun Z., Lorthioir, Aurélien, Pappaccogli, Marco, Prejbisz, Aleksander, Smigielski, Witold, Stanley, James C., Zawistowski, Matthew, Zhou, Xiang, Zöllner, Sebastian, Amouyel, Philippe, De Buyzere, Marc L., Debette, Stéphanie, Dobrowolski, Piotr, Drygas, Wojciech, Gornik, Heather L., Olin, Jeffrey W., Piwonski, Jerzy, Rietzschel, Ernst R., Ruigrok, Ynte M., Vikkula, Miikka, Warchol Celinska, Ewa, Januszewicz, Andrzej, Kullo, Iftikhar J., Azizi, Michel, Jeunemaitre, Xavier, Persu, Alexandre, Kovacic, Jason C., Ganesh, Santhi K., and Bouatia-Naji, Nabila

Published
2022
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25. Four putative pathogenic ARHGAP29variants in patients with non-syndromic orofacial clefts (NsOFC)

Author

Ranji, Peyman, Pairet, Eleonore, Helaers, Raphael, Bayet, Bénédicte, Gerdom, Alexander, Gil-da-Silva-Lopes, Vera Lúcia, Revencu, Nicole, and Vikkula, Miikka

Abstract

The pathophysiological basis of non-syndromic orofacial cleft (NsOFC) is still largely unclear. However, exome sequencing (ES) has led to identify several causative genes, often with reduced penetrance. Among these, the Rho GTPase activating protein 29 (ARHGAP29) has been previously implicated in 7 families with NsOFC. We investigated a cohort of 224 NsOFCs for which no genetic pathogenic variant had been identified by diagnostic testing. We used ES and bioinformatic variant filtering and identified four novel putative pathogenic variants in ARHGAP29in four families. One was a missense variant leading to the substitution of the first methionine with threonine, two were heterozygous frameshift variants leading to a premature termination codon, and one was a nonsense variant. All variants were predicted to result in loss of function, either through mRNA decay, truncated ARHGAP29, or abnormal N-terminal initiation of translation of ARHGAP29. The truncated ARHGAP29 proteins would lack the important RhoGAP domain. The variants were either absent or rare in the control population databases, and the loss of intolerance score (pLI) of ARHGAP29 is 1.0, suggesting that ARHGAP29 haploinsufficiency is not tolerated. Phenotypes ranged from microform cleft lip (CL) to complete bilateral cleft lip and palate (CLP), with one unaffected mutation carrier. These results extend the mutational spectrum of ARHGAP29and show that it is an important gene underlying variable NsOFC phenotypes. ARHGAP29should be included in diagnostic genetic testing for NsOFC, especially familial cases, as it may be mutated in ∼4% of them (4/97 in our cohort) with high penetrance (89%).

Published
2025
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28. A New Tool to Identify Pediatric Patients with Atypical Diabetes Associated with Gene Polymorphisms.

Author

Welsch, Sophie, Harvengt, Antoine, Gallo, Paola, Martin, Manon, Beckers, Dominique, Mouraux, Thierry, Seret, Nicole, Lebrethon, Marie-Christine, Helaers, Raphaël, Brouillard, Pascal, Vikkula, Miikka, and Lysy, Philippe A.

Subjects
MATURITY onset diabetes of the young, TYPE 1 diabetes, TYPE 2 diabetes, DIABETES in children, CHILD patients
Abstract

Background: Recent diabetes subclassifications have improved the differentiation between patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus despite several overlapping features, yet without considering genetic forms of diabetes. We sought to facilitate the identification of monogenic diabetes by creating a new tool that we validated in a pediatric maturity-onset diabetes of the young (MODY) cohort. Methods: We first created the DIAgnose MOnogenic DIAbetes (DIAMODIA) criteria based on the pre-existing, but incomplete, MODY calculator. This new score is composed of four strong and five weak criteria, with patients having to display at least one weak and one strong criterion. Results: The effectiveness of the DIAMODIA criteria was evaluated in two patient cohorts, the first consisting of patients with confirmed MODY diabetes (n=34) and the second of patients with T1DM (n=390). These DIAMODIA criteria successfully detected 100% of MODY patients. Multiple correspondence analysis performed on the MODY and T1DM cohorts enabled us to differentiate MODY patients from T1DM. The three most relevant variables to distinguish a MODY from T1DM profile were: lower insulin-dose adjusted A1c score ≤9, glycemic target-adjusted A1c score ≤4.5, and absence of three anti-islet cell autoantibodies. Conclusion: We validated the DIAMODIA criteria, as it effectively identified all monogenic diabetes patients (MODY cohort) and succeeded to differentiate T1DM from MODY patients. The creation of this new and effective tool is likely to facilitate the characterization and therapeutic management of patients with atypical diabetes, and promptly referring them for genetic testing which would markedly improve clinical care and counseling, as well. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Pathogenic variants in HGF give rise to childhood-to-late onset primary lymphoedema by loss of function

Author

Alpaslan, Murat, primary, Fastré, Elodie, additional, Mestre, Sandrine, additional, van Haeringen, Arie, additional, Repetto, Gabriela M, additional, Keymolen, Kathelijn, additional, Boon, Laurence M, additional, Belva, Florence, additional, Giacalone, Guido, additional, Revencu, Nicole, additional, Sznajer, Yves, additional, Riches, Katie, additional, Keeley, Vaughan, additional, Mansour, Sahar, additional, Gordon, Kristiana, additional, Martin-Almedina, Silvia, additional, Dobbins, Sara, additional, Ostergaard, Pia, additional, Quere, Isabelle, additional, Brouillard, Pascal, additional, and Vikkula, Miikka, additional

Published
2024
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35. Genetic investigation of fibromuscular dysplasia identifies risk loci and shared genetics with common cardiovascular diseases

Author

Georges, Adrien, Yang, Min-Lee, Berrandou, Takiy-Eddine, Bakker, Mark K., Dikilitas, Ozan, Kiando, Soto Romuald, Ma, Lijiang, Satterfield, Benjamin A., Sengupta, Sebanti, Yu, Mengyao, Deleuze, Jean-François, Dupré, Delia, Hunker, Kristina L., Kyryachenko, Sergiy, Liu, Lu, Sayoud-Sadeg, Ines, Amar, Laurence, Brummett, Chad M., Coleman, Dawn M., d’Escamard, Valentina, de Leeuw, Peter, Fendrikova-Mahlay, Natalia, Kadian-Dodov, Daniella, Li, Jun Z., Lorthioir, Aurélien, Pappaccogli, Marco, Prejbisz, Aleksander, Smigielski, Witold, Stanley, James C., Zawistowski, Matthew, Zhou, Xiang, Zöllner, Sebastian, Amouyel, Philippe, De Buyzere, Marc L., Debette, Stéphanie, Dobrowolski, Piotr, Drygas, Wojciech, Gornik, Heather L., Olin, Jeffrey W., Piwonski, Jerzy, Rietzschel, Ernst R., Ruigrok, Ynte M., Vikkula, Miikka, Warchol Celinska, Ewa, Januszewicz, Andrzej, Kullo, Iftikhar J., Azizi, Michel, Jeunemaitre, Xavier, Persu, Alexandre, Kovacic, Jason C., Ganesh, Santhi K., and Bouatia-Naji, Nabila

Published
2021
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36. Primary lymphoedema

Author

Brouillard, Pascal, Witte, Marlys H., Erickson, Robert P., Damstra, Robert J., Becker, Corinne, Quéré, Isabelle, and Vikkula, Miikka

Published
2021
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40. Epilepsy with faint capillary malformation or reticulated telangiectasia associated with mosaic AKT3 pathogenic variants

Author

De Bortoli, Martina, primary, Ivars, Marta, additional, Revencu, Nicole, additional, Nassogne, Marie‐Cécile, additional, Lavarino, Cinzia, additional, Paco, Sonia, additional, Lammens, Martin, additional, Renders, Anne, additional, Dumitriu, Dana, additional, Helaers, Raphaël, additional, Boon, Laurence M., additional, Baselga, Eulalia, additional, and Vikkula, Miikka, additional

Published
2024
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41. An endothelial SOX18-mevalonate pathway axis enables repurposing of statins for infantile hemangioma

Author

Holm, Annegret, primary, Graus, Matthew, additional, Wylie-Sears, Jill, additional, Borgelt, Luke, additional, Tan, Jerry Wei Heng, additional, Nasim, Sana, additional, Chung, Long, additional, Jain, Ashish, additional, Sun, Mingwei, additional, Sun, Liang, additional, Brouillard, Pascal, additional, Lekwuttikarn, Ramrada, additional, Kozakewich, Harry, additional, Qi, Yanfei Jacob, additional, Teng, Joyce, additional, Mulliken, John, additional, Vikkula, Miikka, additional, Francois, Mathias, additional, and Bischoff, Joyce, additional

Published
2024
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42. Mutations in Chromatin Modifier and Ephrin Signaling Genes in Vein of Galen Malformation

Author

Duran, Daniel, Zeng, Xue, Jin, Sheng Chih, Choi, Jungmin, Nelson-Williams, Carol, Yatsula, Bogdan, Gaillard, Jonathan, Furey, Charuta Gavankar, Lu, Qiongshi, Timberlake, Andrew T., Dong, Weilai, Sorscher, Michelle A., Loring, Erin, Klein, Jennifer, Allocco, August, Hunt, Ava, Conine, Sierra, Karimy, Jason K., Youngblood, Mark W., Zhang, Jinwei, DiLuna, Michael L., Matouk, Charles C., Mane, Shrikant, Tikhonova, Irina R., Castaldi, Christopher, López-Giráldez, Francesc, Knight, James, Haider, Shozeb, Soban, Mariya, Alper, Seth L., Komiyama, Masaki, Ducruet, Andrew F., Zabramski, Joseph M., Dardik, Alan, Walcott, Brian P., Stapleton, Christopher J., Aagaard-Kienitz, Beverly, Rodesch, Georges, Jackson, Eric, Smith, Edward R., Orbach, Darren B., Berenstein, Alejandro, Bilguvar, Kaya, Vikkula, Miikka, Gunel, Murat, Lifton, Richard P., and Kahle, Kristopher T.

Published
2019
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44. Recalibrating vascular malformations and mechanotransduction by pharmacological intervention

Author

Abdelilah-Seyfried, Salim, Iruela-Arispe, M. Luisa, Penninger, Josef M., Tournier-Lasserve, Elisabeth, Vikkula, Miikka, and Cleaver, Ondine

Subjects
Drug therapy, Physiological aspects, Development and progression, Genetic aspects, Health aspects, Arteriovenous malformations -- Genetic aspects -- Drug therapy -- Development and progression, Cellular signal transduction -- Health aspects -- Physiological aspects -- Genetic aspects
Abstract

Introduction Circulation of blood throughout the cardiovascular system results in biomechanical forces that profoundly influence vessel development and maintenance. Fluid shear stress along the inner lining of blood vessels imparts [...]

Published
2022
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49. Parkes Weber Syndrome: Contribution of the Genotype to the Diagnosis

Author

Andreoti, Themis-Areti A., primary, Tuleja, Aleksandra, additional, Döring, Yvonne, additional, Maiolo, Massimo, additional, Schaller, André, additional, Vassella, Erik, additional, Zweier, Christiane, additional, Boon, Laurence M., additional, Vikkula, Miikka, additional, Rössler, Jochen, additional, Bernhard, Sarah M., additional, and Baumgartner, Iris, additional

Published
2023
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50. Preliminary results of the European multicentric phase III trial regarding sirolimus in slow-flow vascular malformations

Author

Seront, Emmanuel, primary, Van Damme, An, additional, Legrand, Catherine, additional, Bisdorff-Bresson, Annouk, additional, Orcel, Philippe, additional, Funck-Brentano, Thomas, additional, Sevestre, Marie-Antoinette, additional, Dompmartin, Anne, additional, Quere, Isabelle, additional, Brouillard, Pascal, additional, Revencu, Nicole, additional, De Bortoli, Martina, additional, Hammer, Frank, additional, Clapuyt, Philippe, additional, Dumitriu, Dana, additional, Vikkula, Miikka, additional, and Boon, Laurence M., additional

Published
2023
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