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202 results on '"Scotton, C."'

1. Starship: Study of Telomeres and Role of Sex Hormones in Pulmonary Fibrosis

Author

Duckworth, A., primary, Prague, J.K., additional, Norris, K.T., additional, Emms, H., additional, Sayers, R., additional, Steward, M., additional, Thould, H., additional, Savill, A., additional, Lines, S., additional, Mandizha, J., additional, Almond, H., additional, Baird, D., additional, Russell, A.-M., additional, Gibbons, M.A., additional, and Scotton, C., additional

Published
2024
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2. Chapter Biomarkers in Rare Genetic Diseases

Author

Ferlini, Alessandra and Scotton, C.

Subjects
bone regeneration, bioinspired materials, biomineralization, biomorphic transformation, magnetic activation, bic Book Industry Communication::M Medicine::MN Surgery::MNS Orthopaedics & fractures
Abstract

Today, as the need of new regenerative solutions is steadily increasing, the demand for new bio-devices with smart functionality is pushing material scientists to develop new synthesis concepts. Indeed, the conventional approaches for biomaterials fail when it comes to generate nano-biocomposites with designed biomimetic composition and hierarchically organized architecture mimicking biologically relevant tissue features. In this respect, an emerging concept in material science is to draw inspiration from natural processes and products, which we may consider as the most advanced examples of smart nanotechnology. Natural processes of supramolecular assembly and mineralization of organic macromolecules, known as biomineralization, generate complex hybrid 3D constructs that are the basis of skeletons, exoskeletons, nacre and shells. On the other hand, natural structures such as woods and plants exhibit multi-scale hierarchic organization that is the source of smart and anisotropic mechanical properties associated with high porosity and lightness. The association of nature-inspired nano-technological products with smart functionalization can provide new advanced solutions to critical and still unmet clinical needs. In this respect, magnetic activation of biomaterials by the use of a recently developed biocompatible, resorbable magnetic apatite promises to represent a new safe and effective switching tool, enabling personalized applications in regenerative medicine and theranostics that so far were not feasible, due to the cytotoxicity of the currently used magnetic materials.

Published
2016
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4. Modification of the Rheumatoid Arthritis (RA) Patient Reported Experience Measure (PREM) for patients with Interstitial Lung Disease (ILD)

Author

Mandizha, J, primary, Duckworth, A, additional, Almond, H, additional, Brown, G, additional, Lines, S, additional, Jorge Da Ponte, A, additional, Shuttleworth, R, additional, Lanario, J, additional, Steward, M, additional, Sayers, R, additional, Scotton, C, additional, Gibbons, M, additional, and Russell, A, additional

Published
2022
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11. TCTEX1D1 is a genetic modifier of disease progression in Duchenne muscular dystrophy

Author

Spitali, P., Zaharieva, I., Bohringer, S., Hiller, M., Chaouch, A., Roos, A., Scotton, C., Claustres, M., Bello, L., McDonald, C.M., Hoffman, E.P., Koeks, Z., Suchiman, H.E., Cirak, S., Scoto, M., Reza, M., Hoen, P.A.C. t, Niks, E.H., Tuffery-Giraud, S., Lochmuller, H., Ferlini, A., Muntoni, F., Aartsma-Rus, A., Dubrovsky, A., Kornberg, A., North, K., Ryan, M., Webster, R., Biggar, W.D., McAdam, L.C., Mah, J.K., Kolski, H., Vishwanathan, V., Chidambaranathan, S., Nevo, Y., Gorni, K., Carlo, J., Tulinius, M., Lotze, T., Bertorini, T.E., Day, J.W., Karachunski, P., Clemens, P.R., Abdel-Hamid, H., Teasley, J., Kuntz, N., Driscoll, S., Bodensteiner, J.B., Connolly, A.M., Pestronk, A., Abresch, R.T., Henricson, E.K., Joyce, N.C., Cnaan, A., Gordish-Dressmsn, H., Morgenroth, L.P., Leshner, R., Tesi-Rocha, C., Thangarajh, M., Duong, T., CINRG Investigators, Leibniz-Institut für Analytische Wissenschaften - ISAS - e.V., Laboratoire de génétique des maladies rares. Pathologie moleculaire, etudes fonctionnelles et banque de données génétiques (LGMR), IFR3, Université Montpellier 1 (UM1)-Université Montpellier 1 (UM1)-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Universita degli Studi di Padova, Newcastle University [Newcastle], Department of Reproduction and Growth, UOL of Medical Genetics (University Hospital St Anna, Ferrara), University of Ferrara at St. Anna Hospital, Dubowitz Neuromuscular Center, Institute of Child Health, and Human Genetics

Subjects
Male, 0301 basic medicine, Adolescent, Duchenne muscular dystrophy, [SDV]Life Sciences [q-bio], Locus (genetics), Polymorphism, Single Nucleotide, Genome-wide association studies, Article, Prognostic markers, 03 medical and health sciences, Exon, 0302 clinical medicine, Genotype, Genetics, medicine, Humans, Allele, Muscular dystrophy, Child, Genetics (clinical), Genes, Modifier, biology, business.industry, Neuromuscular disease, medicine.disease, Muscular Dystrophy, Duchenne, Phenotype, 030104 developmental biology, Disease Progression, biology.protein, Human genome, Dystrophin, business, 030217 neurology & neurosurgery
Abstract

Duchenne muscular dystrophy (DMD) is caused by pathogenic variants in the DMD gene leading to the lack of dystrophin. Variability in the disease course suggests that other factors influence disease progression. With this study we aimed to identify genetic factors that may account for some of the variability in the clinical presentation. We compared whole-exome sequencing (WES) data in 27 DMD patients with extreme phenotypes to identify candidate variants that could affect disease progression. Validation of the candidate SNPs was performed in two independent cohorts including 301 (BIO-NMD cohort) and 109 (CINRG cohort of European ancestry) DMD patients, respectively. Variants in the Tctex1 domain containing 1 (TCTEX1D1) gene on chromosome 1 were associated with age of ambulation loss. The minor alleles of two independent variants, known to affect TCTEX1D1 coding sequence and induce skipping of its exon 4, were associated with earlier loss of ambulation. Our data show that disease progression of DMD is affected by a new locus on chromosome 1 and demonstrate the possibility to identify genetic modifiers in rare diseases by studying WES data in patients with extreme phenotypes followed by multiple layers of validation.

Published
2020

13. Corrigendum to: 'Transcriptional and epigenetic analyses of the DMD locus reveal novel cis-acting DNA elements that govern muscle dystrophin expression'. [Biochim. Biophys. Acta Gene Regul. Mech. 2017 Nov;1860(11):1138–1147.] (Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms (2017) 1860(11) (1138–1147), (S1874939917301359), (10.1016/j.bbagrm.2017.08.010))

Author

Gherardi, S., Bovolenta, M., Passarelli, C., Falzarano, M. S., Pigini, P., Scotton, C., Neri, M., Armaroli, A., Osman, H., Selvatici, R., Gualandi, F., Recchia, A., Mora, M., Bernasconi, P., Maggi, L., Morandi, L., Ferlini, A., and Perini, G.

Published
2020

14. TCTEX1D1 is a genetic modifier of disease progression in Duchenne muscular dystrophy

Author

Spitali, P, Zaharieva, I, Bohringer, S, Hiller, M, Chaouch, A, Roos, A, Scotton, C, Claustres, M, Bello, L, McDonald, CM, Hoffman, EP, Koeks, Z, Suchiman, HE, Cirak, S, Scoto, M, Reza, M, 't Hoen, PAC, Niks, EH, Tuffery-Giraud, S, Lochmueller, H, Ferlini, A, Muntoni, F, Aartsma-Rus, A, Dubrovsky, A, Kornberg, A, North, K, Ryan, M, Webster, R, Biggar, WD, McAdam, LC, Mah, JK, Kolski, H, Vishwanathan, V, Chidambaranathan, S, Nevo, Y, Gorni, K, Carlo, J, Tulinius, M, Lotze, T, Bertorini, TE, Day, JW, Karachunski, P, Clemens, PR, Abdel-Hamid, H, Teasley, J, Kuntz, N, Driscoll, S, Bodensteiner, JB, Connolly, AM, Pestronk, A, Abresch, RT, Henricson, EK, Joyce, NC, Cnaan, A, Gordish-Dressmsn, H, Morgenroth, LP, Leshner, R, Tesi-Rocha, C, Thangarajh, M, Duong, T, Spitali, P, Zaharieva, I, Bohringer, S, Hiller, M, Chaouch, A, Roos, A, Scotton, C, Claustres, M, Bello, L, McDonald, CM, Hoffman, EP, Koeks, Z, Suchiman, HE, Cirak, S, Scoto, M, Reza, M, 't Hoen, PAC, Niks, EH, Tuffery-Giraud, S, Lochmueller, H, Ferlini, A, Muntoni, F, Aartsma-Rus, A, Dubrovsky, A, Kornberg, A, North, K, Ryan, M, Webster, R, Biggar, WD, McAdam, LC, Mah, JK, Kolski, H, Vishwanathan, V, Chidambaranathan, S, Nevo, Y, Gorni, K, Carlo, J, Tulinius, M, Lotze, T, Bertorini, TE, Day, JW, Karachunski, P, Clemens, PR, Abdel-Hamid, H, Teasley, J, Kuntz, N, Driscoll, S, Bodensteiner, JB, Connolly, AM, Pestronk, A, Abresch, RT, Henricson, EK, Joyce, NC, Cnaan, A, Gordish-Dressmsn, H, Morgenroth, LP, Leshner, R, Tesi-Rocha, C, Thangarajh, M, and Duong, T

Abstract

Duchenne muscular dystrophy (DMD) is caused by pathogenic variants in the DMD gene leading to the lack of dystrophin. Variability in the disease course suggests that other factors influence disease progression. With this study we aimed to identify genetic factors that may account for some of the variability in the clinical presentation. We compared whole-exome sequencing (WES) data in 27 DMD patients with extreme phenotypes to identify candidate variants that could affect disease progression. Validation of the candidate SNPs was performed in two independent cohorts including 301 (BIO-NMD cohort) and 109 (CINRG cohort of European ancestry) DMD patients, respectively. Variants in the Tctex1 domain containing 1 (TCTEX1D1) gene on chromosome 1 were associated with age of ambulation loss. The minor alleles of two independent variants, known to affect TCTEX1D1 coding sequence and induce skipping of its exon 4, were associated with earlier loss of ambulation. Our data show that disease progression of DMD is affected by a new locus on chromosome 1 and demonstrate the possibility to identify genetic modifiers in rare diseases by studying WES data in patients with extreme phenotypes followed by multiple layers of validation.

Published
2020

17. Corrigendum to: “Transcriptional and epigenetic analyses of the DMD locus reveal novel cis-acting DNA elements that govern muscle dystrophin expression”. [Biochim. Biophys. Acta Gene Regul. Mech. 2017 Nov;1860(11):1138–1147.]

Author

Gherardi, S., primary, Bovolenta, M., additional, Passarelli, C., additional, Falzarano, M.S., additional, Pigini, P., additional, Scotton, C., additional, Neri, M., additional, Armaroli, A., additional, Osman, H., additional, Selvatici, R., additional, Gualandi, F., additional, Recchia, A., additional, Mora, M., additional, Bernasconi, P., additional, Maggi, L., additional, Morandi, L., additional, Ferlini, A., additional, and Perini, G., additional

Published
2020
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25. Clinical gene panel in UNIFE patients orphans of genetic diagnosis

Author

Neri, M., Selvatici, R., Scotton, C., Storbeck, M., Vezyroglou, K., Heller, R., Tugnoli, V., Bigoni, S., Timmerman, V., Wirth, B., De, D., Gualandi, F., Ferlini, A., Neri, M., Selvatici, R., Scotton, C., Storbeck, M., Vezyroglou, K., Heller, R., Tugnoli, V., Bigoni, S., Timmerman, V., Wirth, B., De, D., Gualandi, F., and Ferlini, A.

Published
2017

26. The success of whole exome sequencing analysis in neuromuscular diseases patients: the UNIFE experience within neuromics project

Author

Neri, M., Scotton, C., Selvatici, R., Gualandi, F., Wirth, B., Schols, L., Klockgether, T., Lochmuller, H., Muntoni, F., D'Amico, A., Bertini, E., Pane, M., Mercuri, E., Ferlini, A., Neri, M., Scotton, C., Selvatici, R., Gualandi, F., Wirth, B., Schols, L., Klockgether, T., Lochmuller, H., Muntoni, F., D'Amico, A., Bertini, E., Pane, M., Mercuri, E., and Ferlini, A.

Published
2017

27. Recessive mutations in MSTO1 cause mitochondrial dynamics impairment, leading to myopathy and ataxia

Author

Nasca, A., Scotton, C., Zaharieva, I., Neri, M., Selvatici, R., Magnusson, O. T., Gal, A., Weaver, D., Rossi, R., Armaroli, A., Pane, Marika, Phadke, R., Sarkozy, A., Muntoni, F., Hughes, I., Cecconi, Arianna Veronica, Hajnoczky, G., Donati, Andrea, Mercuri, Eugenio Maria, Zeviani, M., Ferlini, A., Ghezzi, Daniele Maria, Pane M. (ORCID:0000-0002-4851-6124), Cecconi A., Donati A., Mercuri E. (ORCID:0000-0002-9851-5365), Ghezzi D., Nasca, A., Scotton, C., Zaharieva, I., Neri, M., Selvatici, R., Magnusson, O. T., Gal, A., Weaver, D., Rossi, R., Armaroli, A., Pane, Marika, Phadke, R., Sarkozy, A., Muntoni, F., Hughes, I., Cecconi, Arianna Veronica, Hajnoczky, G., Donati, Andrea, Mercuri, Eugenio Maria, Zeviani, M., Ferlini, A., Ghezzi, Daniele Maria, Pane M. (ORCID:0000-0002-4851-6124), Cecconi A., Donati A., Mercuri E. (ORCID:0000-0002-9851-5365), and Ghezzi D.

Abstract

We report here the first families carrying recessive variants in the MSTO1 gene: compound heterozygous mutations were identified in two sisters and in an unrelated singleton case, who presented a multisystem complex phenotype mainly characterized by myopathy and cerebellar ataxia. Human MSTO1 is a poorly studied protein, suggested to have mitochondrial localization and to regulate morphology and distribution of mitochondria. As for other mutations affecting genes involved in mitochondrial dynamics, no biochemical defects typical of mitochondrial disorders were reported. Studies in patients’ fibroblasts revealed that MSTO1 protein levels were strongly reduced, the mitochondrial network was fragmented, and the fusion events among mitochondria were decreased, confirming the deleterious effect of the identified variants and the role of MSTO1 in modulating mitochondrial dynamics. We also found that MSTO1 is mainly a cytosolic protein. These findings indicate recessive mutations in MSTO1 as a new cause for inherited neuromuscular disorders with multisystem features.

Published
2017

28. Developing a collaborative agenda for humanities and social scientific research on laboratory animal science and welfare

Author

Davies, G, Greenhough, B, Hobson-West, P, Kirk, R, Applebee, K, Bellingan, L, Berdoy, M, Buller, H, Cassaday, H, Davies, K, Diefenbacher, D, Druglitrø, T, Escobar, M, Friese, C, Herrmann, K, Hinterberger, A, Jarrett, W, Jayne, K, Johnson, A, Johnson, E, Konold, T, Leach, M, Leonelli, S, Lewis, D, Lilley, E, Longridge, E, McLeod, C, Miele, M, Nelson, N, Ormandy, E, Pallett, H, Poort, L, Pound, P, Ramsden, E, Roe, E, Scalway, H, Schrader, A, Scotton, C, Scudamore, C, Smith, J, Whitfield, L, and Wolfensohn, S

Subjects
Research Facilities, Economics, Science, Animal Types, Social Sciences, Interdisciplinary Studies, Animal Welfare, Research and Analysis Methods, Welfare Economics, Q1, Humanities, Sociology, Laboratory Animal Science, Animals, Humans, Laboratory Animals, Cooperative Behavior, Animal Management, Social Research, Organisms, Biology and Life Sciences, HM Sociology, Agriculture, Labor Economics, Medicine, Research Laboratories, Zoology, Social Welfare, Research Article
Abstract

Improving laboratory animal science and welfare requires both new scientific research and insights from research in the humanities and social sciences. Whilst scientific research provides evidence to replace, reduce and refine procedures involving laboratory animals (the '3Rs'), work in the humanities and social sciences can help understand the social, economic and cultural processes that enhance or impede humane ways of knowing and working with laboratory animals. However, communication across these disciplinary perspectives is currently limited, and they design research programmes, generate results, engage users, and seek to influence policy in different ways. To facilitate dialogue and future research at this interface, we convened an interdisciplinary group of 45 life scientists, social scientists, humanities scholars, non-governmental organisations and policy-makers to generate a collaborative research agenda. This drew on methods employed by other agenda-setting exercises in science policy, using a collaborative and deliberative approach for the identification of research priorities. Participants were recruited from across the community, invited to submit research questions and vote on their priorities. They then met at an interactive workshop in the UK, discussed all 136 questions submitted, and collectively defined the 30 most important issues for the group. The output is a collaborative future agenda for research in the humanities and social sciences on laboratory animal science and welfare. The questions indicate a demand for new research in the humanities and social sciences to inform emerging discussions and priorities on the governance and practice of laboratory animal research, including on issues around: international harmonisation, openness and public engagement, 'cultures of care', harm-benefit analysis and the future of the 3Rs. The process outlined below underlines the value of interdisciplinary exchange for improving communication across different research cultures and identifies ways of enhancing the effectiveness of future research at the interface between the humanities, social sciences, science and science policy.

Published
2016

29. Recessive mutations in novel gene MST01 cause early onset neuromuscular condition

Author

Sarkozy, A., primary, Zaharieva, I., additional, Nasca, A., additional, Scotton, C., additional, Selvatici, R., additional, Neri, M., additional, Magnusson, O., additional, Gal, A., additional, Weaver, D., additional, Armaroli, A., additional, Pane, M., additional, Hajnóczky, G., additional, Sewry, C., additional, Phadke, R., additional, Donati, A., additional, Mercuri, E., additional, Zeviani, M., additional, Muntoni, F., additional, Ghezzi, D., additional, and Ferlini, A., additional

Published
2017
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30. Clinical gene panel in UNIFE patients orphans of genetic diagnosis

Author

Neri, M., primary, Selvatici, R., additional, Scotton, C., additional, Storbeck, M., additional, Vezyroglou, K., additional, Heller, R., additional, Tugnoli, V., additional, Bigoni, S., additional, Timmerman, V., additional, Wirth, B., additional, De, D., additional, Gualandi, F., additional, and Ferlini, A., additional

Published
2017
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31. The success of whole exome sequencing analysis in neuromuscular diseases patients: the UNIFE experience within neuromics project

Author

Neri, M., primary, Scotton, C., additional, Selvatici, R., additional, Gualandi, F., additional, Wirth, B., additional, Schols, L., additional, Klockgether, T., additional, Lochmüller, H., additional, Muntoni, F., additional, D'Amico, A., additional, Bertini, E., additional, Pane, M., additional, Mercuri, E., additional, and Ferlini, A., additional

Published
2017
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32. COL6A genes transcriptomic by RNAseq and fluidic card tools

Author

Rossi, R., primary, Scotton, C., additional, Falzarano, M., additional, Armaroli, A., additional, Osman, H., additional, Neri, M., additional, Pesole, G., additional, Mora, M., additional, Pegoraro, E., additional, Merlini, L., additional, Ferlini, A., additional, and Gualandi, F., additional

Published
2017
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34. Multilevel molecular analysis identifies all dystrophin gene mutations pointing out that DMD is a genetically homogenous disease: repercussions on diagnosis, prevention and therapy

Author

Neri, M., primary, Selvatici, R., additional, Falzarano, M., additional, Trabanelli, C., additional, Ravani, A., additional, Rimessi, P., additional, Fabris, M., additional, Scotton, C., additional, Mauro, A., additional, Fortunato, F., additional, Osman, H., additional, Rossi, R., additional, Armaroli, A., additional, Buldrini, B., additional, Fini, S., additional, Gualandi, F., additional, Group, x. Clinical Study, additional, and Ferlini, A., additional

Published
2017
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36. A missense mutation of POPDC1 affecting cAMP-binding causes limb-girdle muscular dystrophy and cardiac arrhythmia

Author

Schindler, RF, Scotton, C, Simrick, SL, Passarelli, C, Rinne, S, Poon, KL, Nikolaev, VO, Decher, N, Ferlini, A, Brand, T, Medical Research Council (MRC), and British Heart Foundation

Subjects
Science & Technology, Cardiac & Cardiovascular Systems, Cardiovascular Medicine And Haematology, Cardiovascular System & Hematology, Cardiovascular System & Cardiology, Life Sciences & Biomedicine
Published
2015

37. CLINICAL NEXT GENERATION SEQUENCING GENE PANEL IDENTIFIED A NOVEL ATP7A MUTATION IN TWO BROTHERS WITH DISTAL HEREDITARY MOTOR NEUROPATHY AND AUTONOMIC DYSFUNCTION

Author

Gualandi, F., Italyankina, E., Storbeck, M., Vezyroglou, K., Heller, R., Scotton, C., Di Raimo, F., Mauro, A., Tugnoli, V, Timmerman, V, Wirth, B., De Grandis, D., Ferlini, A., Gualandi, F., Italyankina, E., Storbeck, M., Vezyroglou, K., Heller, R., Scotton, C., Di Raimo, F., Mauro, A., Tugnoli, V, Timmerman, V, Wirth, B., De Grandis, D., and Ferlini, A.

Published
2016

41. Isolation and characterization of human urinary stem cells from healthy donors and DMD patients as in vitro cell model for functional studies and drug testing

Author

Falzarano, M., primary, D'Amario, D., additional, Osman, H., additional, Siracusano, A., additional, Scotton, C., additional, Maroni, C., additional, Massetti, M., additional, Amodeo, A., additional, Mercuri, E., additional, Manchi, M., additional, Crea, F., additional, and Ferlini, A., additional

Published
2016
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42. Transcriptomics analysis in collagen VI myopathy: Role of circadian genes using novel fluidic card tools

Author

Scotton, C., primary, Schwartz, E., additional, Falzarano, M., additional, Bovolenta, M., additional, Rossi, R., additional, Armaroli, A., additional, Osman, H., additional, Gualandi, F., additional, Neri, M., additional, Lochmuller, H., additional, Pesole, G., additional, Sabatelli, P., additional, Merlini, L., additional, Bonaldo, P., additional, Muntoni, F., additional, Gelfi, C., additional, Lebowitz, M., additional, Esser, K., additional, and Ferlini, A., additional

Published
2016
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44. Deep RNA profiling identified clock and molecular clock genes as pathophysiological signatures in collagen VI myopathy

Author

Scotton, C., primary, Bovolenta, M., additional, Schwartz, E., additional, Falzarano, M. S., additional, Martoni, E., additional, Passarelli, C., additional, Armaroli, A., additional, Osman, H., additional, Rodolico, C., additional, Messina, S., additional, Pegoraro, E., additional, D'Amico, A., additional, Bertini, E., additional, Gualandi, F., additional, Neri, M., additional, Selvatici, R., additional, Boffi, P., additional, Maioli, M. A., additional, Lochmüller, H., additional, Straub, V., additional, Bushby, K., additional, Castrignanò, T., additional, Pesole, G., additional, Sabatelli, P., additional, Merlini, L., additional, Braghetta, P., additional, Bonaldo, P., additional, Bernardi, P., additional, Foley, R., additional, Cirak, S., additional, Zaharieva, I., additional, Muntoni, F., additional, Capitanio, D., additional, Gelfi, C., additional, Kotelnikova, E., additional, Yuryev, A, additional, Lebowitz, M., additional, Zhang, X., additional, Hodge, B., additional, Esser, K. A., additional, and Ferlini, A., additional

Published
2016
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45. Next generation sequencing identifies a novel ATP7A mutation in two brothers with distal hereditary motor neuropathy and autonomic dysfunction

Author

Scotton, C., Italyankina, E., Storbeck, M., Vezyroglou, K., Heller, R., Neri, M., Di Raimo, F., Mauro, A., Tugnoli, V., Timmerman, V., Wirth, B., De Grandis, D., Gualandi, F., Ferlini, A., Scotton, C., Italyankina, E., Storbeck, M., Vezyroglou, K., Heller, R., Neri, M., Di Raimo, F., Mauro, A., Tugnoli, V., Timmerman, V., Wirth, B., De Grandis, D., Gualandi, F., and Ferlini, A.

Published
2015

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