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520 results on '"Häusler M"'

1. From Technology to Strategy: Robotic Fabrication and Human Robot Collaboration for Increasing AEC Capacities

Author

Reinhardt, Dagmar, Haeusler, M. Hank, Chaari, Fakher, Series Editor, Gherardini, Francesco, Series Editor, Ivanov, Vitalii, Series Editor, Haddar, Mohamed, Series Editor, Cavas-Martínez, Francisco, Editorial Board Member, di Mare, Francesca, Editorial Board Member, Kwon, Young W., Editorial Board Member, Trojanowska, Justyna, Editorial Board Member, Xu, Jinyang, Editorial Board Member, Barberio, Maurizio, editor, Colella, Micaela, editor, Figliola, Angelo, editor, and Battisti, Alessandra, editor

Published
2024
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7. Outcome and Brain Volume Changes over Time in Children with Autoimmune Encephalitis and MOG Antibodies.

Author

Bertolini, A., Bartels, F., Wegener-Panzer, A., Cleaveland, R., Ullmann, F., Olive, G., Armangue, T., Häusler, M., Wendel, E. M., Knierim, E., Reiter-Fink, E., Breu, M., Marina, A. Della, Baumann, B. Tro, Reindl, M., Finke, C., and Rostasy, K.

Subjects
ENCEPHALITIS, IMMUNOGLOBULINS, GRAY matter (Nerve tissue), EPILEPSY, VOLUME (Cubic content), BRAIN diseases
Abstract

This article, published in the journal Neuropediatrics, examines the outcome and brain volume changes over time in children with MOG-encephalitis (MOG-E), a rare clinical phenotype of MOGAD. The study included 21 children with MOG-E, who presented with symptoms such as encephalopathy, headache, focal neurological signs, seizures, or CSF pleocytosis. The results showed that the majority of children had a good clinical outcome, with resolution of MRI changes and decreasing MOG antibodies over time. However, brain volumetry measurements indicated a decrease in whole brain volume, particularly in gray matter, after onset. [Extracted from the article]

Published
2023
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8. Long-Term Follow-up of Children with Pre- and (Post) Pubertal MS.

Author

Kauth, F., Bertolini, A., Koukou, G., Naggar, I. El, Baumann, M., Schödl, C., Bigi, S., Wendel, E.-M., Blaschek, A., Hengstler, J., Schimmel, M., Nosadini, M., Sartori, S., Puthenparampil, M., Gravesande, K. Storm van's, Drenckhahn, A., Nikolaus, M. J., Kauffmann, B., Thiels, C., and Häusler, M. G.

Subjects
CHILDREN'S hospitals, MULTIPLE sclerosis, AGE groups
Abstract

This article, published in the journal Neuropediatrics, explores the differences between prepubertal and (post)pubertal children with multiple sclerosis (MS) in terms of clinical, laboratory, and imaging features. The study included 248 MS patients from various European pediatric hospitals who were diagnosed before the age of 18. The results showed that prepubertal children had an equal distribution of MS between sexes, while postpubertal children had a higher prevalence in females. Prepubertal children also had more relapses in the first two years and a different range of MRI features compared to (post)pubertal children. Overall, the findings suggest both similarities and differences between the two age groups in terms of MS characteristics. [Extracted from the article]

Published
2023
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17. New Diagnoses of Children with Multiple Sclerosis in the Years 2015–2019 in North Rhine-Westphalia with the Help of the Patient Registry for Children with Multiple Sclerosis

Author

Kyprianou, A., additional, Deba, T., additional, Karenfort, M., additional, Thiels, C., additional, Häusler, M., additional, Rademacher, N., additional, Mause, U., additional, Koy, A., additional, Lutz, S., additional, Vaassen, P., additional, Ebinger, F., additional, Classen, G., additional, Erdlenbruch, B., additional, Schlump, J., additional, Pritsch, M., additional, Kreth, J., additional, Flechtenmacher, A., additional, Stahmann, A., additional, and Rostásy, K., additional

Published
2021
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18. Role of Filler Content and Morphology in LLZO/PEO Membranes

Author

Din, Mir Mehraj Ud, primary, Häusler, M., additional, Fischer, S. M., additional, Ratzenböck, K., additional, Chamasemani, F. F., additional, Hanghofer, I., additional, Henninge, V., additional, Brunner, R., additional, Slugovc, C., additional, and Rettenwander, D., additional

Published
2021
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28. Epilepsy subtype-specific copy number burden observed in a genome-wide study of 17458 subjects

Author

Niestroj, LM, Perez-Palma, E, Howrigan, DP, Zhou, Y, Cheng, F, Saarentaus, E, Nürnberg, P, Stevelink, R, Daly, MJ, Palotie, A, Lal, D, Feng, YCA, Abbott, LE, Tashman, K, Cerrato, F, Churchhouse, C, Gupta, N, Neale, BM, Berkovic, SF, Lerche, H, Goldstein, DB, Lowenstein, DH, Cavalleri, GL, Cossette, P, Cotsapas, C, De Jonghe, P, Dixon-Salazar, T, Guerrini, R, Hakonarson, H, Heinzen, EL, Helbig, I, Kwan, P, Marson, AG, Petrovski, S, Kamalakaran, S, Sisodiya, SM, Stewart, R, Weckhuysen, S, Depondt, C, Dlugos, DJ, Scheffer, IE, Striano, P, Freyer, C, Krause, R, May, P, McKenna, K, Regan, BM, Leu, C, Bennett, CA, Bellows, Susannah, Johns, EMC, MacDonald, A, Shilling, H, Burgess, R, Weckhuysen, D, Bahlo, M, O'Brien, TJ, Todaro, M, Stamberger, H, Andrade, DM, Sadoway, TR, Mo, K, Krestel, H, Gallati, S, Papacostas, SS, Kousiappa, I, Tanteles, GA, Šterbová, K, Vlcková, M, Sedlácková, L, Laššuthová, P, Martin, K, Rosenow, F, Reif, PS, Knake, S, Kunz, WS, Zsurka, G, Elger, CE, Bauer, J, Rademacher, M, Pendziwiat, M, Muhle, H, Rademacher, A, Van Baalen, A, Von Spiczak, S, Stephani, U, Afawi, Z, Korczyn, AD, Kanaan, M, Canavati, C, Kurlemann, G, Müller-Schlüter, K, Kluger, G, Häusler, M, Blatt, I, Lemke, JR, Krey, I, Weber, YG, Wolking, S, Becker, F, Niestroj, LM, Perez-Palma, E, Howrigan, DP, Zhou, Y, Cheng, F, Saarentaus, E, Nürnberg, P, Stevelink, R, Daly, MJ, Palotie, A, Lal, D, Feng, YCA, Abbott, LE, Tashman, K, Cerrato, F, Churchhouse, C, Gupta, N, Neale, BM, Berkovic, SF, Lerche, H, Goldstein, DB, Lowenstein, DH, Cavalleri, GL, Cossette, P, Cotsapas, C, De Jonghe, P, Dixon-Salazar, T, Guerrini, R, Hakonarson, H, Heinzen, EL, Helbig, I, Kwan, P, Marson, AG, Petrovski, S, Kamalakaran, S, Sisodiya, SM, Stewart, R, Weckhuysen, S, Depondt, C, Dlugos, DJ, Scheffer, IE, Striano, P, Freyer, C, Krause, R, May, P, McKenna, K, Regan, BM, Leu, C, Bennett, CA, Bellows, Susannah, Johns, EMC, MacDonald, A, Shilling, H, Burgess, R, Weckhuysen, D, Bahlo, M, O'Brien, TJ, Todaro, M, Stamberger, H, Andrade, DM, Sadoway, TR, Mo, K, Krestel, H, Gallati, S, Papacostas, SS, Kousiappa, I, Tanteles, GA, Šterbová, K, Vlcková, M, Sedlácková, L, Laššuthová, P, Martin, K, Rosenow, F, Reif, PS, Knake, S, Kunz, WS, Zsurka, G, Elger, CE, Bauer, J, Rademacher, M, Pendziwiat, M, Muhle, H, Rademacher, A, Van Baalen, A, Von Spiczak, S, Stephani, U, Afawi, Z, Korczyn, AD, Kanaan, M, Canavati, C, Kurlemann, G, Müller-Schlüter, K, Kluger, G, Häusler, M, Blatt, I, Lemke, JR, Krey, I, Weber, YG, Wolking, S, and Becker, F

Abstract

Cytogenic testing is routinely applied in most neurological centres for severe paediatric epilepsies. However, which characteristics of copy number variants (CNVs) confer most epilepsy risk and which epilepsy subtypes carry the most CNV burden, have not been explored on a genome-wide scale. Here, we present the largest CNV investigation in epilepsy to date with 10 712 European epilepsy cases and 6746 ancestry-matched controls. Patients with genetic generalized epilepsy, lesional focal epilepsy, non-acquired focal epilepsy, and developmental and epileptic encephalopathy were included. All samples were processed with the same technology and analysis pipeline. All investigated epilepsy types, including lesional focal epilepsy patients, showed an increase in CNV burden in at least one tested category compared to controls. However, we observed striking differences in CNV burden across epilepsy types and investigated CNV categories. Genetic generalized epilepsy patients have the highest CNV burden in all categories tested, followed by developmental and epileptic encephalopathy patients. Both epilepsy types also show association for deletions covering genes intolerant for truncating variants. Genome-wide CNV breakpoint association showed not only significant loci for genetic generalized and developmental and epileptic encephalopathy patients but also for lesional focal epilepsy patients. With a 34-fold risk for developing genetic generalized epilepsy, we show for the first time that the established epilepsy-associated 15q13.3 deletion represents the strongest risk CNV for genetic generalized epilepsy across the whole genome. Using the human interactome, we examined the largest connected component of the genes overlapped by CNVs in the four epilepsy types. We observed that genetic generalized epilepsy and non-acquired focal epilepsy formed disease modules. In summary, we show that in all common epilepsy types, 1.5-3% of patients carry epilepsy-associated CNVs. The character

Published
2020

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