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194 results on '"Nevsimalova S"'

18. Stable or improved neurological manifestations during miglustat therapy in patients from the international disease registry for Niemann-Pick disease type C: An observational cohort study

Author

Patterson, M. C, Mengel, E, Vanier, M. T, Schwierin, B, Muller, A, Cornelisse, P, Pineda, M, Amado-Fondo, A, Amraoui, Y, Andria, G, Arellano, M, Audoin, B, Azcona, C, Barr, C, Baruteau, J, Baumgartner, C, Bell, L, Bembi, B, Benneddif, K, Bernard, G, Bobocea, N, Bodzioch, M, Boettcher, T, Bonnan, M, Broue, P, Bruni, A, Caceres, M, Camino, R, Campbell, E, Cances, C, Cannell, P, Cesar, J, Chabrol, B, Chakrapani, A, Colao, R, Collet, A, Corsetti, T, Cousins, A, Covanis, A, Cox, T, Cuisset, J. M, Dardis, A, Das, A, Deegan, P, Dengler, T, Deodato, F, Derralynn, H, Di Donato, I, Di Rocco, M, Dinopoulos, A, Pakiela, D, Eckehard, S, Engelen, M, Eyer, D, Fecarotta, S, Federico, A, Filla, A, Fiumara, A, Fonseca, M. J, Gabrielli, O, Garcia, T, Garrote, J, Gissen, P, Giugliani, L, Greenberg, C, Heron, B, Hertzberg, C, Higgins, F, Hill, A, Hiwot, T, Hlavata, A, Hörbe-Blindt, A, Howley, E, Hussain, N, Illsinger, S, Imrie, J, Jacklin, E, Jones, S, Jovanovic, A, Kaczmarek, V, Kaphan, E, Kibaek, M, Kleinhans, P, Klünemann, Kh, Koch, S. M, Koegl-Wallner, W, Kolnikova, M, Korenke, G. C, Korinthenberg, R, Kumari, S, Lachmann, R, Lee Ann, L, Likopoulou, L, Lilienthal, E, Link, B, Lippold, M, Lopez-Laso, E, Luecke, T, Lundgren, J, Mackrell, M, Madruga, M, Maletta, R, Malinova, V, Manners, J, Marinei, R, Marquardt, T, Martins, E, Martins, A. M, Martins, N, Mcalister, L, Mccabe, A, Mckie, M, Mcmahon, S, Meehan, M, Meldgaard Lund, A, Mendozah, C, Meyer, A, Mielke, S, Milligan, A, Mir, P, Moisa, M, Mombelli, C, Morris, L, Müller Vom Hagen, J, Munoz, B, Murphy, E, Nagarajan, L, Neto, P. B, Nevsimalova, S, Nia, S, Nicolai, J, Niemann, D, Niktari, G, O'Callaghan, M. D. M, Paucar-Arce, M, Peers, K, Peintinger, L, Peralta, M, Pérez, J, Perez-Poyato, M, Petrariu, A, Puschmann, A, Raiman, J, Rask, O, Rataj, J, Raymond-Gaynor, C, Reichelt, G, Ribeiro, E, Riches, V, Roberts, A, Roelants, J, Rohrbach, M, Rokicki, D, Rolfs, A, Russo, C, Rutsch, F, Saleem, R, Santos, M, Schmutz, P, Schwahn, B, Sedel, F, Semotok, J, Sharma, R, Silska, S, Silva, A, Simmons, L, Sivera, R, Skorpen, J, Sole, G, Souza, C, Stadlober-Degwerth, M, Starling, J, Temudo, T, Tomas, M, Tranchant, C, Uziel, G, Valayannopoulous, V, Van Den Hout, H, Van Der Tol, L, Van Spronsen, F, Vellodi, A, Verdu, A, Vilchez, J. J, Vinaixa, A, Visser, G, Voelker, J, Waldek, S, Walter, A, Walterfang, M, Wein, U, Widner, H, Wilcke, C, Wildish, L, Wraith, E, Wright, N, Xaidara, A, Yamamoto, M, Zallocco, F, Zielke, S, Patterson, Mc, Mengel, E, Vanier, Mt, Schwierin, B, Muller, A, Cornelisse, P, Pineda, M, Registry investigators, Npc, Filla, Alessandro, Russo, CINZIA VALERIA, Neurology, Paediatric Neurology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, ANS - Amsterdam Neuroscience, and Graduate School

Subjects
Male, Pediatrics, Neurology, Cohort Studies, 0302 clinical medicine, Miglustat, Medicine, Enzyme Inhibitor, Genetics(clinical), Pharmacology (medical), Prospective Studies, Young adult, Enzyme Inhibitors, Prospective cohort study, Child, Genetics (clinical), Medicine(all), 0303 health sciences, Medicine (all), Niemann-Pick disease type C, Niemann-Pick Disease, Type C, General Medicine, 3. Good health, Treatment Outcome, Child, Preschool, Cohort, Disease Progression, Female, medicine.drug, Cohort study, Human, Adult, medicine.medical_specialty, Registry, 1-Deoxynojirimycin, Adolescent, 03 medical and health sciences, Young Adult, Disease registry, Swallowing, Humans, 030304 developmental biology, business.industry, Research, Prospective Studie, Cohort Studie, business, 030217 neurology & neurosurgery
Abstract

BACKGROUND: Niemann-Pick disease type C (NP-C) is a rare neurovisceral disease characterised by progressive neurological degeneration, where the rate of neurological disease progression varies depending on age at neurological onset. We report longitudinal data on functional disease progression and safety observations in patients in the international NPC Registry who received continuous treatment with miglustat. METHODS: The NPC Registry is a prospective observational cohort of NP-C patients. Enrolled patients who received ≥1 year of continuous miglustat therapy (for ≥90 % of the observation period, with no single treatment interruption >28 days) were included in this analysis. Disability was measured using a scale rating the four domains, ambulation, manipulation, language and swallowing from 0 (normal) to 1 (worst). Neurological disease progression was analysed in all patients based on: 1) annual progression rates between enrolment and last follow up, and; 2) categorical analysis with patients categorised as 'improved/stable' if ≥3/4 domain scores were lower/unchanged, and as 'progressed' if

Published
2015

19. Clinical experience suggests that modafinil is an effective and safe treatment for paediatric narcolepsy

Author

Lecendreux, M., Bruni, O., Franco, P., Gringras, P., Konofal, E., Nevsimalova, S., Paiva, T., Partinen, M., Peeters, E., Peraita-Adrados, R., Plazzi, G., Poli, F., Lecendreux M., Bruni O., Franco P., Gringras P., Konofal E., Nevsimalova S., Paiva T., Partinen M., Peeters E., Peraita-Adrados R., Plazzi G., and Poli F.

Subjects
Male, Adolescent, CHILDREN, CATAPLEXY, CHILDHOOD, Modafinil, Child, Preschool, Humans, Central Nervous System Stimulants, Female, Benzhydryl Compounds, Child, Narcolepsy
Abstract

N.A.

Published
2012

20. De novo mutations in ATP1A3 cause alternating hemiplegia of childhood

Author

Heinzen EL, Swoboda KJ, Hitomi Y, Gurrieri F, Nicole S, de Vries B, Tiziano FD, Fontaine B, Walley NM, Heavin S, Panagiotakaki E, European Alternating Hemiplegia of Childhood Genetics Consortium, Neri G, Koelewijn S, Kamphorst J, Geilenkirchen M, Pelzer N, Laan L, Haan J, Ferrari M, van den Maagdenberg A, Biobanca e. Registro Clinico per l'Emiplegia Alternante Consortium, Zucca C, Bassi MT, Franchini F, Vavassori R, Giannotta M, Gobbi G, Granata T, Nardocci N, De Grandis E, Veneselli E, Stagnaro M, Vigevano F, European Network for Research on Alternating Hemiplegia for Small, Medium sized Enterpriese Consortium, Oechsler C, Arzimanoglou A, Ninan M, Neville B, Ebinger F, Fons C, Campistol J, Kemlink D, Nevsimalova S, Peeters Scholte C, Casaer P, Sange G, Spiel G, Martinelli Boneschi F, Schyns T, Crawley F, Poncelin D, Fiori S, Abiusi E, Di Pietro L, Sweney MT, Newcomb TM, Viollet L, Huff C, Jorde LB, Reyna SP, Murphy KJ, Shianna KV, Gumbs CE, Little L, Silver K, Ptáček LJ, Ferrari MD, Bye AM, Herkes GK, Whitelaw CM, Webb D, Lynch BJ, Uldall P, King MD, Scheffer IE, van den Maagdenberg AM, Sisodiya SM, Mikati MA, Goldstein D.B., CASARI , GIORGIO NEVIO, Heinzen, El, Swoboda, Kj, Hitomi, Y, Gurrieri, F, Nicole, S, de Vries, B, Tiziano, Fd, Fontaine, B, Walley, Nm, Heavin, S, Panagiotakaki, E, European Alternating Hemiplegia of Childhood Genetics, Consortium, Neri, G, Koelewijn, S, Kamphorst, J, Geilenkirchen, M, Pelzer, N, Laan, L, Haan, J, Ferrari, M, van den Maagdenberg, A, Biobanca e., Registro Clinico per l'Emiplegia Alternante Consortium, Zucca, C, Bassi, Mt, Franchini, F, Vavassori, R, Giannotta, M, Gobbi, G, Granata, T, Nardocci, N, De Grandis, E, Veneselli, E, Stagnaro, M, Vigevano, F, European Network for Research on Alternating Hemiplegia for, Small, Medium sized Enterpriese, Consortium, Oechsler, C, Arzimanoglou, A, Ninan, M, Neville, B, Ebinger, F, Fons, C, Campistol, J, Kemlink, D, Nevsimalova, S, Peeters Scholte, C, Casaer, P, Casari, GIORGIO NEVIO, Sange, G, Spiel, G, Martinelli Boneschi, F, Schyns, T, Crawley, F, Poncelin, D, Fiori, S, Abiusi, E, Di Pietro, L, Sweney, Mt, Newcomb, Tm, Viollet, L, Huff, C, Jorde, Lb, Reyna, Sp, Murphy, Kj, Shianna, Kv, Gumbs, Ce, Little, L, Silver, K, Ptáček, Lj, Ferrari, Md, Bye, Am, Herkes, Gk, Whitelaw, Cm, Webb, D, Lynch, Bj, Uldall, P, King, Md, Scheffer, Ie, van den Maagdenberg, Am, Sisodiya, Sm, Mikati, Ma, and Goldstein, D. B.

Subjects
Nonsynonymous substitution, Genetics, 0303 health sciences, Mutation, Alternating hemiplegia of childhood, Neurological disorder, Biology, Settore MED/03 - GENETICA MEDICA, medicine.disease, medicine.disease_cause, Alternating Hemiplegia, Article, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, ATP1A3, medicine, Etiology, 030217 neurology & neurosurgery, Alternating hemiplegia, Exome sequencing, 030304 developmental biology
Abstract

Alternating hemiplegia of childhood (AHC) is a rare, severe neurodevelopmental syndrome characterized by recurrent hemiplegic episodes and distinct neurological manifestations. AHC is usually a sporadic disorder and has unknown etiology. We used exome sequencing of seven patients with AHC and their unaffected parents to identify de novo nonsynonymous mutations in ATP1A3 in all seven individuals. In a subsequent sequence analysis of ATP1A3 in 98 other patients with AHC, we found that ATP1A3 mutations were likely to be responsible for at least 74% of the cases; we also identified one inherited mutation in a case of familial AHC. Notably, most AHC cases are caused by one of seven recurrent ATP1A3 mutations, one of which was observed in 36 patients. Unlike ATP1A3 mutations that cause rapid-onset dystonia-parkinsonism, AHC-causing mutations in this gene caused consistent reductions in ATPase activity without affecting the level of protein expression. This work identifies de novo ATP1A3 mutations as the primary cause of AHC and offers insight into disease pathophysiology by expanding the spectrum of phenotypes associated with mutations in ATP1A3.

Published
2012

23. Clinical profile of patients with ATP1A3 mutations in Alternating Hemiplegia of Childhood-a study of 155 patients

Author

Panagiotakaki, E, De Grandis, E, Stagnaro, M, Heinzen, EL, Fons, C, Sisodiya, S, de Vries, B, Goubau, C, Weckhuysen, S, Kemlink, D, Scheffer, I, Lesca, G, Rabilloud, M, Klich, A, Ramirez-Camacho, A, Ulate-Campos, A, Campistol, J, Giannotta, M, Moutard, M-L, Doummar, D, Hubsch-Bonneaud, C, Jaffer, F, Cross, H, Gurrieri, F, Tiziano, D, Nevsimalova, S, Nicole, S, Neville, B, van den Maagdenberg, AMJM, Mikati, M, Goldstein, DB, Vavassori, R, Arzimanoglou, A, Panagiotakaki, E, De Grandis, E, Stagnaro, M, Heinzen, EL, Fons, C, Sisodiya, S, de Vries, B, Goubau, C, Weckhuysen, S, Kemlink, D, Scheffer, I, Lesca, G, Rabilloud, M, Klich, A, Ramirez-Camacho, A, Ulate-Campos, A, Campistol, J, Giannotta, M, Moutard, M-L, Doummar, D, Hubsch-Bonneaud, C, Jaffer, F, Cross, H, Gurrieri, F, Tiziano, D, Nevsimalova, S, Nicole, S, Neville, B, van den Maagdenberg, AMJM, Mikati, M, Goldstein, DB, Vavassori, R, and Arzimanoglou, A

Abstract

BACKGROUND: Mutations in the gene ATP1A3 have recently been identified to be prevalent in patients with alternating hemiplegia of childhood (AHC2). Based on a large series of patients with AHC, we set out to identify the spectrum of different mutations within the ATP1A3 gene and further establish any correlation with phenotype. METHODS: Clinical data from an international cohort of 155 AHC patients (84 females, 71 males; between 3 months and 52 years) were gathered using a specifically formulated questionnaire and analysed relative to the mutational ATP1A3 gene data for each patient. RESULTS: In total, 34 different ATP1A3 mutations were detected in 85 % (132/155) patients, seven of which were novel. In general, mutations were found to cluster into five different regions. The most frequent mutations included: p.Asp801Asn (43 %; 57/132), p.Glu815Lys (16 %; 22/132), and p.Gly947Arg (11 %; 15/132). Of these, p.Glu815Lys was associated with a severe phenotype, with more severe intellectual and motor disability. p.Asp801Asn appeared to confer a milder phenotypic expression, and p.Gly947Arg appeared to correlate with the most favourable prognosis, compared to the other two frequent mutations. Overall, the comparison of the clinical profiles suggested a gradient of severity between the three major mutations with differences in intellectual (p = 0.029) and motor (p = 0.039) disabilities being statistically significant. For patients with epilepsy, age at onset of seizures was earlier for patients with either p.Glu815Lys or p.Gly947Arg mutation, compared to those with p.Asp801Asn mutation (p < 0.001). With regards to the five mutation clusters, some clusters appeared to correlate with certain clinical phenotypes. No statistically significant clinical correlations were found between patients with and without ATP1A3 mutations. CONCLUSIONS: Our results, demonstrate a highly variable clinical phenotype in patients with AHC2 that correlates with certain mutations and possibly clust

Published
2015

24. Clinical profile of patients with ATP1A3 mutations in Alternating Hemiplegia of Childhood-a study of 155 patients.

Author

Gurrieri, Fiorella, Panagiotakaki, E, De Grandis, E, Stagnaro, M, Heinzen, El, Fons, C, Sisodiya, S, Tiziano, Francesco Danilo, Nicole, Nevsimalova, S, Neville, B, Van Den Maagdenberg, Am, Mikati, M, Goldstein, D., Gurrieri, Fiorella (ORCID:0000-0002-6775-5972), Tiziano, Francesco Danilo (ORCID:0000-0002-5545-6158), Gurrieri, Fiorella, Panagiotakaki, E, De Grandis, E, Stagnaro, M, Heinzen, El, Fons, C, Sisodiya, S, Tiziano, Francesco Danilo, Nicole, Nevsimalova, S, Neville, B, Van Den Maagdenberg, Am, Mikati, M, Goldstein, D., Gurrieri, Fiorella (ORCID:0000-0002-6775-5972), and Tiziano, Francesco Danilo (ORCID:0000-0002-5545-6158)

Abstract

BACKGROUND: Mutations in the gene ATP1A3 have recently been identified to be prevalent in patients with alternating hemiplegia of childhood (AHC2). Based on a large series of patients with AHC, we set out to identify the spectrum of different mutations within the ATP1A3 gene and further establish any correlation with phenotype. METHODS: Clinical data from an international cohort of 155 AHC patients (84 females, 71 males; between 3 months and 52 years) were gathered using a specifically formulated questionnaire and analysed relative to the mutational ATP1A3 gene data for each patient. RESULTS: In total, 34 different ATP1A3 mutations were detected in 85 % (132/155) patients, seven of which were novel. In general, mutations were found to cluster into five different regions. The most frequent mutations included: p.Asp801Asn (43 %; 57/132), p.Glu815Lys (16 %; 22/132), and p.Gly947Arg (11 %; 15/132). Of these, p.Glu815Lys was associated with a severe phenotype, with more severe intellectual and motor disability. p.Asp801Asn appeared to confer a milder phenotypic expression, and p.Gly947Arg appeared to correlate with the most favourable prognosis, compared to the other two frequent mutations. Overall, the comparison of the clinical profiles suggested a gradient of severity between the three major mutations with differences in intellectual (p = 0.029) and motor (p = 0.039) disabilities being statistically significant. For patients with epilepsy, age at onset of seizures was earlier for patients with either p.Glu815Lys or p.Gly947Arg mutation, compared to those with p.Asp801Asn mutation (p < 0.001). With regards to the five mutation clusters, some clusters appeared to correlate with certain clinical phenotypes. No statistically significant clinical correlations were found between patients with and without ATP1A3 mutations. CONCLUSIONS: Our results, demonstrate a highly variable clinical phenotype in patients with AHC2 that correlates with certain mutations and possibly clust

Published
2015

25. Erratum: Common variants in P2RY11 are associated with narcolepsy (Nature Genetics (2011) 43 (66-71))

Author

Kornum, B. R., Kawashima, M., Faraco, J., Lin, L., Rico, T. J., Hesselson, S., Axtell, R. C., Kuipers, H., Weiner, K., Hamacher, A., Kassack, M. U., Han, F., Knudsen, S., Li, J., Dong, X., Winkelmann, J., Plazzi, G., Nevsimalova, S., Hong, S. -C., Honda, Y., Honda, M., Hogl, B., Ton, T. G. N., Montplaisir, J., Bourgin, P., Kemlink, D., Huang, Y. -S., Warby, S., Einen, M., Eshragh, J. L., Miyagawa, T., Desautels, A., Ruppert, E., Hesla, P. E., Poli, F., Pizza, F., Frauscher, B., Jeong, J. -H., Lee, S. -P., Strohl, K. P., Longstreth, W. T., Kvale, M., Dobrovolna, M., Ohayon, M. M., Nepom, G. T., Wichmann, H. -E., Rouleau, G. A., Gieger, C., Levinson, D. F., Gejman, P. V., Meitinger, T., Peppard, P., Young, T., Jennum, P., Steinman, L., Tokunaga, K., Kwok, P. -Y., Risch, N., Hallmayer, J., and Mignot, E.

Published
2011

28. Erratum: Narcolepsy is strongly associated with the T-cell receptor alpha locus (Nature Genetics (2009) 41 (708-711))

Author

Hallmayer, J., Faraco, J., Lin, L., Hesselson, S., Winkelmann, J., Kawashima, M., Mayer, G., Plazzi, G., Nevsimalova, S., Bourgin, P., Hong, S. S. -C., Honda, Y., Honda, M., Hogl, B., Longstreth, W. T., Montplaisir, J., Kemlink, D., Einen, M., Chen, J., Musone, S. L., Akana, M., Miyagawa, T., Duan, J., Desautels, A., Erhardt, C., Hesla, P. E., Poli, F., Frauscher, B., Jeong, J. -H., Lee, S. -P., Ton, T. G. N., Kvale, M., Kolesar, L., Dobrovolna, M., Nepom, G. T., Salomon, D., Wichmann, H. -E., Rouleau, G. A., Gieger, C., Levinson, D. F., Gejman, P. V., Meitinger, T., Young, T., Peppard, P., Tokunaga, K., Kwok, P. -Y., Risch, N., and Mignot, E.

Published
2009

31. ImmunoChip Study Implicates Antigen Presentation to T Cells in Narcolepsy

Author

Faraco, J., Lin, L., Kornum, B.R., Kenny, E.E., Trynka, G., Einen, M., Rico, T.J., Lichtner, P., Dauvilliers, Y., Arnulf, I., Lecendreux, M., Javidi, S., Geisler, P., Mayer, G., Pizza, F., Poli, F., Plazzi, G., Overeem, S., Lammers, G.J., Kemlink, D., Sonka, K., Nevsimalova, S., Rouleau, G., Desautels, A., Montplaisir, J., Frauscher, B., Ehrmann, L., Hogl, B., Jennum, P., Bourgin, P., Peraita-Adrados, R., Iranzo, A., Bassetti, C., Chen, W.M., Concannon, P., Thompson, S.D., Damotte, V., Fontaine, B., Breban, M., Gieger, C., Klopp, N., Deloukas, P., Wijmenga, C., Hallmayer, J., Onengut-Gumuscu, S., Rich, S.S., Winkelmann, J., Mignot, E., Faraco, J., Lin, L., Kornum, B.R., Kenny, E.E., Trynka, G., Einen, M., Rico, T.J., Lichtner, P., Dauvilliers, Y., Arnulf, I., Lecendreux, M., Javidi, S., Geisler, P., Mayer, G., Pizza, F., Poli, F., Plazzi, G., Overeem, S., Lammers, G.J., Kemlink, D., Sonka, K., Nevsimalova, S., Rouleau, G., Desautels, A., Montplaisir, J., Frauscher, B., Ehrmann, L., Hogl, B., Jennum, P., Bourgin, P., Peraita-Adrados, R., Iranzo, A., Bassetti, C., Chen, W.M., Concannon, P., Thompson, S.D., Damotte, V., Fontaine, B., Breban, M., Gieger, C., Klopp, N., Deloukas, P., Wijmenga, C., Hallmayer, J., Onengut-Gumuscu, S., Rich, S.S., Winkelmann, J., and Mignot, E.

Abstract

Contains fulltext : 118596.pdf (publisher's version ) (Open Access), Recent advances in the identification of susceptibility genes and environmental exposures provide broad support for a post-infectious autoimmune basis for narcolepsy/hypocretin (orexin) deficiency. We genotyped loci associated with other autoimmune and inflammatory diseases in 1,886 individuals with hypocretin-deficient narcolepsy and 10,421 controls, all of European ancestry, using a custom genotyping array (ImmunoChip). Three loci located outside the Human Leukocyte Antigen (HLA) region on chromosome 6 were significantly associated with disease risk. In addition to a strong signal in the T cell receptor alpha (TRA@), variants in two additional narcolepsy loci, Cathepsin H () and Tumor necrosis factor (ligand) superfamily member 4 (, also called ), attained genome-wide significance. These findings underline the importance of antigen presentation by HLA Class II to T cells in the pathophysiology of this autoimmune disease.

Published
2013

36. CSF hypocretin/orexin levels in narcolepsy and other neurological conditions

Author

Ripley, B, Overeem, S, Fujiki, N, Nevsimalova, S, Uchino, M, Yesavage, J, Di Monte, D, Dohi, K, Melberg, Atle, Lammers, G J, Nishida , Y, Roelandse, FWC, Hungs, M, Mignot, E, Nishino, S, Ripley, B, Overeem, S, Fujiki, N, Nevsimalova, S, Uchino, M, Yesavage, J, Di Monte, D, Dohi, K, Melberg, Atle, Lammers, G J, Nishida , Y, Roelandse, FWC, Hungs, M, Mignot, E, and Nishino, S

Published
2001

40. NREM sleep alterations in narcolepsy/cataplexy

Author

FERRI, R, primary, MIANO, S, additional, BRUNI, O, additional, VANKOVA, J, additional, NEVSIMALOVA, S, additional, VANDI, S, additional, MONTAGNA, P, additional, FERINISTRAMBI, L, additional, and PLAZZI, G, additional

Published
2005
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44. CSF hypocretin/orexin levels in narcolepsy and other neurological conditions

Author

Ripley, B., primary, Overeem, S., additional, Fujiki, N., additional, Nevsimalova, S., additional, Uchino, M., additional, Yesavage, J., additional, Di Monte, D., additional, Dohi, K., additional, Melberg, A., additional, Lammers, G. J., additional, Nishida, Y., additional, Roelandse, F. W.C., additional, Hungs, M., additional, Mignot, E., additional, and Nishino, S., additional

Published
2001
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