Huppke, Brenda

[["dc.bibliographiccitation.firstpage","92"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Blood Purification"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Koziolek, Michael J."],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Sigler, Matthias"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Mühlhausen, Johannes"],["dc.date.accessioned","2017-09-07T11:48:19Z"],["dc.date.available","2017-09-07T11:48:19Z"],["dc.date.issued","2013"],["dc.description.abstract","Background/Aims: In adults, plasma exchange (PE) has been shown to be an efficient treatment for severe relapses of acute inflammatory CNS demyelinating diseases. The aim of this study was to evaluate the safety and efficacy of this treatment in pediatric patients. Methods: We retrospectively analyzed a single-center cohort of pediatric patients with inflammatory CNS demyelinating disorders who underwent apheresis between 2007 and 2011. Results: Ten patients (mean age: 11.6 +/- 3.4 years) with an acute relapse of multiple sclerosis (n = 5), neuromyelitis optica (n = 2) or acute disseminated encephalomyelitis were included. All received methylprednisolone prior to treatment with either PE (n = 5) or immunoadsorption (n = 5). Apheresis-related side effects were either self-limiting or easily managed. EDSS (Expanded Disability Status Scale) improved in 7 of 8 patients during apheresis and in all patients within 30 days from a median of 7.5 to 1 (p < 0.01). The visual acuity initially worsened during the procedure in 3 of 7 affected eyes (mean 0.09), but improved in all at follow-up (mean: 0.5; p = 0.008). Conclusions: Apheresis was well tolerated and associated with a favorable outcome in all pediatric patients similar to reports in adults. Copyright (C) 2013 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000354077"],["dc.identifier.gro","3142409"],["dc.identifier.isi","000328188600005"],["dc.identifier.pmid","24021839"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10815"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7963"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9735"],["dc.relation.issn","0253-5068"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Therapeutic Apheresis in Pediatric Patients with Acute CNS Inflammatory Demyelinating Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Toxicology"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Kilian, Adrienne"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Groeneveld, Annette"],["dc.contributor.author","Schaper, Andreas"],["dc.date.accessioned","2018-11-07T10:20:30Z"],["dc.date.available","2018-11-07T10:20:30Z"],["dc.date.issued","2016"],["dc.format.extent","381"],["dc.identifier.isi","000374999800032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41905"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.publisher.place","Abingdon"],["dc.relation.issn","1556-9519"],["dc.relation.issn","1556-3650"],["dc.title","Phenethylamines - they have known, but have they loved? Mass intoxication with 2C-E in northern Germany"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1740"],["dc.bibliographiccitation.issue","75"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1744"],["dc.contributor.author","Huppke, P."],["dc.contributor.author","Blüthner, Rosa M."],["dc.contributor.author","Bauer, O."],["dc.contributor.author","Stark, W,"],["dc.contributor.author","Reinhardt, K."],["dc.contributor.author","Huppke, B."],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2019-07-10T08:13:35Z"],["dc.date.available","2019-07-10T08:13:35Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: Neuromyelitis optica (NMO) is currently considered a severe relapsing CNS demyelinating disorder that is associated with aquaporin-4 immunoglobulin G (NMO-IgG) while in earlier reports of NMO in childhood it has been described as a benign and monophasic disorder. This study was performed to analyze the prevalence and the clinical course of NMO in a European pediatric cohort of patients with demyelinating CNS disorders. Methods: A cohort study was performed evaluating 118 pediatric patients presenting at the Center for Multiple Sclerosis in Childhood and Adolescents, Go¨ttingen, Germany, with demyelinating CNS disorders between 2000 and 2009. In all patients, NMO-IgG status was determined. Results: The majority of patients (94%) were diagnosed with remitting recurrent multiple sclerosis. Six patients fulfilled the clinical criteria for NMO but only 1 was seropositive for NMO-IgG. This patient had a severe relapsing course in contrast to the seronegative patients who showed a mild and in the majority of cases monophasic course. Conclusions: The diagnostic criteria clearly distinguished the patients with NMO from patients with other demyelinating CNS disorders. In the European pediatric population, NMO is very rare and in the majority of patients not associated with NMO-IgG. These seronegative cases have a benign and predominantly monophasic course and therefore do not need the immunosuppressant therapy that is recommended for NMO in the recent literature."],["dc.identifier.fs","576516"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6319"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61280"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Neuromyelitis optica and NMO-IgG in European pediatric patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","818"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Weissbach, Susann"],["dc.contributor.author","Church, Joseph A."],["dc.contributor.author","Schnur, Rhonda"],["dc.contributor.author","Krusen, Martina"],["dc.contributor.author","Dreha-Kulaczewski, Steffi"],["dc.contributor.author","Kühn-Velten, W. Nikolaus"],["dc.contributor.author","Wolf, Annika"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Millan, Francisca"],["dc.contributor.author","Begtrup, Amber"],["dc.contributor.author","Almusafri, Fatima"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2018-04-23T11:47:26Z"],["dc.date.available","2018-04-23T11:47:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Transcription factor NRF2, encoded by NFE2L2, is the master regulator of defense against stress in mammalian cells. Somatic mutations of NFE2L2 leading to NRF2 accumulation promote cell survival and drug resistance in cancer cells. Here we show that the same mutations as inborn de novo mutations cause an early onset multisystem disorder with failure to thrive, immunodeficiency and neurological symptoms. NRF2 accumulation leads to widespread misregulation of gene expression and an imbalance in cytosolic redox balance. The unique combination of white matter lesions, hypohomocysteinaemia and increased G-6-P-dehydrogenase activity will facilitate early diagnosis and therapeutic intervention of this novel disorder."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1038/s41467-017-00932-7"],["dc.identifier.gro","3142218"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14817"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13340"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Activating de novo mutations in NFE2L2 encoding NRF2 cause a multisystem disorder"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","382"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Multiple Sclerosis"],["dc.bibliographiccitation.lastpage","387"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Hummel, Hannah-Maria"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stark, Wiebke"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Because of the emergence of novel therapies for multiple sclerosis (MS) and the associated increased risk of progressive multifocal leukoencephalopathy, John Cunningham (JC) virus infection has become a focus of interest for neurologists. However, little is known about JC virus infection in pediatric MS to date. Objective: We aimed to analyze the prevalence of anti-JC virus antibodies, the conversion rate and the influence of the anti-JC virus antibody status on the clinical course in a large pediatric MS cohort. Methods: Anti-JC virus antibodies were analyzed in serum samples within six months of disease onset and during the course of the disease. Clinical data were extracted from a pediatric MS databank. Results: A total of 51.6% of 256 patients were found to be positive for anti-JC virus antibodies at onset of disease. No correlation between antibody status and clinical course was seen. Analyzing 693 follow-up serum samples revealed high titer stability, and an annual conversion rate of 4.37% was seen. Conclusion: No evidence was found that seropositivity for anti-JC virus antibodies influences the clinical course. Surprisingly, seroprevalence for anti-JC virus antibodies was more than twice as high as anticipated in this age group, raising the question of whether the infection increases the risk of MS development."],["dc.identifier.doi","10.1177/1352458514543340"],["dc.identifier.gro","3141931"],["dc.identifier.isi","000352165000006"],["dc.identifier.pmid","25070674"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2668"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","JC virus antibody status in a pediatric multiple sclerosis cohort: Prevalence, conversion rate and influence on disease severity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","232"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Pediatric Neurology"],["dc.bibliographiccitation.lastpage","234"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Heise, Alexander"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:46:52Z"],["dc.date.available","2017-09-07T11:46:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Idiopathic hypothalamic dysfunction is a rare disorder presenting at age 3-7 years. Severe hypothalamic and brainstem dysfunction leads to death in 25% of patients. The disease is presumed to be autoimmune, or in some cases paraneoplastic. No successful treatment has been reported. Patient V. developed hyperphagia, hypersomnia, and extreme aggression at age 7 years, accompanied by episodes of hyperthermia, hypothermia, sinus bradycardia, hypernatremia, hyponatremia, persistent hyperprolactinemia, hypothyroidism, and growth-hormone deficiency. At age 9 years, a diagnosis of idiopathic hypothalamic dysfunction was rendered, and immunoglobulin therapy was commenced. Nine courses of immunoglobulins, at a dose of 2 g/kg every 4 weeks, were administered. Reproducible improvements in behavior and no further episodes of hyponatremia or hypernatremia and sinus bradycardia were evident. The endocrinologic abnormalities and poor thermoregulation remained. Administration of immunoglobulins during late stages of idiopathic hypothalamic dysfunction led to improvement in some but not all signs. Assuming an autoimmune basis for this disorder, treatment during early stages of disease should be more effective. To facilitate such early treatment, increased awareness of this disorder is necessary, to allow for early diagnosis. (C) 2009 by Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.pediatrneurol.2009.03.017"],["dc.identifier.gro","3143067"],["dc.identifier.isi","000268866200018"],["dc.identifier.pmid","19664546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/540"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0887-8994"],["dc.title","Immunoglobulin Therapy in Idiopathic Hypothalamic Dysfunction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1655"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Archives of Neurology"],["dc.bibliographiccitation.lastpage","1658"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Stark, Wiebke"],["dc.contributor.author","Zuercher, Claudia"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:48:08Z"],["dc.date.available","2017-09-07T11:48:08Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Natalizumab, a humanized monoclonal antibody raised against alpha(4) integrins, is approved for treatment of active relapsing-remitting multiple sclerosis (RRMS) in adult patients. Objective: To determine the safety, effectiveness, and tolerability of natalizumab use in pediatric patients with MS. Design: Case report. Setting: Center for MS in childhood and adolescents, Gottingen, Germany. Patients: Three pediatric patients with RRMS having a poor response to other immunomodulatory therapies or having intolerable adverse effects. Interventions: Natalizumab given every 4 weeks at a dosage of 3 to 5 mg/kg of body weight. Main Outcome Measures: Cranial magnetic resonance (MR) imaging before treatment and every 6 months thereafter. Results: During 24, 16, and 15 months of treatment, no further relapses occurred in the 3 pediatric patients; all reported significant improvement in their quality of life. Follow-up MR imaging showed no new T2-weighted lesions or gadolinium-enhancing lesions. No adverse events were seen when dosage was adjusted to body weight. Conclusions: Natalizumab treatment was effective and well tolerated in our pediatric patients with RRMS who did not respond to initial immunomodulatory treatments. Therefore, it is a promising second-line therapy for pediatric patients with RRMS."],["dc.identifier.doi","10.1001/archneur.65.12.1655"],["dc.identifier.gro","3143197"],["dc.identifier.isi","000261483100015"],["dc.identifier.pmid","19064754"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/685"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Natalizumab Use in Pediatric Multiple Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","135245851773284"],["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Hummel, Hannah"],["dc.contributor.author","Stark, Wiebke"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2018-04-23T11:47:25Z"],["dc.date.available","2018-04-23T11:47:25Z"],["dc.date.issued","2019-01"],["dc.description.abstract","Objective: Study aims were to determine the frequency of highly active disease in pediatric multiple sclerosis (MS), the response to natalizumab (NTZ) and fingolimod (FTY) treatment, and the impact of current treatment modalities on the clinical course. Methods: Retrospective single-center study in the German Center for MS in Childhood and Adolescence. Results: Of 144 patients with first MS manifestation between 2011 and 2015, 41.6% fulfilled the criteria for highly active MS. In total, 55 patients treated with NTZ and 23 with FTY demonstrated a significant reduction in relapse rate (NTZ: 95.2%, FTY: 75%), new T2 lesions (NTZ: 97%, FTY: 81%), and contrast-enhancing lesions (NTZ: 97%, FTY: 93%). However, seven patients switched from NTZ to FTY experienced an increase in disease activity. Comparing pediatric MS patients treated in 2005 with those treated in 2015 showed a 46% reduction in relapse rate and a 44% reduction in mean Expanded Disability Status Scale (EDSS). Conclusion: The rate of highly active disease among pediatric MS patients is high; more than 40% in our cohort. Response to NTZ and FTY treatment is similar if not better than observed in adults. Current treatment modalities including earlier treatment initiation and the introduction of NTZ and FTY have significantly improved the clinical course of pediatric MS."],["dc.identifier.doi","10.1177/1352458517732843"],["dc.identifier.gro","3142216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13338"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.publisher","SAGE Publications"],["dc.relation.eissn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Therapy of highly active pediatric multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","941"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Multiple Sclerosis"],["dc.bibliographiccitation.lastpage","946"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Karenfort, Michael"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Seidl, Rainer"],["dc.contributor.author","Leiz, Steffen"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:47:41Z"],["dc.date.available","2017-09-07T11:47:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Some pediatric patients with inflammatory demyelinating central nervous system disorders cannot be classified under any of the established disease entities, making their treatment and prognosis difficult. Objective: The objective of this study is to characterize a subgroup of pediatric patients with recurrent demyelinating central nervous system disorders. Methods: This study includes a case series of pediatric patients with monophasic or recurrent acute disseminated encephalomyelitis (ADEM) who later presented with either monophasic or recurrent optic neuritis (ON). Results: We describe seven patients with a median follow-up of six years (five females, two males) who presented at a median age of 6 years (range 4-8 years) with monophasic (n = 4) or recurrent ADEM (two to four attacks) followed by monophasic (n = 3) or recurrent ON (two to nine attacks). Cranial magnetic resonance imaging (MRI) was typical for ADEM (n = 6) with complete or almost complete resolution of lesions on follow-up. Cerebrospinal (CSF) studies at the time of ADEM showed a pleocytosis in six patients and were negative for oligoclonal bands (OCBs) in all. In all patients high titers for serum anti-MOG antibodies were detected. Conclusion: ADEM followed by ON is a rare but distinct clinical phenotype among pediatric patients. Further studies are needed to allow recommendations on treatment or prognosis."],["dc.identifier.doi","10.1177/1352458512466317"],["dc.identifier.gro","3142346"],["dc.identifier.isi","000319567900018"],["dc.identifier.pmid","23128668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7264"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Acute disseminated encephalomyelitis followed by recurrent or monophasic optic neuritis in pediatric patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1157"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","JAMA Neurology"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Hummel, Hannah-Maria"],["dc.contributor.author","Stark, Wiebke"],["dc.contributor.author","Röbl, Markus"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Huppke, Peter"],["dc.date.accessioned","2020-04-02T09:57:28Z"],["dc.date.available","2020-04-02T09:57:28Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1001/jamaneurol.2019.1997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63492"],["dc.relation.issn","2168-6149"],["dc.title","Association of Obesity With Multiple Sclerosis Risk and Response to First-line Disease Modifying Drugs in Children"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]