Brockmann, Knut

[["dc.bibliographiccitation.firstpage","268"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuropediatrics"],["dc.bibliographiccitation.lastpage","271"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Shoukier, Moneef"],["dc.contributor.author","Fuchs, Sigrid"],["dc.contributor.author","Schwaibold, Eva"],["dc.contributor.author","Lingen, Michael"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Zirn, Birgit"],["dc.date.accessioned","2017-09-07T11:47:08Z"],["dc.date.available","2017-09-07T11:47:08Z"],["dc.date.issued","2013"],["dc.description.abstract","Terminal deletions of chromosome 3p26.3 confined to the CHL1 gene have previously been described in children with intellectual disability and epilepsy. Here, we report for the first time, a 3p26.3 duplication including only the CHL1 gene in an intellectually disabled girl with epilepsy. The penetrance of both deletions and duplications in 3p26.3 is reduced because all chromosomal imbalances were inherited from healthy parents. Further studies are needed to specify the pathogenic mechanism of 3p26.3 imbalances and to estimate recurrence risks in genetic counseling. However, the description of both deletions and duplications of chromosome 3p26.3 in nonsyndromic intellectual disability suggests that CHL1 is a dosage-sensitive gene with an important role for normal cognitive development."],["dc.identifier.doi","10.1055/s-0033-1333874"],["dc.identifier.gro","3142278"],["dc.identifier.isi","000324755000006"],["dc.identifier.pmid","23436495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6509"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0174-304X"],["dc.title","Microduplication of 3p26.3 in Nonsyndromic Intellectual Disability Indicates an Important Role of CHL1 for Normal Cognitive Function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","143"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","156"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Namavar, Yasmin"],["dc.contributor.author","Barth, Peter G."],["dc.contributor.author","Kasher, Paul R."],["dc.contributor.author","van Ruissen, Fred"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Bernert, Guenther"],["dc.contributor.author","Writzl, Karin"],["dc.contributor.author","Ventura, Karen"],["dc.contributor.author","Cheng, Edith Y."],["dc.contributor.author","Ferriero, Donna M."],["dc.contributor.author","Basel-Vanagaite, Lina"],["dc.contributor.author","Eggens, Veerle R. C."],["dc.contributor.author","Kraegeloh-Mann, Ingeborg"],["dc.contributor.author","De Meirleir, Linda"],["dc.contributor.author","King, Mary"],["dc.contributor.author","Graham, John M., Jr."],["dc.contributor.author","von Moers, Arpad"],["dc.contributor.author","Knoers, Nine"],["dc.contributor.author","Sztriha, Laszlo K."],["dc.contributor.author","Korinthenberg, Rudolf"],["dc.contributor.author","Dobyns, William B."],["dc.contributor.author","Baas, Frank"],["dc.contributor.author","Poll-The, Bwee Tien"],["dc.date.accessioned","2018-11-07T09:00:54Z"],["dc.date.available","2018-11-07T09:00:54Z"],["dc.date.issued","2011"],["dc.description.abstract","Pontocerebellar hypoplasia is a group of autosomal recessive neurodegenerative disorders with prenatal onset. The common characteristics are cerebellar hypoplasia with variable atrophy of the cerebellum and the ventral pons. Supratentorial involvement is reflected by variable neocortical atrophy, ventriculomegaly and microcephaly. Mutations in the transfer RNA splicing endonuclease subunit genes (TSEN54, TSEN2, TSEN34) were found to be associated with pontocerebellar hypoplasia types 2 and 4. Mutations in the mitochondrial transfer RNA arginyl synthetase gene (RARS2) were associated with pontocerebellar hypoplasia type 6. We studied a cohort of 169 patients from 141 families for mutations in these genes, of whom 106 patients tested positive for mutations in one of the TSEN genes or the RARS2 gene. In order to delineate the neuroradiological and clinical phenotype of patients with mutations in these genes, we compared this group with 63 patients suspected of pontocerebellar hypoplasia who were negative on mutation analysis. We found a strong correlation (P < 0.0005) between TSEN54 mutations and a dragonfly-like cerebellar pattern on magnetic resonance imaging, in which the cerebellar hemispheres are flat and severely reduced in size and the vermis is relatively spared. Mutations in TSEN54 are clinically associated with dyskinesia and/or dystonia and variable degrees of spasticity, in some cases with pure generalized spasticity. Nonsense or splice site mutations in TSEN54 are associated with a more severe phenotype of more perinatal symptoms, ventilator dependency and early death. In addition, we present ten new mutations in TSEN54, TSEN2 and RARS2. Furthermore, we show that pontocerebellar hypoplasia type 1 together with elevated cerebrospinal fluid lactate may be caused by RARS2 mutations."],["dc.identifier.doi","10.1093/brain/awq287"],["dc.identifier.isi","000285625000014"],["dc.identifier.pmid","20952379"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24277"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical, neuroradiological and genetic findings in pontocerebellar hypoplasia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","10"],["dc.bibliographiccitation.journal","Molecular Cytogenetics"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Bruemmer, Verena"],["dc.contributor.author","Zoll, Barbara"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Boehm, Detlef"],["dc.contributor.author","Liehr, Thomas"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Wilichowski, Ekkehard"],["dc.contributor.author","Argyriou, Loukas"],["dc.contributor.author","Bartels, Iris"],["dc.date.accessioned","2018-11-07T08:35:08Z"],["dc.date.available","2018-11-07T08:35:08Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Submicroscopic imbalances in the subtelomeric regions of the chromosomes are considered to play an important role in the aetiology of mental retardation (MR). The aim of the study was to evaluate a quantitative PCR (qPCR) protocol established by Boehm et al. (2004) in the clinical routine of subtelomeric testing. Results: 296 patients with MR and a normal karyotype (500-550 bands) were screened for subtelomeric imbalances by using qPCR combined with SYBR green detection. In total, 17 patients (5.8%) with 20 subtelomeric imbalances were identified. Six of the aberrations (2%) were classified as causative for the symptoms, because they occurred either de novo in the patients (5 cases) or the aberration were be detected in the patient and an equally affected parent (1 case). The extent of the deletions ranged from 1.8 to approximately 10 Mb, duplications were 1.8 to approximately 5 Mb in size. In 6 patients, the copy number variations (CNVs) were rated as benign polymorphisms, and the clinical relevance of these CNVs remains unclear in 5 patients (1.7%). Therefore, the overall frequency of clinically relevant imbalances ranges between 2% and 3.7% in our cohort."],["dc.identifier.doi","10.1186/1755-8166-2-10"],["dc.identifier.isi","000208460900009"],["dc.identifier.pmid","19284615"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5765"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17987"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1755-8166"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Identification of subtelomeric genomic imbalances and breakpoint mapping with quantitative PCR in 296 individuals with congenital defects and/or mental retardation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","64"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Orphanet Journal of Rare Diseases"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Pacheu-Grau, David"],["dc.contributor.author","Catarino, Claudia B."],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Schittkowski, Michael Peter"],["dc.contributor.author","Wilichowski, Ekkehard"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2021-04-14T08:28:08Z"],["dc.date.available","2021-04-14T08:28:08Z"],["dc.date.issued","2021"],["dc.date.updated","2022-07-29T12:17:42Z"],["dc.description.abstract","Background Leber hereditary optic neuropathy (LHON) is the most common mitochondrial disorder and characterized by acute or subacute painless visual loss. Environmental factors reported to trigger visual loss in LHON mutation carriers include smoking, heavy intake of alcohol, raised intraocular pressure, and some drugs, including several carbonic anhydrase inhibitors. The antiepileptic drug sulthiame (STM) is effective especially in focal seizures, particularly in benign epilepsy of childhood with centrotemporal spikes, and widely used in pediatric epileptology. STM is a sulfonamide derivate and an inhibitor of mammalian carbonic anhydrase isoforms I–XIV. Results We describe two unrelated patients, an 8-year-old girl and an 11-year-old boy, with cryptogenic focal epilepsy, who suffered binocular (subject #1) or monocular (subject #2) visual loss in close temporal connection with starting antiepileptic pharmacotherapy with STM. In both subjects, visual loss was due to LHON. We used real-time respirometry in fibroblasts derived from LHON patients carrying the same mitochondrial mutations as our two subjects to investigate the effect of STM on oxidative phosphorylation. Oxygen consumption rate in fibroblasts from a healthy control was not impaired by STM compared with a vehicle control. In contrast, fibroblasts carrying the m.14484T>C or the m.3460G>A LHON mutation displayed a drastic reduction of the respiration rate when treated with STM compared to vehicle control. Conclusions Our observations point to a causal relationship between STM treatment and onset or worsening of visual failure in two subjects with LHON rather than pure coincidence. We conclude that antiepileptic medication with STM may pose a risk for visual loss in LHON mutation carriers and should be avoided in these patients."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.citation","Orphanet Journal of Rare Diseases. 2021 Feb 04;16(1):64"],["dc.identifier.doi","10.1186/s13023-021-01690-y"],["dc.identifier.pmid","33541401"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82509"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/219"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/102"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A06: Mitochondrienfunktion und -umsatz in Synapsen"],["dc.relation.eissn","1750-1172"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Sulthiame"],["dc.subject","Carbonic anhydrase inhibitor"],["dc.subject","Adverse effects"],["dc.subject","Leber hereditary optic neuropathy"],["dc.subject","LHON"],["dc.subject","Oxygen consumption rate"],["dc.title","Sulthiame impairs mitochondrial function in vitro and may trigger onset of visual loss in Leber hereditary optic neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","772"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Medical Genetics"],["dc.bibliographiccitation.lastpage","775"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Banne, Ehud"],["dc.contributor.author","Atawneh, Osama"],["dc.contributor.author","Henneke, Marco"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Elpeleg, Orly"],["dc.contributor.author","Edvardson, Simon"],["dc.date.accessioned","2017-09-07T11:47:04Z"],["dc.date.available","2017-09-07T11:47:04Z"],["dc.date.issued","2013"],["dc.description.abstract","West syndrome (WS) is an epileptic encephalopathy of childhood, defined by the presence of clustered spasms usually occurring before the age of 1year, hypsarrhythmia on EEG that is notoriously difficult to define, and developmental arrest or regression. The incidence of WS is 1:3200 live births with an aetiology-dependent prognosis. Up to 80% of children with symptomatic WS suffer from mental retardation, and approximately 50% develop Lennox-Gastaut syndrome. Using homozygosity mapping followed by exome sequencing, we identified a ADP-ribosylation factor (ARF) guanine nucleotide-exchange factor two (brefeldin A-inhibited) (ARFGEF2) mutation in five related infants with WS. ARFGEF2 is involved in the activation of ARFs by accelerating replacement of bound guanosine diphosphate (GDP) with Guanosine triphosphate (GTP), and is involved in Golgi transport. A mutation in ARFGEF2 has been previously described only once, causing microcephaly and periventricular heterotopia. Here, we describe a novel ARFGEF2 mutation in five related patients presenting with WS, microcephaly, periventricular heterotopia and thin corpus callosum."],["dc.identifier.doi","10.1136/jmedgenet-2013-101752"],["dc.identifier.gro","3142256"],["dc.identifier.isi","000328141400009"],["dc.identifier.pmid","23812912"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6265"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation [Ga354/9-1]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Bmj Publishing Group"],["dc.relation.eissn","1468-6244"],["dc.relation.issn","0022-2593"],["dc.title","West syndrome, microcephaly, grey matter heterotopia and hypoplasia of corpus callosum due to a novel ARFGEF2 mutation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","10"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Paediatric Neurology"],["dc.bibliographiccitation.lastpage","16"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Koehler, Karola"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Stettner, Georg M."],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:49:52Z"],["dc.date.available","2017-09-07T11:49:52Z"],["dc.date.issued","2007"],["dc.description.abstract","Introduction: Epilepsy is very frequent in Rett syndrome (RTT) patients and often difficult to treat. Because most cases of RTT are caused by mutations in the MECP2 gene it is reasonable to assume that convulsions are based on common pathogenetic mechanisms and thus should have a similar response to antiepileptic drugs. Purpose: To find the optimal treatment for epilepsy in RTT. Methods: We performed a retrospective study on 110 female patients with confirmed MECP2 mutations. Results: The median age was 10 years, 58% had a history of epilepsy and 55% received antiepileptic drugs (AEDs). Only sulthiame, carbamazepine and valproate were administered in an adequate frequency to allow statistical analysis. The best anticonvulsive results were seen in the RTT group that was treated with carbamazepine. Sulthiame was slightly less effective while valproate was significantly less effective. The rate of side effects was equivalent in all groups. In conclusion, carbamazepine should be recommended as first choice AED in RTT. If carbamazepine is not effective or not well tolerated sulthiame ought to be taken as second choice AED. (c) 2006 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ejpn.2006.09.003"],["dc.identifier.gro","3143557"],["dc.identifier.isi","000244178200002"],["dc.identifier.pmid","17178248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1084"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","1090-3798"],["dc.title","Treatment of epilepsy in Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","152"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","331"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Kretzschmar, Benedikt"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Pauli, Silke"],["dc.contributor.author","Schramm, Peter"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2018-11-07T09:21:15Z"],["dc.date.available","2018-11-07T09:21:15Z"],["dc.date.issued","2013"],["dc.description.abstract","Adult-onset Alexander disease (AOAD) is a rare leukoencephalopathy affecting predominantly the brainstem and cervical cord with insidious onset of clinical features. Acute onset is very rare and has yet been described only twice, to our knowledge. We report a 32-year-old hitherto healthy male who, after excessive consumption of alcohol, presented with stroke-like onset of symptoms including rigidospasticity, loss of consciousness, and bulbar dysfunction. MRI features comprised bilateral T2-hyperintensities of frontal white matter and basal ganglia as well as atrophy of medulla oblongata with a peculiar \"tadpole\" appearance, a pattern characteristic of AOAD. Mutation analysis of the GFAP gene revealed a heterozygous de novo 9-bp microduplication in exon 1. Adult Alexander disease may present with stroke-like features. MRI patterns of chronic neurodegenerative conditions may be recognizable even in acute neurological emergencies. (C) 2013 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2013.05.006"],["dc.identifier.isi","000322415000030"],["dc.identifier.pmid","23706596"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29072"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0022-510X"],["dc.title","Acute onset of adult Alexander disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","580"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Developmental Medicine & Child Neurology"],["dc.bibliographiccitation.lastpage","581"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2018-11-07T08:54:53Z"],["dc.date.available","2018-11-07T08:54:53Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1111/j.1469-8749.2011.03946.x"],["dc.identifier.isi","000291398700004"],["dc.identifier.pmid","21585366"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22775"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0012-1622"],["dc.title","Towards a more palatable treatment for Glut1 deficiency syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","48"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Gerstner, Thorsten"],["dc.contributor.author","Buesing, Deike"],["dc.contributor.author","Bell, Nellie"],["dc.contributor.author","Longin, Elke"],["dc.contributor.author","Kasper, Johannes-Martin"],["dc.contributor.author","Klostermann, Wolfgang"],["dc.contributor.author","Hebing, Burkhard"],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Eckel, Ulrich"],["dc.contributor.author","Hoffmann, Reiner"],["dc.contributor.author","Bettendorf, Ulrich"],["dc.contributor.author","Weidner, Birgit"],["dc.contributor.author","Wiemer-Kruel, Adelheid"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Neumann, Fritz-Wilhelm"],["dc.contributor.author","Sandrieser, Thorsten"],["dc.contributor.author","Wolff, Markus"],["dc.contributor.author","Koenig, Stephan"],["dc.date.accessioned","2018-11-07T11:06:51Z"],["dc.date.available","2018-11-07T11:06:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Background Acute pancreatitis is rarely seen in children, and, in contrast to cases in adults, it is often drug induced. One possible medication is the antiepileptic drug valproic acid (VPA), which is commonly prescribed for generalized and focal epilepsy, migraine, neuropathic pain, and bipolar disorder. The common side effects associated with VPA are typically benign, but less common but more serious adverse effects may occur. These include hepatotoxicity, hyperammonemic encephalopathy, coagulation disorders, and pancreatitis. Since 1979, a few cases of pancreatitis induced by VPA have been published in the medical literature. Methods We mailed a questionnaire to all members of the \"German Section of the International League against Epilepsy,\" asking about VPA-induced side effects. We also reviewed the medical literature for VPA-induced pancreatitis. Results Fifty-three publications (90 patients) published from 1979 to 2005 were found. Our survey in Germany, however, yielded 16 cases of pancreatitis from 1994 to 2003 whose original files we could study in detail. None of these patients had been published previously. Conclusion The difference between 90 patients reported worldwide from 1979 to 2005 and the 16 new documented cases from only Germany over 10 years corroborates that the occurrence of this severe side effect is under reported."],["dc.identifier.doi","10.1007/s00535-006-1961-4"],["dc.identifier.isi","000244483900005"],["dc.identifier.pmid","17322992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52417"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Tokyo"],["dc.relation.issn","0944-1174"],["dc.title","Valproic acid-induced pancreatitis: 16 new cases and a review of the literature"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","739"],["dc.bibliographiccitation.issue","9-10"],["dc.bibliographiccitation.journal","Neuromuscular Disorders"],["dc.bibliographiccitation.lastpage","740"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Zou, Y."],["dc.contributor.author","Zwolanek, D."],["dc.contributor.author","Hu, Y."],["dc.contributor.author","Schreiber, Gudrun"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Izu, Yayoi"],["dc.contributor.author","Tian, Z."],["dc.contributor.author","Devoto, Marcella"],["dc.contributor.author","Gandhy, S."],["dc.contributor.author","Meier, M."],["dc.contributor.author","Stetefeld, J."],["dc.contributor.author","Hicks, Pamela J."],["dc.contributor.author","Straub, Volker"],["dc.contributor.author","Voermans, N."],["dc.contributor.author","Birk, D. E."],["dc.contributor.author","Barton, E. R."],["dc.contributor.author","Koch, M."],["dc.contributor.author","Bönnemann, C. G."],["dc.date.accessioned","2018-11-07T09:19:35Z"],["dc.date.available","2018-11-07T09:19:35Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.nmd.2013.06.380"],["dc.identifier.isi","000324972500007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28674"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","CA"],["dc.title","Collagen type XII: A new congenital matrix and muscle disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]