Hunneman, Donald H.

[["dc.bibliographiccitation.firstpage","220"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","MEDICAL AND PEDIATRIC ONCOLOGY"],["dc.bibliographiccitation.lastpage","223"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Hero, Barbara"],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Gahr, M."],["dc.contributor.author","Berthold, F."],["dc.date.accessioned","2018-11-07T09:36:29Z"],["dc.date.available","2018-11-07T09:36:29Z"],["dc.date.issued","2001"],["dc.description.abstract","Background. The early biological response has been proved an excellent predictor in acute lymphoblastic leukemia and nephroblastoma. We asked whether catecholamine metabolites, mIBG scan, and bone marrow evaluation might be relevant response markers in disseminated neuroblastoma. Procedure. Three hundred sixty-seven unselected stage 4 neuroblastoma patients treated according the German cooperative trial NB90 were entered into the study. Catecholamine plasma and urine levels were centrally determined by gas chromatography/ mass spectrometry. Bone marrow cytology and mIBG scans were evaluated by local investigators. Results. Ar diagnosis, mIBG scan was positive in 306 patients (92%), borderline in seven patients (2%), and negative in 19 patients (6%). Bone marrow aspirates were cytologically positive in 292 patients (84%) and negative in 57 patients (16%). Plasma catecholamine levels were elevated in 79% (206 of 260 patients.), urinary levers in 92% (307 of 338 patients). The outcome of patients with normalized mIBG scan after four courses of chemotherapy [5 year EFS (event free survival) 0.22 +/- 0.071 was not superior to the outcome of patients with still abnormal uptake (5 year EFS 0.30 +/- 0.05). The event free survival of patients with still positive bone marrow aspirates after four courses (0.16 +/- 0.06) was inferior to the EFS of patients with negative bone marrow aspirates (0.26 +/- 0.04, P = 0.0054). Urinary catecholamine normalization after four cycles of chemotherapy (5 year EFS 0.35 +/- 0.06 Versus 0.26 +/- 0.10) had no influence on outcome, whereas plasma catecholamine normalization after the first (5 year EFS 0.40 +/- 0.09 versus 0.14 +/- 0.07, P = 0.0364) or the fourth cycle (5 year EFS 0.35 +/- 0.06 versus 0.26 +/- 0.10, P = 0.0242) indicated a better outcome. Conclusions. These data show that serial plasma catecholamine levels and bone marrow aspirates in the course of the disease are useful toots in predicting outcome. Med. Pediatr. Oncol. 36:220-223, 2001. (C) 2001 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/1096-911X(20010101)36:1<220::AID-MPO1053>3.0.CO;2-6"],["dc.identifier.isi","000166167300053"],["dc.identifier.pmid","11464889"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32629"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","New york"],["dc.relation.conference","Advances in Neuroblastoma Research Meeting"],["dc.relation.eventlocation","BATH, ENGLAND"],["dc.relation.issn","0098-1532"],["dc.title","Evaluation of catecholamine metabolites, mIBG scan, and bone marrow cytology as response markers in stage 4 neuroblastoma"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Bizzi, A."],["dc.contributor.author","Bugiani, M."],["dc.contributor.author","Salomons, G. S."],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Moroni, I."],["dc.contributor.author","Estienne, M."],["dc.contributor.author","Danesi, U."],["dc.contributor.author","Jakobsen, Jannik E."],["dc.contributor.author","Uziel, G."],["dc.date.accessioned","2018-11-07T10:11:34Z"],["dc.date.available","2018-11-07T10:11:34Z"],["dc.date.issued","2002"],["dc.description.abstract","Among creatine deficiency syndromes, an X-linked condition related to a defective creatine transport into the central nervous system has been described recently. Hallmarks of the disease are the absence of a creatine signal at brain spectroscopy, increased creatine levels in blood and urine, ineffectiveness of oral supplementation, and a mutation in the SLC6A8 (Online Mendelian Inheritance in Man [OMIM] 300036) creatine transporter gene. We report on a patient in whom a novel mutation (1221-1223delTTC) was identified."],["dc.identifier.doi","10.1002/ana.10246"],["dc.identifier.isi","177140000015"],["dc.identifier.pmid","12210795"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40074"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","X-linked creatine deficiency syndrome: A novel mutation in creatine transporter gene SLC6A8"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","475"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics"],["dc.bibliographiccitation.lastpage","478"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Heim, P."],["dc.contributor.author","Claussen, M."],["dc.contributor.author","Hoffmann, B."],["dc.contributor.author","Conzelmann, E."],["dc.contributor.author","Gärtner, J."],["dc.contributor.author","Harzer, K."],["dc.contributor.author","Hunneman, D. H."],["dc.contributor.author","Kohler, W."],["dc.contributor.author","Kurlemann, G."],["dc.contributor.author","Kohlschütter, A."],["dc.date.accessioned","2018-04-23T11:47:32Z"],["dc.date.available","2018-04-23T11:47:32Z"],["dc.date.issued","1997"],["dc.description.abstract","Through a survey of all departments of pediatrics, neurology and neuropathology in Germany, we calculated the incidence of all major forms of leukodystrophy. Only diagnoses based on specific biochemical tests in association with typical findings and/or neuroradiologically proven white matter involvement were accepted, In accordance with these strict criteria, 617 cases of leuko-dystrophy were found (incidence of all forms: app. 2.0/100,000), Minimal incidence was estimated at 0.8/100,000 for adrenoleugodystrophy/adrenomyeloneuropathy (ALD/AMN), 0.6/100,000 for metachromatic leukodystrophy (MLD), and 0.6/100,000 for Krabbe disease. Thus ALD/AMN is apparently underdiagnosed in Germany. A considerable proportion of leukodystrophies could not be classified in spite of adequate diagnostic procedures in experienced centers."],["dc.identifier.gro","3144591"],["dc.identifier.isi","A1997XT64000020"],["dc.identifier.pmid","9286459"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2231"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0148-7299"],["dc.relation.issn","0148-7299"],["dc.title","Leukodystrophy incidence in Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuropediatrics"],["dc.bibliographiccitation.lastpage","98"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Waterham, Hans R."],["dc.contributor.author","Wanders, Ronald J. A."],["dc.contributor.author","Ferdinandusse, Sacha"],["dc.contributor.author","Henneke, Marco"],["dc.contributor.author","Hunneman, D. H."],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:53:15Z"],["dc.date.available","2017-09-07T11:53:15Z"],["dc.date.issued","2006"],["dc.description.abstract","We present a rare case of peroxisomal acyl-CoA oxidase deficiency that was not detected by the common metabolic screening program for peroxisomal disorders. The patient presented with a typical MRI pattern showing pachygyria, perisylvian polymicrogyria, cerebral and cerebellar white matter abnormalities, and facial dysmorphia, progressive psychomotor retardation, deafness, retinopathy, peripheral neuropathy, and infantile seizures strongly indicative for a peroxisomal disorder. Yet, repetitive measurements of very long-chain fatty acids (VLCFAs) and phytanic acid in serum and plasma as well as plasmalogens in erythrocytes revealed normal values apparently excluding a peroxisomal defect (methods of measurement published by Moser and co-workers in 1980 [4] and 1981 [2]). Subsequent biochemical investigation in cultured skin fibroblasts of the patient, however, revealed elevated concentrations of VLCFAs, deficient oxidation of C26:0, but normal oxidation of both phytanic acid and pristanic acid and normal de novo plasmalogen synthesis, indicative for a defect in the peroxisomal P-oxidation system. Enzymatic studies in these fibroblasts pointed to peroxisomal acyl-CoA oxidase deficiency and subsequent molecular analyses revealed a homozygous acceptor splice site mutation IVS3-1G > A in the ACOX1 gene (MIM 609 751)."],["dc.identifier.doi","10.1055/s-2006-923943"],["dc.identifier.gro","3143717"],["dc.identifier.isi","000238839300007"],["dc.identifier.pmid","16773508"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1262"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0174-304X"],["dc.title","Pitfall in metabolic screening in a patient with fatal peroxisomal beta-oxidation defect"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1899"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.lastpage","1903"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Simon, T."],["dc.contributor.author","Hero, Barbara"],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Berthold, F."],["dc.date.accessioned","2018-11-07T10:36:27Z"],["dc.date.available","2018-11-07T10:36:27Z"],["dc.date.issued","2003"],["dc.description.abstract","The value of the tumour markers vanillylmandelic acid (VMA) and homovanillic acid (HVA) in urine (u) and serum (s), neurone-specific enolase (NSE). and lactate dehydrogenase (LDH) in the early prediction of relapse/progression in neuroblastoma is not known. We analysed the data of neuroblastoma patients who had successfully completed first-line treatment and had laboratory results available from their initial diagnosis and from relapse/progression (n = 196). Patients' overall survival from relapse or progression was 21.5 +/- 4.2% (mean standard deviation). At diagnosis, we found abnormal results in 75% for VMA and/or HVA (s), 92% for VMA and/or HVA (u), 90% for NSE, and 81% for LDH. We found a lower incidence of abnormal results at relapse or progression,with 40% for VMA and/or HVA (s), 54% for HVA and/or VMA (u), 61% for NSE, and 48% for LDH. Sensitivity of markers was higher for metastatic compared with local recurrence. NSE was the best, being able to detect 42% of the localised relapses. 77% of the combined local/metastatic relapses, and 69% of the metastatic recurrences. Relapse or progression in neuroblastoma cannot be detected reliably by monitoring tumour markers alone. Therefore, follow-up of neuroblastoma patients must include clinical assessment and imaging studies. (C) 2003 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0959-8049(03)00376-9"],["dc.identifier.isi","000185327400013"],["dc.identifier.pmid","12932669"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0959-8049"],["dc.title","Tumour markers are poor predictors for relapse or progression in neuroblastoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","496"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pediatric Research"],["dc.bibliographiccitation.lastpage","501"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Roth, Christian L."],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Gebhardt, Ursel"],["dc.contributor.author","Stoffel-Wagner, Birgit"],["dc.contributor.author","Reinehr, Thomas"],["dc.contributor.author","Mueller, Hermann L."],["dc.date.accessioned","2018-11-07T11:03:52Z"],["dc.date.available","2018-11-07T11:03:52Z"],["dc.date.issued","2007"],["dc.description.abstract","Severe obesity is a major problem in patients suffering from craniopharyngioma (CP), a benign tumor located in pituitary and hypothalamic regions. In this study, the hypothesis that hypothalamic damage leads to a reduction in overall sympathetic tone was tested. Catecholamines, as well as their metabolites homovanillic acid (HVA) and vanillylmandelic acid (VMA), markers of catecholamine turnover, were measured in morning voided urine of 109 patients participating in a German pediatric CP study, and their physical activity was analyzed using a questionnaire. HVA and VMA results were compared with age-matched HVA and VMA in urine of patients proven to not have a catecholamine-secreting tumor. Patients with the most severe obesity displayed the lowest urine HVA and VMA values. Patients with hypothalamic CP had 3.2-fold higher BMI values (p < 0.0001), lower HVA (0.72-fold, p < 0.001), and VMA (0.84-fold, p < 0.01) values, and significantly lower activity scores than those without hypothalamic involvement, but their epinephrine- and norepinephrine/creatinine ratios were not significantly different, possibly due to low levels. The low HVA and VMA values suggest decreased sympathetic outflow contributing to reduced physical activity and severe obesity, especially in patients with a hypothalamic tumor. In further studies investigating treatment options for hypothalamic obesity, disturbed sympathetic tone should be considered."],["dc.identifier.doi","10.1203/pdr.0b013e3180332cd6"],["dc.identifier.isi","000245224400021"],["dc.identifier.pmid","17515878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51706"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Pediatric Research Foundation, Inc"],["dc.relation.issn","0031-3998"],["dc.title","Reduced sympathetic metabolites in urine of obese patients with craniopharyngioma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","113"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Inherited Metabolic Disease"],["dc.bibliographiccitation.lastpage","119"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Barmaki Pour, R."],["dc.contributor.author","Stockler-Ipsiroglu, S."],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Gahr, M."],["dc.contributor.author","Korenke, Christoph"],["dc.contributor.author","Pabst, W."],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Peters, A."],["dc.date.accessioned","2018-11-07T09:21:59Z"],["dc.date.available","2018-11-07T09:21:59Z"],["dc.date.issued","2000"],["dc.description.abstract","Lymphocytopenia and depression of natural killer cells have been observed in patients with adrenoleukodystrophy (ALD) treated with glycerol trioleate and glycerol trierucate ('Lorenzo's oil'). To investigate possible alterations of cellular immunoreactivity, we measured lymphocyte proliferation in response to mitogens (PHA, Con A, PWM, OKT3) in 27 patients on treatment and in 14 patients without treatment. In patients on treatment, lymphocyte proliferation in response to the mitogens PHA and Con A was significantly higher than in patients without treatment. Lymphocyte proliferation in patients without treatment was comparable to that of normal control lymphocytes. Additionally, we found increased concentrations of erucic acid, C-22:1, in lymphocytes from patients with treatment. The enhanced proliferation of lymphocytes in response to mitogens is an indication of increased reactivity of cellular immunity to unspecific immunological stimuli. Long-term side-effects on cellular immunoreactivity have to be considered in ALD patients treated with Lorenzo's oil."],["dc.identifier.doi","10.1023/A:1005657530372"],["dc.identifier.isi","000085803300003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29235"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Kluwer Academic Publ"],["dc.relation.issn","0141-8955"],["dc.title","Enhanced lymphocyte proliferation in patients with adrenoleukodystrophy treated with erucic acid (22 : 1)-rich triglycerides"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","196"],["dc.bibliographiccitation.issue","4-5"],["dc.bibliographiccitation.journal","European Journal of Pediatrics"],["dc.bibliographiccitation.lastpage","201"],["dc.bibliographiccitation.volume","163"],["dc.contributor.author","Korenke, Christoph"],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Eber, S."],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:49:52Z"],["dc.date.available","2018-11-07T10:49:52Z"],["dc.date.issued","2004"],["dc.description.abstract","Vitamin B-12 deficiency is one of the major causes of megaloblastic anaemia with or without neurological symptoms. We report on a patient manifesting acute encephalopathy, epilepsy, microcephaly and megaloblastic anaemia at the age of 4 months. Vitamin B-12 deficiency in the patient was due to subclinical pernicious anaemia of the mother who exhibited neither haematological nor neurological symptoms. Mother and child both had elevated methylmalonic acid in their urine which is a sensitive parameter of vitamin B-12 deficiency. Vitamin B-12 therapy resulted in arrest of convulsions within 24 h. There were no further seizures although the patient showed moderate mental retardation at the age of 7 years but a normal head circumference. Long-term MRI follow-up, performed at the age of 7 years, showed moderate enlargement of the ventricles with reduction of myelin and hypoplasia of the corpus callosum. Conclusion:vitamin B-12 deficiency due to maternal pernicious anaemia should always be considered in the differential diagnosis of neurological symptoms in infants and especially in combination with megaloblastic anaemia. Since the age of onset and the duration of neurological symptoms may contribute to the development of long-term symptoms, early diagnosis and treatment is important for vitamin B-12 deficient children."],["dc.identifier.doi","10.1007/s00431-004-1402-4"],["dc.identifier.isi","000220298900003"],["dc.identifier.pmid","14762712"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48528"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-6199"],["dc.title","Severe encephalopathy with epilepsy in an infant caused by subclinical maternal pernicious anaemia: case report and review of the literature"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S28"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","S29"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Kuehl, J.-S."],["dc.contributor.author","Strauss, G."],["dc.contributor.author","Weschke, Bernhard"],["dc.contributor.author","Koehler, Wolfgang"],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Weddige, Almut"],["dc.contributor.author","Steinfeld, Robert"],["dc.contributor.author","Gaertner, J."],["dc.contributor.author","Ebell, Wolfram"],["dc.date.accessioned","2018-11-07T11:17:24Z"],["dc.date.available","2018-11-07T11:17:24Z"],["dc.date.issued","2008"],["dc.identifier.isi","000254359200071"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54796"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","London"],["dc.relation.conference","34th Annual Meeting of the European-Group-for-Blood-and-Marrow-Transplantation/24nd Meeting of the EBMT-Nurses-Group/7th Meeting of the EBMT-Data-Management-Group"],["dc.relation.eventlocation","Florence, ITALY"],["dc.relation.issn","0268-3369"],["dc.title","HSCT in childhood-onset cerebral X-linked adrenoleukodystrophy: the updated Berlin experience"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Pediatrics"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","162"],["dc.contributor.author","Baumann, M."],["dc.contributor.author","Korenke, Christoph"],["dc.contributor.author","Weddige-Diedrichs, A."],["dc.contributor.author","Wilichowski, E."],["dc.contributor.author","Hunneman, Donald H."],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Klingebiel, T."],["dc.contributor.author","Niethammer, D."],["dc.contributor.author","Kuhl, J."],["dc.contributor.author","Ebell, Wolfram"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:42:22Z"],["dc.date.available","2018-11-07T10:42:22Z"],["dc.date.issued","2003"],["dc.description.abstract","In an attempt to elucidate prognostic factors, the data on 12 boys who underwent haematopoietic stem cell transplantation (HSCT) for cerebral X-linked adrenoleukodystrophy were evaluated. Two further patients received HSCT but died from transplantation-related complications. The data included neurological examination, neuropsychological testing and magnetic resonance imaging (MRI). Follow-up after HSCT was up to 5.5 years. Six patients showed a moderate to severe clinical deterioration after HSCT including two who died within 6 months. In this group, a MRI severity score of 10 or higher before HSCT was associated with severe impairment and a score of more than 12 was followed by rapid deterioration and death after HSCT. The presence of neurological symptoms before HSCT also affected prognosis. Six patients showed no deterioration in neurological or neuropsychological assessment after HSCT. Conclusion: our data confirm that haematopoietic stem cell transplantation can stop the progress of demyelination when performed at a critical early stage of the disease. The prognosis in an individual patient for the clinical course after stem cell transplantation can in general be given based on the status before transplantation, although individual patients may show an unexpected course."],["dc.identifier.doi","10.1007/s00431-002-1097-3"],["dc.identifier.isi","000180613300002"],["dc.identifier.pmid","12486501"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46778"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-6199"],["dc.title","Haematopoietic stem cell transplantation in 12 patients with cerebral X-linked adrenoleukodystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]