Prange, Hilmar Walter

[["dc.bibliographiccitation.firstpage","690"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","694"],["dc.bibliographiccitation.volume","248"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Henkel, Karsten"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Poser, S."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Creutzfeldt-Jakob disease (CJD) belongs to the group of transmissible spongiform encephalopathies. It is suspected that a pathologically altered form of the prion protein (PrPSc) is the decisive trigger of the disease. Data from animal experiments suggest an involvement of the lymphatic system in the intracorporal transport of PrPSc. However, it has not so far been possible to detect PrPSc on mononuclear cells (MNCs) either in the sporadic form of CJD or in the new variant of CJD (vCJD). In order to determine a possible alteration of MNCs in CJD, we investigated the natural and induced apoptotic behaviour of these cells.MNCs from 19 patients with sporadic CJD and from 20 patients with other neurological disorders were used. The cells were analysed by fluorescence cytometry with and without apoptosis induction by xanthine oxidase and hypoxanthine. The apoptosis rate was quantified using the stain 7-amino-actinomycin D (7-AAD). In the morphological investigation of the cells before apoptosis induction, there were no significant differences between the groups with regard to cell size and granularity of the MNCs. After apoptosis induction, the typical significant decrease in cell size and increase in granularity of the cells occurred in both groups. Significant differences between the patient populations were not found.For the first time, our investigation has demonstrated that a functional impairment of MNCs with regard to their apoptotic behaviour does not occur in sporadic CJD. It remains open to question whether this mechanism plays an important role in forms of transmissible encephalopathy other than sporadic CJD, especially after oral transmission."],["dc.identifier.doi","10.1007/pl00007834"],["dc.identifier.gro","3151691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8510"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.relation.issn","0340-5354"],["dc.title","Unaltered apoptotic behaviour of mononuclear cells from patients with sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","51"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Horn, C."],["dc.contributor.author","Kemmling, Y."],["dc.contributor.author","Seipelt, M."],["dc.contributor.author","Hellenbrand, U."],["dc.contributor.author","Stiefel, M."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:03Z"],["dc.date.available","2018-11-07T10:33:03Z"],["dc.date.issued","2002"],["dc.description.abstract","Biochemical markers of brain damage, e.g. ischemic stroke, should reflect the volume of irreversibly damaged brain parenchyma and the clinical outcome in a single patient in order to allow estimation of prognosis at an early stage. Tau protein, which derives predominantly from neurons and axons, is elevated in the cerebrospinal fluid of patients with neurodegenerative disease. This makes tau protein a potential marker of neuronal/axonal injury. In order to test this hypothesis, the current study aimed at showing that tau protein is measurable in the blood after acute ischemic stroke and that it correlates with clinical disability and stroke volume. In a longitudinal prospective study we measured tau protein serum levels with an ELISA in 30 patients longitudinally after ischemic stroke. Tau protein was detectable within 5 days after ischemia in the sera of 7/20 patients with MRI-proven infarction and in 2/10 patients with transitory ischemic attack; both of them had a small infarction visible on the MRI scan. Tau protein was measurable within 6 h after symptom onset, peaked after 3-5 days and correlated with infarct volume and disability after 3 months. In conclusion, serum tau protein is a candidate marker of axonal injury. In stroke, its clinical use is limited, because it is detectable only in a proportion of patients. Copyright (C) 2002 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000047946"],["dc.identifier.isi","000173547300008"],["dc.identifier.pmid","11803192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44511"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0014-3022"],["dc.title","Serum tau protein level as a marker of axonal damage in acute ischemic stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Piotr, L."],["dc.contributor.author","Dembowski, C."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Stiefel, M."],["dc.contributor.author","Rustenbeck, Hans Heino"],["dc.contributor.author","Jacob, S."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Siren, A. L."],["dc.date.accessioned","2018-11-07T10:33:49Z"],["dc.date.available","2018-11-07T10:33:49Z"],["dc.date.issued","2002"],["dc.format.extent","354"],["dc.identifier.isi","000173147700143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0039-2499"],["dc.title","Erythropoietin treatment for acute stroke: A randomized double-blind proof-of concept trial in man"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","112"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","115"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Mohr, A."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Prange, Hilmar"],["dc.date.accessioned","2018-11-07T10:24:16Z"],["dc.date.available","2018-11-07T10:24:16Z"],["dc.date.issued","2006"],["dc.description.abstract","Hypothermia is a rare condition in multiple sclerosis (MS). We report on a patient with a long-standing secondary progressive MS and six episodes of recurring hypothermia down to 29.9 degrees C with associated hypotension, bradycardia, coagulopathy and electrolyte dysequilibrium. Magnetic resonance imaging (MRI) demonstrated severe involvement of the corpus callosum with an associated lesion in the right posterior thalamus. These findings may link hypothermia in MS with callosal and associated thalamic pathology to Shapiro's syndrome, where agenesis of the corpus callosum and associated abnormalities are related to episodic spontaneous hypothermia. In MS, hypothermic episodes may be triggered by preceding infections, as shown in the present case."],["dc.identifier.doi","10.1191/135248506ms1268cr"],["dc.identifier.isi","000235338300017"],["dc.identifier.pmid","16459729"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42624"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hodder Arnold, Hodder Headline Plc"],["dc.relation.issn","1352-4585"],["dc.title","Core hypothermia in multiple sclerosis: case report with magnetic resonance imaging localization of a thalamic lesion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","505"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Dembowski, Christoph"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Lewczuk, Pjotr"],["dc.contributor.author","Stiefel, Michael"],["dc.contributor.author","Rustenbeck, Hans-Heino"],["dc.contributor.author","Breiter, Norbert"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Kochen, Michael"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Wessel, Thomas C."],["dc.contributor.author","Ryck, Marc de"],["dc.contributor.author","Itri, Loretta"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Siren, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2002"],["dc.description.abstract","Background: Erythropoietin (EPO) and its receptor play a major role in embryonic brain, are weakly expressed in normal postnatal/adult brain and up-regulated upon metabolic stress. EPO protects neurons from hypoxic/ ischemic injury. The objective of this trial is to study the safety and efficacy of recombinant human EPO (rhEPO) for treatment of ischemic stroke in man. Materials and Methods: The trial consisted of a safety part and an efficacy part. in the safety study, 13 patients received rhEPO intravenously (3.3 x 10(4) IU/50 m/130 min) once daily for the first 3 days after stroke. in the double-blind randomized proof-of-concept trial, 40 patients received either rhEPO or saline. Inclusion criteria were age {.extbackslash}textless80 years, ischemic stroke within the middle cerebral artery territory confirmed by diffusion-weighted MRI, symptom onset {.extbackslash}textless8 hr before drug administration, and deficits on stroke scales. The study endpoints were functional outcome at day 30 (Barthel index, modified Rankin scale), NIH and Scandinavian stroke scales, evolution of infarct size (sequential MRI evaluation using diffusion-weighted [DWI] and fluid-attenuated inversion recovery sequences [FLAIR]) and the damage marker S100ss. Results: No safety concerns were identified. Cerebrospinal fluid EPO increased to 60-100 times that of nontreated patients, proving that intravenously administered rhEPO reaches the brain. in the efficacy trial, patients received rhEPO within 5 hr of onset of symptoms (median, range 2:40-7:55). Admission neurologic scores and serum S100beta concentrations were strong predictors of outcome. Analysis of covariance controlled for these two variables indicated that rhEPO treatment was associated with an improvement in follow-up and outcome scales. A strong trend for reduction in infarct size in rhEPO patients as compared to controls was observed by MRI. Conclusion: intravenous high-dose rhEPO is well tolerated in acute ischemic stroke and associated with an improvement in clinical outcome at 1 month. A larger scale clinical trial is warranted."],["dc.identifier.gro","3150429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7192"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1076-1551"],["dc.relation.orgunit","Institut für Allgemeinmedizin"],["dc.title","Erythropoietin therapy for acute stroke is both safe and beneficial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","810"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","812"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","Arlt, Soenke"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Rustenbeck, Hans Heino"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Reimers, Carl Detlev"],["dc.date.accessioned","2018-11-07T11:01:59Z"],["dc.date.available","2018-11-07T11:01:59Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1007/s00415-006-0439-x"],["dc.identifier.isi","000247654300019"],["dc.identifier.pmid","17401744"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51272"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Gadolinium encephalopathy due to accidental intrathecal administration of gadopentetate dimeglumine"],["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","29"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","32"],["dc.bibliographiccitation.volume","343"],["dc.contributor.author","Ratzka, Peter"],["dc.contributor.author","Döhlinger, Susanne"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Arlt, Sönke"],["dc.contributor.author","Jacobi, Christian"],["dc.contributor.author","Schröter, Andreas"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2021-06-01T10:50:14Z"],["dc.date.available","2021-06-01T10:50:14Z"],["dc.date.issued","2003"],["dc.description.abstract","In Creutzfeldt-Jakob disease (CJD), progressive neuronal cell death probably occurs as a result of a change in conformation of the physiological prion protein (PrPC). There is evidence of participation of the lymphatic system and in particular of lymphocytes in the intracorporeal transportation of the pathological prion protein (PrPSc) in new variant CJD and scrapie. Using fluorescence cytometry, we investigated a possible alteration of PrPC on lymphocytes of patients with sporadic CJD. We demonstrated a significantly lower binding pattern of antibodies (3F4) against physiological prion protein to lymphocytes of patients with sporadic CJD (n = 16) compared with control patients. In contrast this difference was not found on platelets (n = 23). For the first time we were able to present a measurable difference of antibody binding on lymphocytes of patients with CID. One interpretation of this finding is that lymphocytes patrolling the brain bind and transport PrPSc which has a lower binding affinity for the antibodies directed against physiological PrP. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(03)00315-X"],["dc.identifier.isi","000183128900008"],["dc.identifier.pmid","12749990"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86584"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Different binding pattern of antibodies to prion protein on lymphocytes from patients with sporadic Creutzfeldt–Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","714"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","718"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Otto, M."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Doehlinger, S."],["dc.contributor.author","Boekhoff, I."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Irle, E."],["dc.contributor.author","Pergande, G."],["dc.contributor.author","Ellers-Lenz, B."],["dc.contributor.author","Prange, H."],["dc.date.accessioned","2021-06-01T10:48:09Z"],["dc.date.available","2021-06-01T10:48:09Z"],["dc.date.issued","2004"],["dc.description.abstract","Background: In cell culture experiments, flupirtine maleate ( FLU), a triaminopyridine compound, was able to protect neuronal cells from apoptotic cell death induced by prion protein fragments and beta-amyloid peptides. As FLU is a clinically safe drug, the authors started a double-blind placebo-controlled study in patients with Creutzfeldt - Jakob disease (CJD). Methods: Twenty-eight patients with CJD were randomized to an oral treatment with either FLU ( n = 13) or matching placebo (PLA; n = 15). For inclusion and continuing the study, the patients had to achieve at least 50% in two of the subscales of the dementia tests employed. A battery of standardized questionnaires was employed to monitor the progression of the disease. The main outcome variable was the cognitive part of the Alzheimer's Disease Assessment Scale (ADAS-Cog); the difference between baseline and the best score under treatment was defined as the primary efficacy variable for hypothesis testing. Results: CJD types were homogeneously distributed among the treatment groups. Patients treated with FLU showed significantly less deterioration in the dementia tests than patients treated with PLA. The mean change in ADAS-Cog ( baseline to best) was + 8.4 ( +/- 15.3) in the FLU group and + 20.6 ( +/- 15.1) in the PLA group ( p = 0.02, one-sided t-test). Conclusions: FLU has beneficial effects on cognitive function in patients with CJD. These positive results also may suggest a treatment potential of FLU in other neurodegenerative disorders. However, further studies are necessary."],["dc.identifier.doi","10.1212/01.WNL.0000113764.35026.EF"],["dc.identifier.isi","000220083000008"],["dc.identifier.pmid","15007119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85845"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Efficacy of flupirtine on cognitive function in patients with CJD: A double-blind study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]