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","e647"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","e656"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Schneider, Dietmar"],["dc.contributor.author","Weimar, Christian"],["dc.contributor.author","Wartenberg, Katja"],["dc.contributor.author","Schellinger, Peter D."],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Becker, Harald"],["dc.contributor.author","Wegrzyn, Martin"],["dc.contributor.author","Jähnig, Peter"],["dc.contributor.author","Herrmann, Manfred"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Heide, Wolfgang"],["dc.contributor.author","Wagner, Armin"],["dc.contributor.author","Schwab, Stefan"],["dc.contributor.author","Reichmann, Heinz"],["dc.contributor.author","Schwendemann, Günther"],["dc.contributor.author","Dengler, Reinhard"],["dc.contributor.author","Kastrup, Andreas"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2017-09-07T11:46:20Z"],["dc.date.available","2017-09-07T11:46:20Z"],["dc.date.issued","2009-12"],["dc.description.abstract","Background and Purpose— Numerous preclinical findings and a clinical pilot study suggest that recombinant human erythropoietin (EPO) provides neuroprotection that may be beneficial for the treatment of patients with ischemic stroke. Although EPO has been considered to be a safe and well-tolerated drug over 2 decades, recent studies have identified increased thromboembolic complications and/or mortality risks on EPO administration to patients with cancer or chronic kidney disease. Accordingly, the double-blind, placebo-controlled, randomized German Multicenter EPO Stroke Trial (Phase II/III; ClinicalTrials.gov Identifier: NCT00604630) was designed to evaluate efficacy and safety of EPO in stroke.Methods— This clinical trial enrolled 522 patients with acute ischemic stroke in the middle cerebral artery territory (intent-to-treat population) with 460 patients treated as planned (per-protocol population). Within 6 hours of symptom onset, at 24 and 48 hours, EPO was infused intravenously (40 000 IU each). Systemic thrombolysis with recombinant tissue plasminogen activator was allowed and stratified for.Results— Unexpectedly, a very high number of patients received recombinant tissue plasminogen activator (63.4%). On analysis of total intent-to-treat and per-protocol populations, neither primary outcome Barthel Index on Day 90 (P=0.45) nor any of the other outcome parameters showed favorable effects of EPO. There was an overall death rate of 16.4% (n=42 of 256) in the EPO and 9.0% (n=24 of 266) in the placebo group (OR, 1.98; 95% CI, 1.16 to 3.38; P=0.01) without any particular mechanism of death unexpected after stroke.Conclusions— Based on analysis of total intent-to-treat and per-protocol populations only, this is a negative trial that also raises safety concerns, particularly in patients receiving systemic thrombolysis."],["dc.identifier.doi","10.1161/STROKEAHA.109.564872"],["dc.identifier.gro","3150483"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7252"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","clinical trial; hematopoietic growth factor; neuroprotection; NIHSS; rtPA"],["dc.title","Recombinant Human Erythropoietin in the Treatment of Acute Ischemic Stroke"],["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.firstpage","1001.2"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1002"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Reiber, Hansotto"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Volles, Erwin"],["dc.date.accessioned","2021-06-01T10:48:11Z"],["dc.date.available","2021-06-01T10:48:11Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1212/WNL.0000000000009539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85852"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Reader response: The two lives of neurologist Helmut J. Bauer (1914–2008): Renowned MS specialist and National Socialist"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","1330"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Weber, T."],["dc.date.accessioned","2018-11-07T08:51:14Z"],["dc.date.available","2018-11-07T08:51:14Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1007/s00115-011-3284-9"],["dc.identifier.isi","000295678400013"],["dc.identifier.pmid","21503715"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21884"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Vanishing white matter disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3283"],["dc.bibliographiccitation.issue","51-52"],["dc.bibliographiccitation.journal","Deutsches Ärzteblatt"],["dc.bibliographiccitation.lastpage","3286"],["dc.bibliographiccitation.volume","95"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Boekhoff, Immo"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Prange, Hilmar Walter"],["dc.date.accessioned","2017-11-21T12:33:49Z"],["dc.date.available","2017-11-21T12:33:49Z"],["dc.date.issued","1998"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10140"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.title","Therapeutische Ansätze bei der Creutzfeldt-Jakob-Krankheit"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","132"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","AKTUELLE NEUROLOGIE"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Weber, F."],["dc.contributor.author","Neurath, H."],["dc.contributor.author","Desel, Herbert"],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Prange, Hilmar"],["dc.date.accessioned","2018-11-07T09:10:47Z"],["dc.date.available","2018-11-07T09:10:47Z"],["dc.date.issued","2001"],["dc.description.abstract","Venlafaxin is a serotonine-noradrenaline reuptake inhibitor that is used for treatment of depression and concomitant anxiety disorders. We report on a 38 years old woman, who developed a generalised seizure, agitation and somnolence, fever, hyponatriemia, rhabdomyolysis and a tachyarrhytmia absoluta. In a blood sample, which was collected about one day after the ingestion of venlafaxin, we detected 12 ng/ml venlafaxin and 105 ng/ml of its active metabolite O-desmethyl-venlafaxin. Considering the pharmacokinetic of venlafaxin and O-desmethyl-venlafaxin toxic plasma levels of both substances can be calculated for the time when symptoms had occurred. Under treatment with volume, diuretics and substitution of electrolytes the patient recovered consciousness very quickly. However, serum levels of creatine-kinase increased steadily to a maximum of 14 926 U/I on day 3 and declined slowly thereafter. In addition, a tachyarrhytmia absoluta developed suddenly on day 4 and reversed spontaneously one day later. While seizures, fever, hyponatriemia and loss of consciousness are typical symptoms of intoxication with venlafaxin, rhabdomyolysis and the late occurrence of tachyarrhytmia absoluta are uncommon."],["dc.identifier.doi","10.1055/s-2001-12522"],["dc.identifier.isi","000168288700008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26573"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0302-4350"],["dc.title","Rhabdomyolysis after intake of Venlafaxin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","592"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","British Journal of Clinical Pharmacology"],["dc.bibliographiccitation.lastpage","603"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Meineke, Ingolf"],["dc.contributor.author","Freudenthaler, S."],["dc.contributor.author","Hofmann, U."],["dc.contributor.author","Schaeffeler, E."],["dc.contributor.author","Mikus, G."],["dc.contributor.author","Schwab, M."],["dc.contributor.author","Prange, H. W."],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T09:43:46Z"],["dc.date.available","2018-11-07T09:43:46Z"],["dc.date.issued","2002"],["dc.description.abstract","Aims Concentrations in the cerebrospinal fluid (CSF) are a useful approximation to the effect site for drugs like morphine. However, CSF samples, are available only in rare circumstances. If they can be obtained they may provide important insights into the pharmacokinetics/pharmacodynamics of opioids. Methods Nine neurological and neurosurgical patients (age 19-69 years) received 0.5 mg kg(-1) morphine sulphate pentahydrate as an intravenous infusion over 30 min. Plasma and CSF were collected for up to 48 h. Concentration time-course and interindividual variability of morphine (M), morphine-3-glucuronide (M3G) and morphine-6 glucuronide (M6G) were analysed using population pharmacokinetic modelling. Results While morphine was rapidly cleared from plasma (total clearance = 1838 ml min(-1) (95% CI 1668, 2001 ml min(-1) )) the glucuronide metabolites were eliminated more slowly (clearance M3G = 44.5 ml min(-1) (35.1, 53.9 ml min(-1) ), clearance M6G = 42.1 ml min(-1) (36.4, 47.7 ml min(-1) )) and their clearance could be described as a function of creatinine clearance. The central volumes of distribution were estimated to be 12.7 l (11.1, 14.3 l) for morphine. Transfer from the central compartment into the CSF was also rapid for M and considerably slower for both glucuronide metabolites. Maximum concentrations were achieved after 102 min (M), 417 min (M3G) and 443 min (M6G). A P-glycoprotein exon 26 polymorphism previously found to be linked with transport activity could be involved in CSF accessibility, since the homozygous mutant genotype was associated (P < 0.001) with high maximum CSF concentrations of M but not M3G or M6G. Conclusions From the population pharmacokinetic model presented, CSF concentration profiles can be derived for M, M3G and M6G on the basis of dosing information and creatinine clearance without collecting CSF samples. Such profiles may then serve as the link between dose regimen and effect measurements in future clinical effect studies."],["dc.identifier.doi","10.1046/j.1365-2125.2002.t01-1-01689.x"],["dc.identifier.isi","000179909500005"],["dc.identifier.pmid","12492606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34251"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0306-5251"],["dc.title","Pharmacokinetic modelling of morphine, morphine-3-glucuronide and morphine-6-glucuronide in plasma and cerebrospinal fluid of neurosurgical patients after short-term infusion of morphine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]