Bohn, Matthias

[["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","2273"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The American Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Schworer, H."],["dc.contributor.author","Bohn, M."],["dc.contributor.author","Waezsada, S. Y."],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:53:17Z"],["dc.date.available","2018-11-07T08:53:17Z"],["dc.date.issued","2001"],["dc.identifier.isi","000169839600062"],["dc.identifier.pmid","11467676"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22373"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0002-9270"],["dc.title","Successful treatment of megacolon associated with colitis with a nitric oxide synthase inhibitor"],["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","20992"],["dc.bibliographiccitation.issue","49"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","20997"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Bohn, S."],["dc.contributor.author","Beck, F."],["dc.contributor.author","Sakata, E."],["dc.contributor.author","Walzthoeni, T."],["dc.contributor.author","Beck, M."],["dc.contributor.author","Aebersold, R."],["dc.contributor.author","Forster, F."],["dc.contributor.author","Baumeister, W."],["dc.contributor.author","Nickell, S."],["dc.date.accessioned","2022-03-01T11:46:22Z"],["dc.date.available","2022-03-01T11:46:22Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1073/pnas.1015530107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103646"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Structure of the 26S proteasome from Schizosaccharomyces pombe at subnanometer resolution"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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","1479"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","1484"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Sakata, E."],["dc.contributor.author","Bohn, S."],["dc.contributor.author","Mihalache, O."],["dc.contributor.author","Kiss, P."],["dc.contributor.author","Beck, F."],["dc.contributor.author","Nagy, I."],["dc.contributor.author","Nickell, S."],["dc.contributor.author","Tanaka, K."],["dc.contributor.author","Saeki, Y."],["dc.contributor.author","Forster, F."],["dc.contributor.author","Baumeister, W."],["dc.date.accessioned","2022-03-01T11:46:23Z"],["dc.date.available","2022-03-01T11:46:23Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1073/pnas.1119394109"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103649"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Localization of the proteasomal ubiquitin receptors Rpn10 and Rpn13 by electron cryomicroscopy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","14870"],["dc.bibliographiccitation.issue","37"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","14875"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Beck, F."],["dc.contributor.author","Unverdorben, P."],["dc.contributor.author","Bohn, S."],["dc.contributor.author","Schweitzer, A."],["dc.contributor.author","Pfeifer, G."],["dc.contributor.author","Sakata, E."],["dc.contributor.author","Nickell, S."],["dc.contributor.author","Plitzko, J. M."],["dc.contributor.author","Villa, E."],["dc.contributor.author","Baumeister, W."],["dc.contributor.author","Forster, F."],["dc.date.accessioned","2022-03-01T11:46:23Z"],["dc.date.available","2022-03-01T11:46:23Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1073/pnas.1213333109"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103650"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Near-atomic resolution structural model of the yeast 26S proteasome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","313"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","323"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Pölking, Esther"],["dc.contributor.author","Dietrich, Jeannine"],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Poeggeler, Burkhard"],["dc.contributor.author","Mertens, Nina"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Hüther, Gerald"],["dc.contributor.author","Schneider, Armin"],["dc.contributor.author","Bach, Alfred"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Hardeland, Rüdiger"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:31Z"],["dc.date.available","2017-09-07T11:46:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by classical antioxidants. In preparation of a possible future clinical trial, we explored the potential of melatonin as neuroprotective compound and antioxidant in: (1) cultured motoneuronal cells (NSC-34), (2) a genetic mouse model of ALS (SOD1(G93A)-transgenic mice), and (3) a group of 31 patients with sporadic ALS. We found that melatonin attenuates glutamate-induced cell death of cultured motoneurons. In SOD1(G93A)-transgenic mice, high-dose oral melatonin delayed disease progression and extended survival. In a clinical safety study, chronic high-dose (300 mg/day) rectal melatonin was well tolerated during an observation period of up to 2 yr. Importantly, circulating serum protein carbonyls, which provide a surrogate marker for oxidative stress, were elevated in ALS patients, but were normalized to control values by melatonin treatment. This combination of preclinical effectiveness and proven safety in humans suggests that high-dose melatonin is suitable for clinical trials aimed at neuroprotection through antioxidation in ALS."],["dc.identifier.doi","10.1111/j.1600-079X.2006.00377.x"],["dc.identifier.gro","3150526"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7299"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0742-3098"],["dc.title","Reduced oxidative damage in ALS by high-dose enteral melatonin treatment"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","206"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hinze-Selch, D."],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Aust, Carlotta"],["dc.contributor.author","Knolle-Veentjer, S."],["dc.contributor.author","Wilms, S."],["dc.contributor.author","Heinz, G."],["dc.contributor.author","Erdag, S."],["dc.contributor.author","Jahn, H."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Ritzen, M."],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Wagner, M."],["dc.contributor.author","Schneider, U."],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Huber, Martin"],["dc.contributor.author","Czernik, Adelheid"],["dc.contributor.author","Pollmacher, T."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Sirén, A-L."],["dc.contributor.author","Klosterkötter, J."],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Aldenhoff, Josef B."],["dc.contributor.author","Krampe, Henning"],["dc.date.accessioned","2017-09-07T11:46:24Z"],["dc.date.available","2017-09-07T11:46:24Z"],["dc.date.issued","2007"],["dc.description.abstract","Schizophrenia is increasingly recognized as a neurodevelopmental disease with an additional degenerative component, comprising cognitive decline and loss of cortical gray matter. We hypothesized that a neuroprotective/neurotrophic add-on strategy, recombinant human erythropoietin (rhEPO) in addition to stable antipsychotic medication, may be able to improve cognitive function even in chronic schizophrenic patients. Therefore, we designed a double-blind, placebo-controlled, randomized, multicenter, proof-of-principle (phase II) study. This study had a total duration of 2 years and an individual duration of 12 weeks with an additional safety visit at 16 weeks. Chronic schizophrenic men (N=39) with defined cognitive deficit (greater than or equal to1 s.d. below normal in the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)), stable medication and disease state, were treated for 3 months with a weekly short (15 min) intravenous infusion of 40 000 IU rhEPO (N=20) or placebo (N=19). Main outcome measure was schizophrenia-relevant cognitive function at week 12. The neuropsychological test set (RBANS subtests delayed memory, language–semantic fluency, attention and Wisconsin Card Sorting Test (WCST-64) – perseverative errors) was applied over 2 days at baseline, 2 weeks, 4 weeks and 12 weeks of study participation. Both placebo and rhEPO patients improved in all evaluated categories. Patients receiving rhEPO showed a significant improvement over placebo patients in schizophrenia-related cognitive performance (RBANS subtests, WCST-64), but no effects on psychopathology or social functioning. Also, a significant decline in serum levels of S100B, a glial damage marker, occurred upon rhEPO. The fact that rhEPO is the first compound to exert a selective and lasting beneficial effect on cognition should encourage new treatment strategies for schizophrenia."],["dc.identifier.doi","10.1038/sj.mp.4001907"],["dc.identifier.gro","3150509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7281"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1359-4184"],["dc.subject","S100B; plasticity; neuropsychology; psychopathology; high-dose EPO"],["dc.title","Improvement of cognitive functions in chronic schizophrenic patients by recombinant human erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]