Rüther, Eckart

[["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Haust, Merle"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Meller, J."],["dc.date.accessioned","2018-11-07T10:36:28Z"],["dc.date.available","2018-11-07T10:36:28Z"],["dc.date.issued","2003"],["dc.format.extent","S232"],["dc.identifier.doi","10.1016/S0924-977X(03)91847-5"],["dc.identifier.isi","000185412300253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45332"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","16th Congress of the European-College-of-Neuropsychopharmacology"],["dc.relation.eventlocation","PRAGUE, CZECH REPUBLIC"],["dc.relation.issn","0924-977X"],["dc.title","Autoimmune thyroiditis (AIT) and affective disorders - a prospective pilot study"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PSYCHOPHARMAKOTHERAPIE"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Fiege, O."],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Grohmann, Renate"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T08:47:19Z"],["dc.date.available","2018-11-07T08:47:19Z"],["dc.date.issued","2005"],["dc.identifier.isi","000227807100009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20924"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wissenschaftliche Verlag Mbh"],["dc.relation.issn","0944-6877"],["dc.title","Oculogyric crisis under aripiprazol in combination with fluoxetin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Schlautmann, V."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T09:29:24Z"],["dc.date.available","2018-11-07T09:29:24Z"],["dc.date.issued","2000"],["dc.format.extent","369S"],["dc.identifier.doi","10.1016/S0924-9338(00)94588-7"],["dc.identifier.isi","000165731700527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31020"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Editions Scientifiques Medicales Elsevier"],["dc.publisher.place","Paris cedex 15"],["dc.relation.issn","0924-9338"],["dc.title","Thyroid axis alterations in psychoses"],["dc.type","conference_abstract"],["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","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Kern, V."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Emrich, H. M."],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:20:37Z"],["dc.date.available","2018-11-07T11:20:37Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurotoxicity of first-generation antipsychotics: (FGAs) may be involved in lipid peroxidation, which is the pathogenesis of extrapyramidal symptoms, including tardive dyskinesia (TD). Blood samples at day 0, 7, and 21 drawn from patients taking antipsychotics were analyzed for malondialdehyde (MDA) in plasma, a marker of lipid peroxidation, by high-performance liquid chromatography. Of 115 patients enrolled, 92 patients completed the study. Most MDA levels were within normal ranges (<1.0 mu mol/liter). Malondialdehyde levels in patients receiving clozapine (p = 0.002), quetiapine (p = 0.003), amisulpride (p = 0.008), and risperidone (p = 0.008) were significantly lower than within the first generation antipsychotic group. The authors conclude that lipid peroxidation is significantly higher in treatment with FGAs."],["dc.identifier.doi","10.1176/appi.neuropsych.17.2.227"],["dc.identifier.isi","000229541000014"],["dc.identifier.pmid","15939978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Publishing, Inc"],["dc.publisher.place","Arlington"],["dc.relation.conference","Annual Meeting of the Nordic-Association-for-Psychiatric-Epidemiology"],["dc.relation.eventlocation","REYKJAVIK, ICELAND"],["dc.relation.issn","1545-7222"],["dc.relation.issn","0895-0172"],["dc.title","Oxidative stress during treatment with first- and second-generation antipsychotics"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","466"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","475"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Maler, Manuel"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Rüther, Eckart"],["dc.date.accessioned","2017-09-07T11:44:45Z"],["dc.date.available","2017-09-07T11:44:45Z"],["dc.date.issued","2008"],["dc.description.abstract","The spectrum of action of flupirtine includes analgesic, muscle-relaxant and neuroprotective properties. The substance's mechanism of action has yet to be fully explained. Over the past few years, however, evidence has accumulated that flupirtine interacts with the glutamatergic N-Methyl-D-Aspartate (NMDA) receptor. Although it was not possible to demonstrate a direct effect on the NMDA receptor, all of the findings pointed to an indirect influence on the NMDA receptor in the sense of a functional NMDA antagonism. It was thus postulated that a site of action \"up- or downstream\" of the NMDA receptor is influenced. Such a site of action proved to be the G-protein-activated inwardly rectifying K+ channels (GIRK), the opening of which leads to a stabilisation of the resting membrane potential of neuronal cells and thus causes an indirect inhibition of the NMDA receptor. At therapeutically relevant concentrations, flupirtine is a neuronal potassium channel opener. This mechanism may explain the spectrum of action of flupirtine. Selective neuronal potassium channel opening (SNEPCO) thus proves to be a new principle of action, making flupirtine the prototype of a new substance class with analgesic, muscle-relaxant and neuroprotective properties. The experimental basis for this working hypothesis and the resulting model concepts are presented from the perspective of a four-stage approach."],["dc.description.abstract","Das Wirkspektrum von Flupirtin umfaßt analgetische, muskelentspannende und neuroprotektive Eigenschaften. Der Wirkmechanismus der Substanz war bislang unzureichend bekannt. In den letzten Jahren verdichteten sich jedoch Hinweise auf eine Interaktion von Flupirtin mit dem glutamatergen N-Methyl-D-Aspartat (NMDA)-Rezeptor. Obwohl eine direkte Wirkung am NMDA-Rezeptor nicht nachweisbar war. sprachen alle Befunde für eine indirekte Beeinflussung des NMDA-Rezeptors im Sinne eines funktionellen NMDA-Antagonismus. Es wurde somit postuliert, daß ein Wirkort ,,up- oder downstream\" vom NMDA-Rezeptor beeinflußt wird. Als solcher erwiesen sich die G-Protein gesteuerten einwärts gleichrichtenden K\"-Kanale (GIRK), deren Öffnung zu einer Stabilisierung des Ruhemembranpotentials neuronaler Zellen führt und dadurch eine indirekte Hemmung des NMDA-Rezeptors bewirkt. Flupirtin ist in therapeutisch relevanten Konzentrationen ein neuronaler K'-Kanalöffner (neuronal potassium Channel opener). Dieser Mechanismus vermag das Wirkspektrum von Flupirtin zu erklären. Damit erweist sich die selektive neuronale K+-Kanaloffnung (SNEPCO) als ein neues Wirkprinzip und Flupirtin als Prototyp einer neuen Substanzklasse mit analgetischen, muskelrelaxierenden und neuroprotektiven Eigenschaften. Die experimentellen Grundlagen dieser Arbeitshypothese und der daraus resultierenden Modellvorstellungen werden in einer vierstufigen Betrachtungsebene vorgestellt."],["dc.identifier.doi","10.1055/s-2007-994997"],["dc.identifier.gro","3151740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8561"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0720-4299"],["dc.title","Neuronale Kaliumkanalöffnung durch Flupirtin"],["dc.title.subtitle","Opening of Neuronal K+ Channels by Flupirtine"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","532"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","533"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Meller, J."],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Schlautmann, V."],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T08:43:19Z"],["dc.date.available","2018-11-07T08:43:19Z"],["dc.date.issued","2001"],["dc.identifier.doi","10.1176/appi.neuropsych.13.4.532"],["dc.identifier.isi","000172707700015"],["dc.identifier.pmid","11748327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19933"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Press, Inc"],["dc.relation.issn","0895-0172"],["dc.title","Affective disorders associated with autoimmune thyroiditis"],["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","42"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Degner, D."],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Behe, M."],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Jacob, Silke"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Brück, W."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Cerami, A."],["dc.contributor.author","Becker, Wolfgang"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:26Z"],["dc.date.available","2017-09-07T11:46:26Z"],["dc.date.issued","2004"],["dc.description.abstract","Erythropoietin (EPO) is a candidate compound for neuroprotection in human brain disease capable of combating a spectrum of pathophysiological processes operational during the progression of schizophrenic psychosis. The purpose of the present study was to prepare the ground for its application in a first neuroprotective add-on strategy in schizophrenia, aiming at improvement of cognitive brain function as well as prevention/slowing of degenerative processes. Using rodent studies, primary hippocampal neurons in culture, immunohistochemical analysis of human post-mortem brain tissue and nuclear imaging technology in man, we demonstrate that: (1) peripherally applied recombinant human (rh) EPO penetrates into the brain efficiently both in rat and humans, (2) rhEPO is enriched intracranially in healthy men and more distinctly in schizophrenic patients, (3) EPO receptors are densely expressed in hippocampus and cortex of schizophrenic subjects but distinctly less in controls, (4) rhEPO attenuates the haloperidol-induced neuronal death in vitro, and (4) peripherally administered rhEPO enhances cognitive functioning in mice in the context of an aversion task involving cortical and subcortical pathways presumably affected in schizophrenia. These observations, together with the known safety of rhEPO, render it an interesting compound for neuroprotective add-on strategies in schizophrenia and other human diseases characterized by a progressive decline in cognitive performance."],["dc.identifier.doi","10.1038/sj.mp.4001442"],["dc.identifier.gro","3150503"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7274"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1359-4184"],["dc.subject","recombinant human erythropoietin; EPO; schizophrenia; clinical; rodent; SPECT"],["dc.title","Erythropoietin: a candidate compound for neuroprotection in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","254"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Pajonk, Frank-Gerald B."],["dc.contributor.author","Schreiner, A."],["dc.contributor.author","Peters, S."],["dc.contributor.author","Rettig, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T10:39:10Z"],["dc.date.available","2018-11-07T10:39:10Z"],["dc.date.issued","2003"],["dc.description.abstract","Objective: The effectiveness of atypical antipsychotic agents in the treatment of acute schizophrenic episodes is still a subject of controversial debate. The objective, therefore, was to investigate the efficacy and tolerability of an initial therapy with the atypical antipsychotic agent risperidone in acutely exacerbated patients under the conditions of clinical practice. A sub-analysis was performed to show if highly agitated and aggressive patients may profit from an initial risperidone therapy as well. Material and Methods: In a still ongoing prospective multicentre observational trial, schizophrenic patients with acute exacerbations treated with risperidone within 24 hours of in-patient admission were observed for six weeks. Patients showing a total score of greater than or equal to 15 in the items,excitement\" \"hostility\" and \"uncooperativeness\" of the Positive and Negative Syndrome Scale (PANSS) were defined as highly agitated patients. Evaluation of efficacy was carried out according to a modified PANSS, the Clinical Global Impression (CGI) and the Brief Psychiatric Rating Scale (BPRS). Results: 1,117 patients were evaluated. An improvement of all parameters was shown in the whole study group (51% males, age 39.8 + 14.3 years, paranoid schizophrenia in 70.1% of cases) and in particular in the subgroup of highly agitated patients. In these patients (n = 163), a greater improvement of symptoms was observed. Only in 4,1% of cases was risperidone discontinued because of side effects. At the end of the observation, the mean dosage was 5.1 mg/day in both groups. More than 50% of the patients were finally treated with a risperidone monotherapy. Conclusion: The initial acute treatment with risperidone proves to be effective and safe even for highly agitated schizophrenic patients under the conditions of clinical practice."],["dc.identifier.doi","10.1055/s-2003-39063"],["dc.identifier.isi","000182999900005"],["dc.identifier.pmid","12740756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45982"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0720-4299"],["dc.title","Initial use of risperidone in the treatment of acutely exacerbated schizophrenic patients - An interim analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","293"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Clinical Psychopharmacology"],["dc.bibliographiccitation.lastpage","300"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Pajonk, Frank-Gerald B."],["dc.contributor.author","Schreiner, A."],["dc.contributor.author","Peters, S."],["dc.contributor.author","Rettig, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T10:57:42Z"],["dc.date.available","2018-11-07T10:57:42Z"],["dc.date.issued","2005"],["dc.description.abstract","Objective: Efficacy of atypical antipsychotic in acute schizophrenic episodes is still in debate. This study evaluated treatment practices over 7 years of initial treatment with oral risperidone in acutely exacerbated patients with schizophrenia and in a subgroup of highly agitated, tense, and aggressive patients. Additionally, the study investigated the efficacy and tolerability of risperidone in routine clinical practice. Methods: In a prospective, multicenter, observational trial from 1996 to 2002, patients with schizophrenia experiencing acute symptom exacerbations were treated with risperidone within 24 hours of inpatient admission. Patients with a total score of >= 15 points on the agitation subscale of the Positive and Negative Syndrome Scale (PANSS) were defined as highly agitated. Efficacy measures were carried out with a modified PANSS, the Clinical Global Impression (CGI) and the Brief Psychiatric Rating Scale (BPRS). Results: A total of 1625 patients were evaluated. Despite prescription of decreasing risperidone dosages over 7 years, efficacy was maintained and tolerability improved significantly. Significant symptom relief occurred in all patients and was more pronounced in the subgroup of highly agitated patients (n = 256; P < 0.001 for PANSS, BPRS, and CGI). At Week 6, the mean daily dosage of risperidone was 4.8 mg in the highly agitated patients and 4.7 mg in the remaining patients, and more than 55% of all patients were receiving risperidone as monotherapy. Conclusions: Prescribing patterns with risperidone in patients with acutely exacerbated schizophrenia, including highly agitated patients, changed with the experience gained with this compound. In routine clinical practice in this indication, risperidone was found to be effective and well tolerated."],["dc.identifier.doi","10.1097/01.jcp.0000170686.27476.ab"],["dc.identifier.isi","000230876800002"],["dc.identifier.pmid","16012270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50315"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0271-0749"],["dc.title","Risperidone - An open-label, observational study of the efficacy, tolerability, and prescribing behavior in acutely exacerbated patients with schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S79"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.lastpage","S83"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Grohmann, Renate"],["dc.contributor.author","Hauser, U."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Degner, Detlef"],["dc.date.accessioned","2018-11-07T10:50:59Z"],["dc.date.available","2018-11-07T10:50:59Z"],["dc.date.issued","2004"],["dc.description.abstract","The introduction of new antipsychotics has resulted in the availability of drugs with improved safety and tolerability as well as proven efficacy compared to the older antipsychotics. New compounds might show new or different adverse effects that arise in the post-marketing phase when a greater number of patients are treated. One goal of the drug safety program in psychiatry AMSP (Arzneimittelsicherheit in der Psychiatrie) is the detection and description of severe, new, or rare adverse drug reactions (ADRs). Between 1993 and 2000, 122,562 patients were monitored in 35 psychiatric institutions, 86,349 patients of which received antipsychotics. Hyperglycemia related to antipsychotics was observed in association with only two compounds so far: A clozapine and olanzapine (clozapine 2 cases, olanzapine 7 cases). In 6 of 9 patients, weight gain preceded hyperglycemia. The relative frequency of these adverse drug related events was 0.013% for clozapine and 0.075% for olanzapine. The symptomatology included reversible hyperglycemia, worsening of existing diabetes, and new-onset diabetes. Control for glycemic dysregulation should be maintained in clinical practice with these drugs."],["dc.identifier.doi","10.1055/s-2004-815514"],["dc.identifier.isi","000221126100012"],["dc.identifier.pmid","15052518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48780"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0176-3679"],["dc.title","Hyperglycemia associated with antipsychotic treatment in a multicenter drug safety project"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]