Bleich, Stefan

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.date.accessioned","2018-11-07T08:51:05Z"],["dc.date.available","2018-11-07T08:51:05Z"],["dc.date.issued","2000"],["dc.format.extent","215"],["dc.identifier.doi","10.1093/alcalc/35.2.215"],["dc.identifier.isi","000087531200017"],["dc.identifier.pmid","10787401"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21847"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Reversal of ethanol-induced hepatic steatosis and lipid peroxidation by taurine: A study in rats"],["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","296"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","299"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Wilhelm, Julia"],["dc.contributor.author","Frieling, Helge"],["dc.contributor.author","Hillemacher, Thomas"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:15:16Z"],["dc.date.available","2018-11-07T11:15:16Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims: The individual extent of structural brain tissue changes in patients with alcohol dependence is influenced by genetic factors, gender, age and possibly a dose/duration-effect. Aim of the present study was to investigate different types of alcoholic beverages with regard to hippocampal volume loss in patients suffering from alcoholism. Methods: We included 52 patients with alcohol dependence and divided them according to their preferred type of beverage consumption (beer, wine, and spirits). Hippocampal volumes were determined using volumetric high-resolution MR imaging. Results: There was a significant difference in hippocampal volumes between patients consuming different beverages (ANOVA: F = 7.454; df = 2; P = 0.0015) with the smallest volumes in the wine group, followed by the spirits group. Furthermore, patients with a preferred spirits consumption showed significantly higher plasma homocysteine levels (ANOVA: F = 3.39; df = 2; P = 0.042). Linear regression analyses revealed an association of homocysteine and hippocampal volume only in the group of patients preferring spirits (R(2) = 0.364; P = 0.008). Conclusions: Homocysteine-mediated excitotoxicity may be an important pathophysiological mechanism in ethanol-related brain damage, particularly in patients consuming wine and spirits. The extent of brain atrophy in beer consuming patients seems to be more moderate."],["dc.identifier.doi","10.1093/alcalc/agn002"],["dc.identifier.isi","000255756300008"],["dc.identifier.pmid","18238850"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54329"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0735-0414"],["dc.title","Hippocampal volume loss in patients with alcoholism is influenced by the consumed type of alcoholic beverage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.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","857"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Bleich, S."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Maler, M."],["dc.contributor.author","Parsons, C. G."],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","2002"],["dc.description.abstract","The spectrum of action of flupirtine includes analgesia, muscle relaxation and neuroprotection. N-methyl-D-aspartate (NMDA) receptor antagonism has been discussed as a possible mechanism of action of this compound with little direct evidence. The objective of the present study was to develop a plausible model to explain flupirtine's spectrum of action. A four-stage strategy was selected for this purpose: Firstly, the serum concentration of flupirtine under therapeutic conditions was determined on the basis of the current literature. The second stage involved assessing the known in-vitro effects in light of the therapeutic active concentration. Using whole cell patch clamp recordings from cultured rat superior colliculus neurones interactions between flupirtine and NMDA receptors were assessed. Only very high concentrations of flupirtine antagonized inward currents to NMDA (200 μM) at −70 mV with an lC50 against steady-state responses of 182.1 ± 12.1 μM. The effects of flupirtine were voltage-independent and not associated with receptor desensitization making actions within the NMDA receptor channel or at the glycine modulatory site unlikely. NMDA receptor antagonism probably has little relevance for the clinical efficacy of flupirtine as the concentrations needed were far higher than those achieved in clinical practice. However, the activation of a G-protein-regulated inwardly rectifying K+ channel was identified as an interesting molecular target site of flupirtine. In the next stage, the central nervous spectrum of action of experimental K+ channel openers (PCO) was considered. As far as they have been studied, experimental K+ channel openers display a spectrum of action comparable to that of flupirtine. In the final stage, a global model was developed in which flupirtine stabilizes the resting membrane potential by activating inwardly rectifying K+ channels, thus indirectly inhibiting the activation of NMDA receptors. The model presented here reconciles the known functional NMDA receptor antagonism of flupirtine with the activation of K+ channels that occurs at therapeutic concentrations, thus providing an understanding of flupirtine's spectrum of action. This makes flupirtine the prototype of a clinically applicable substance group with analgesic, muscle-relaxant and neuroprotective properties."],["dc.identifier.doi","10.1007/s007020050206"],["dc.identifier.gro","3151702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8521"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0300-9564"],["dc.title","Flupirtine shows functional NMDA receptor antagonism by enhancing Mg 2+ block via activation of voltage independent potassium channels"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","948"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Canadian Journal of Psychiatry"],["dc.bibliographiccitation.lastpage","952"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Tichauer, G. A."],["dc.contributor.author","Spath, C."],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T11:20:34Z"],["dc.date.available","2018-11-07T11:20:34Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: The association between separation anxiety in childhood and actual separation experiences during childhood has not yet been investigated in patients with panic disorder. Methods: In 115 patients with panic disorder with or without agoraphobia and in 124 control subjects without a history of psychiatric illness, we assessed separation anxiety during childhood, retrospectively, using DSM-IV and ICD-10 criteria and the Separation Anxiety Symptom Inventory (SASI). In addition, actual separation experiences from age 0 to 15 years were assessed, retrospectively. Results: A total of 22.6% of the patients and 4.8% of the Control subjects fulfilled both DSM-IV and ICD-10 criteria for childhood separation anxiety (chi(2) = 11.8; P < 0.0001). Further, 57.4% ofthepatients and 37.9% of the control subjects reported actual separation experiences during their childhood (chi(2) = 9. 09, P < 0.003). Separation anxiety and actual separation experiences, however, were independent of each other. Conclusion: These results suggest that separation anxiety during childhood is not a consequence of actual traumatic separation experiences in panic disorder patients."],["dc.identifier.isi","000173099800007"],["dc.identifier.pmid","11816316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Canadian Psychiatric Assoc"],["dc.relation.issn","0706-7437"],["dc.title","Separation anxiety and actual separation experiences during childhood in patients with panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","269"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neurosciences"],["dc.bibliographiccitation.lastpage","271"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schenk-Daprá, Bettina"],["dc.contributor.author","Stiens, Gerthild"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Müller, Peter"],["dc.contributor.author","Niedmann, Paul Dieter"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Rüther, Eckart"],["dc.date.accessioned","2017-09-07T11:44:42Z"],["dc.date.available","2017-09-07T11:44:42Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective The goal of this study was to identify adverse effects of the atypical neuroleptic clozapine on liver function and lipid metabolism. Methods Data which included serum levels of clozapine and its hepatic metabolite N-desmethyl clozapine were collected from medical records of patients treated with clozapine and controls. Results We identified a clozapine-associated marked elevation of plasma cholinesterase (ChE) with unchanged levels of AST, ALT or g-GT. ChE was correlated to the serum level of clozapine and even closer to N-desmethyl clozapine. For the total patient group we observed significant correlations of ChE with the body-mass index and body weight. However, clozapine-treated patients and controls did not differ with regard to body-mass index, triglycerides, and cholesterol. Conclusion We report for the first time a clozapine-associated and dose-dependent elevation of plasma ChE, which may be related to clozapine-associated effects on hepatic lipid metabolism or ChE enzyme induction."],["dc.identifier.doi","10.1007/pl00007544"],["dc.identifier.gro","3151720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8541"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0940-1334"],["dc.title","Clozapine-associated elevation of plasma cholinesterase"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]