Pilz, Jürgen

[["dc.bibliographiccitation.firstpage","161"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","360"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Guan, Z."],["dc.contributor.author","Pohlmann, K."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.date.accessioned","2018-11-07T10:49:33Z"],["dc.date.available","2018-11-07T10:49:33Z"],["dc.date.issued","2004"],["dc.description.abstract","The pathophysiology of periodic leg movements (PLMs) in sleep remains to be elucidated. Among other hypotheses all alteration of dopaminergic function has been suggested. Nocturnal urinary dopamine and 4-hydroxy-3-methoxyphenylacetic acid excretion in otherwise healthy subjects with PLMs was significantly reduced (P < 0.001 and P < 0.05, respectively) compared to subjects without PLMs. This finding, for the first time, demonstrates a correlate of a functionally relevant hypoactivity of the dopaminergic system in subjects with PLMs. (C) 2004 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2004.02.056"],["dc.identifier.isi","000221141400013"],["dc.identifier.pmid","15082158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48459"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Nocturnal urinary dopamine excretion is reduced in otherwise healthy subjects with periodic leg movements in sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Meier, A."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Mayer, G."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:56:34Z"],["dc.date.available","2018-11-07T10:56:34Z"],["dc.date.issued","2005"],["dc.format.extent","252"],["dc.identifier.isi","000232591900119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50044"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","24th Symposium of the Arbeitsgemeinschaft-fur-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Evaluation of oxidative stress measurements in obstructive sleep apnea syndrome"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","239"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","254"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Meier, A."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Mayer, G."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:23:16Z"],["dc.date.available","2018-11-07T10:23:16Z"],["dc.date.issued","2006"],["dc.description.abstract","Assessment of reactive oxygen species (ROS) is highly important in neurodegenerative disorders and neuroleptic treatment. However, conflicting results have been reported, which may arise from methodological difficulties. Obstructive sleep apnea (OSA) syndrome with episodic hypoxia-reoxygenation is proposed as a human model for the investigation of ROS measurements. Despite a broad analytical approach comprising lipid peroxidation and amino acid oxidation products, oxidative DNA damage, and activity of the antioxidant defense, only plasma malondialdehyde (MDA) and urinary o,o'-dityrosine seemed to be appropriate, robust biomarkers of oxidative stress, which are also simple enough for routine clinical use. MDA concentrations correlated with a duration of nocturnal desaturation below 85% (r = 0.77, p < 0.0005), and o,o'-dityrosine levels decreased after therapy (p < 0.05) as a function of baseline concentrations (r = -0.61, p < 0.05). Gender effects in ROS generation also have to be considered. At present, we recommend the application of several oxidative stress measurements at different time points, preferably involving plasma MDA and urinary o,o'-dityrosine."],["dc.identifier.doi","10.1007/s00702-005-0316-2"],["dc.identifier.isi","000234752500013"],["dc.identifier.pmid","15959848"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42424"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Evaluation of oxidative stress measurements in obstructive sleep apnea syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neurologica Scandinavica"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Bleich, S."],["dc.contributor.author","Kropp, S."],["dc.contributor.author","Degner, D."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Gleiter, C. H."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Poser, S."],["dc.date.accessioned","2017-09-07T11:44:36Z"],["dc.date.available","2017-09-07T11:44:36Z"],["dc.date.issued","2000"],["dc.description.abstract","Objectives– Substantial evidence supports the hypothesis that oxygen free radicals are involved in various neurodegenerative disorders. To assess the presence of oxidative stress in Creutzfeldt–Jakob disease (CJD) we examined the concentrations of malondialdehyde (MDA) as an established marker of lipid peroxidation. Material and methods– MDA was quantified by high performance liquid chromatography (HPLC) in cerebrospinal fluid (CSF; n=12) and in serum (n=11) samples of CJD patients and healthy controls (n=15). Results– Mean values in healthy controls: 2.56 nmol/ml±0.46 (CSF) and 1.94 nmol/ml±0.67 (serum); mean values in CJD patients: 2.64 nmol/ml±0.67 (CSF) and 1.68 nmol/ml±0.79 (serum). No significant (P>0.05) difference between CJD patients and controls was observed. Conclusions– The results indicated that the CSF and serum of CJD patients showed no higher endogenous levels of MDA as compared to normal healthy controls. These findings provide no evidence for an additional role of oxidative stress in the pathogenetic mechanism underlying CJD neurodegeneration."],["dc.identifier.doi","10.1034/j.1600-0404.2000.9s290a.x"],["dc.identifier.gro","3151697"],["dc.identifier.pmid","10987323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8516"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0001-6314"],["dc.title","Creutzfeldt-Jakob disease and oxidative stress"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Nolte, Wilhelm"],["dc.contributor.author","von Heppe, J."],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Hajak, G."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Ramadori, G."],["dc.contributor.editor","Hüther, Gerald"],["dc.contributor.editor","Kochen, Walter"],["dc.contributor.editor","Simat, Thomas J."],["dc.contributor.editor","Steinhart, Hans"],["dc.date.accessioned","2017-09-07T11:44:27Z"],["dc.date.available","2017-09-07T11:44:27Z"],["dc.date.issued","2011"],["dc.description.abstract","Neuropsychiatric symptoms due to any type of dysfunction and/or portal-systemic shunting are summarized as hepatic encephalopathy (HE). HE in the presence of liver cirrhosis and/or portal-systemic shunting has been termed portal-systemic encephalopathy (PSE). PSE is most frequent among the HE syndromes and is almost exclusively seen in patients with advanced cirrhosis and portal hypertension. Portal-systemic shunting either spontaneous due to portal hypertension, following surgical portocaval anastomosis, or subsequent to transjugular intrahepatic portosystemic stent-shunt (TIPSS) is regarded as the primary causative condition for PSE, not hepatic dysfunction per se. PSE may be considered as a disorder of multiple neurotransmitter systems among which derangements of the seroton-ergic system have been documented most consistently. Incipient PSE is frequently paralleled by the occurence of sleep disorders, however, their relation to PSE remains unclear. We observed a transient increase of sleep disorders post-TIPSS, which were only in part correlated to other symptoms of PSE. Among the biochemical parameters studied only an association between arterial ammonia levels and sleep disorders became apparent, whereas no significat relation was observed for peripheral tryptophan."],["dc.identifier.doi","10.1007/978-1-4615-4709-9_22"],["dc.identifier.gro","3151664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8481"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.publisher","Springer"],["dc.publisher.place","Boston, MA"],["dc.relation.crisseries","Advances in Experimental Medicine and Biology"],["dc.relation.isbn","978-1-4613-7133-5"],["dc.relation.ispartof","Advances in Experimental Medicine and Biology"],["dc.relation.ispartofseries","Advances in Experimental Medicine and Biology"],["dc.relation.issn","0065-2598"],["dc.title","Sleep Disorders and Portal-Systemic Encephalopathy Following Transjugular Intrahepatic Portosystemic Stent Shunt in Patients with Liver Cirrhosis"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","163"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.lastpage","167"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Bock, Nathalie"],["dc.contributor.author","Moll, Gunther H."],["dc.contributor.author","Wicker, M."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Rothenberger, A."],["dc.date.accessioned","2018-11-07T10:47:54Z"],["dc.date.available","2018-11-07T10:47:54Z"],["dc.date.issued","2004"],["dc.description.abstract","Background: The benzamide tiapride, a selective dopamine D2/D3-receptor antagonist, can be used effectively in children to treat tic disorders and stuttering. Tiapride is a clinically safe substance (even during long-term treatment and when given to young children). Unfortunately, its probable effects on general brain development and the maturation of the dopaminergic system have not been investigated. Thus, important information for drug treatment in children is missing. Therefore, this study in rats describes tiapride's effects on several parameters of dopaminergic activity (dopamine transporter, D2 receptor, dopamine, DOPAC, and homovanillic acid in the striatum) seen after tiapride administration (30 mg/kg/day) to prepubertal (from day 25-39) and postpubertal (from day 50-64) rats. Methods: Three groups of rats (n = 6) received tiapride within their drinking water for 14 days. Two groups were treated before puberty; one of those was killed at day 50, the other at day 90. The group treated after puberty was measured at day 90. A fourth group (n = 6) was treated from day 50 to day 53 and measured under tiapride at day 53. Changes were measured by ligand-binding assays (K-D and B-max values of dopamine transporter by [H-3]-GBR binding and D2 receptor by [H-3]-spiperone binding) and by HPLC (concentrations of dopamine, DOPAC, and homovanillic acid). Results: The density of dopamine transporters and D2 receptors remained unaffected after early (day 25) and late (day 50) tiapride administration. Only during the treatment period could a significant reduction of D2-receptor binding (displacement of spiperone) and of dopamine and DOPAC levels be stated. Conclusions: These data suggest that tiapride treatment during postnatal brain development causes no long-lasting changes in the development of the central dopaminergic system and is in line with clinical experience in children."],["dc.identifier.doi","10.1055/s-2004-827171"],["dc.identifier.isi","000222642000005"],["dc.identifier.pmid","15467972"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48074"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0176-3679"],["dc.title","Early administration of tiapride to young rats without long-lasting changes in the development of the dopaminergic system"],["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","Bleich, Stefan"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T09:30:09Z"],["dc.date.available","2018-11-07T09:30:09Z"],["dc.date.issued","2000"],["dc.format.extent","371S"],["dc.identifier.isi","000165731700530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31234"],["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","Lipid peroxidation after electroconvulsive therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]