Stiens, Gerthild

[["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Stoppe, Gabriela"],["dc.contributor.author","Linkersdrfer, V."],["dc.contributor.author","Maeck, L."],["dc.contributor.author","Stiens, G."],["dc.date.accessioned","2018-11-07T11:04:22Z"],["dc.date.available","2018-11-07T11:04:22Z"],["dc.date.issued","2007"],["dc.format.extent","S41"],["dc.identifier.isi","000245473000150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51829"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier France-editions Scientifiques Medicales Elsevier"],["dc.publisher.place","Paris"],["dc.relation.issn","0924-9338"],["dc.title","Filial maturity as predictor of caregiver burden in adult children of demented patients"],["dc.type","conference_abstract"],["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"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Platzer, Anja"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Stiens, G."],["dc.date.accessioned","2018-11-07T08:32:05Z"],["dc.date.available","2018-11-07T08:32:05Z"],["dc.date.issued","2009"],["dc.format.extent","324"],["dc.identifier.isi","000263520200311"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17262"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","36th Annual Meeting of the Arbeitsgemeinschaft-Dermatologishche-Forschung"],["dc.relation.eventlocation","Heidelberg, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Psychosocial distress in psoriatic out-patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","671"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Ruether, Eckhart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T11:01:11Z"],["dc.date.available","2018-11-07T11:01:11Z"],["dc.date.issued","2007"],["dc.description.abstract","Biomarkers for differential diagnosis of the three most frequent degenerative forms of dementia, Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and frontotemporal dementias (FTD), are currently under intensive investigation, but disease-specific biomarkers for FTD and DLB are still lacking. We analyzed 303 cerebrospinal fluid (CSF) samples of 71 AD, 32 DLB and 36 FTD patients in comparison to 93 various other dementias (OD), 20 peripheral neurologic disease (PND) controls, 25 neurodegenerative disorders without dementia (ND) and 26 depressive cognitive complainers (DCC) for distinct CSF amyloid-beta (Ab) peptide patterns, using the quantitative A beta-SDS-PAGE/immunoblot. Additionally, the novel electrochemiluminescence technique (MSD) was used to validate the measures on A beta 1-38. The main outcome measures were a striking decrease of A beta 1-42 in AD ( P = 7.4 x 10(-19)), and most interestingly a pronounced decrease of A beta 1-38 in FTD ( P = 9.6 x 1 0(-7)). Moreover, a novel peptide that most probably represents an oxidized alpha-helical form of A beta 1-40 (A beta 1-40(ox)) displayed a highly significant increase in DLB ( P = 3.7 x 10(-3)) as compared to non-demented disease controls. The overall diagnostic accuracy of percentage Ab peptide abundances (A beta 1-X%) was clearly superior to absolute CSF Ab levels. A beta 1-42% and A beta 1-38% enabled contrasts of 85% or beyond to distinguish AD and FTD, respectively, from all other investigated subjects. A beta 1-40(ox)% yielded a diagnostic sensitivity and specificity of 88 and 73% for the detection of DLB among all other investigated patients. We found a strong correlation between A beta 1-38 levels as measured by the A beta-SDS-PAGE/immunoblot and MSD, respectively. CSF A beta peptides may reflect disease-specific impact of distinct neurodegenerative processes on A beta peptide metabolism and represent a potential diagnostic biomarker for AD, FTD and DLB."],["dc.identifier.doi","10.1038/sj.mp.4001967"],["dc.identifier.isi","000247619700009"],["dc.identifier.pmid","17339876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51089"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","Validation of amyloid-beta peptides in CSF diagnosis of neurodegenerative dementias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1544"],["dc.bibliographiccitation.issue","28-29"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.lastpage","1546"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Stoppe, Gabriela"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Staedt, J."],["dc.date.accessioned","2018-11-07T10:37:40Z"],["dc.date.available","2018-11-07T10:37:40Z"],["dc.date.issued","2003"],["dc.identifier.isi","000184113500007"],["dc.identifier.pmid","12854065"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45627"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0012-0472"],["dc.title","Dementia - treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0304-3940(02)00968-0"],["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","333"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Stoppe, Gabriela"],["dc.contributor.author","Maeck, Lienhard"],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Stiens, Gerthild"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T09:49:14Z"],["dc.date.available","2018-11-07T09:49:14Z"],["dc.date.issued","2002"],["dc.description.abstract","Primary progressive aphasia (PPA) is a clinical syndrome characterized by a slowly progressive aphasia in the absence of accompanying signs of generalized dementia. While non-fluent PPA tends to progress frontally and is usually linked to frontotemporal degeneration, fluent PPA might be associated with both, frontotemporal degeneration or Alzheimer's disease. Although recent reports suggest that PPA belongs neuropathologically to the group of tauopathias, cerebrospinal fluid analysis has not been established as a means of diagnosis in PPA so far. In this paper we investigated Abeta peptide(1-42) (Abeta(1-42)), Tau protein and S-100B protein level in the cerebrospinal fluid of three patients with PPA. In all patients Tau protein and S-100B level were slightly elevated, however, Abeta(1-42) was found to be in normal range. Thus, our first results point to PPA being neurochemically linked to frontotemporal degeneration. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(02)00968-0"],["dc.identifier.gro","3151712"],["dc.identifier.isi","000179043400009"],["dc.identifier.pmid","12401554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35465"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","A beta peptide(1-42), Tau protein and S-100B protein level in cerebrospinal fluid of three patients with primary progressive aphasia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","443"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","447"],["dc.bibliographiccitation.volume","301"],["dc.contributor.author","Moessner, Rotraut"],["dc.contributor.author","Stiens, Gerthild"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Schmidt, Diane"],["dc.contributor.author","Platzer, Anja"],["dc.contributor.author","Krueger, Ullrich"],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T08:27:58Z"],["dc.date.available","2018-11-07T08:27:58Z"],["dc.date.issued","2009"],["dc.description.abstract","Serotonin is a monoamine acting as a neuromediator in the central and peripheral nervous system. Recently, serotonin has also been shown to influence T- and B-cell function. The serotonin transporter is central in the regulation of the serotonergic system and widely expressed on cells of the immune system. A functional length polymorphism in the promoter of the serotonin transporter gene (5-HTTLPR) has been implicated in the genetic background of depression. Psoriasis is a complex disease with a polygenetic inheritance. In light of the role of T-cell mediated inflammation in psoriasis and the increased prevalence of depression in psoriatic patients, we analyzed the 5-HTTLPR polymorphism in 309 patients with psoriasis vulgaris and 315 healthy control individuals. No significant differences in genotype distribution and allele frequencies were found. There was also no difference in the score of the Hamilton Rating Scale for Depression in patients with psoriasis (n = 137) characterized by carriage of different 5-HTTLPR genotypes. These findings argue against a major contribution of the 5-HTTLPR polymorphism to psoriasis susceptibility and the occurrence of depressive symptoms among psoriatic patients."],["dc.description.sponsorship","Deutscher Psoriasis Bund"],["dc.identifier.doi","10.1007/s00403-008-0909-3"],["dc.identifier.isi","000267389100005"],["dc.identifier.pmid","18979110"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16317"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Analysis of a functional serotonin transporter promoter polymorphism in psoriasis vulgaris"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","933"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","948"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Neubert, K."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T09:19:19Z"],["dc.date.available","2018-11-07T09:19:19Z"],["dc.date.issued","2005"],["dc.description.abstract","Measuring proteins in cerebrospinal fluid (CSF) has gained wide acceptance for the differential diagnosis of dementia. Some groups have already extended these investigations in Alzheimer's disease (AD) by asking how stable these markers are in follow-up analysis, if they depend on the stage of disease and whether they can be used to monitor the progression and biological effects of treatment. We evaluated 21 patients with dementia with Lewy bodies (DLB) and 19 patients with AD, on two occasions, with regard to levels of tau protein, tau protein phosphorylated at threonine 181 (p-tau), A beta 42, A beta 40 and S-100B protein, using a set of commercially available assays. Tau protein levels were lower in DLB in first and second LP compared to AD and decreased during course of both groups. P-tau levels were increased in AD and DLB and decreased during follow-up. A beta 42 and A beta 40 remained relatively stable during follow-up but we found a slight increase of the median A beta 42 level in DLB, whereas in AD, A beta 42 tends to decrease during follow-up. S-100B protein increased during follow-up in both diseases. The protein dynamics in DLB and AD are relatively similar. S-100B protein may be a useful marker for follow-up in neurodegenerative diseases but has to be analysed in longer follow-up periods. Tau protein may be used to differentiate between DLB and AD. Follow-up CSF analyses are of limited value for the differentiation of AD and DLB. We conclude that more specific markers have to be established for the differentiation and follow-up of these diseases."],["dc.identifier.doi","10.1007/s00702-004-0235-7"],["dc.identifier.isi","000229624600008"],["dc.identifier.pmid","15937638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28602"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Follow-up investigations in cerebrospinal fluid of patients with dementia with Lewy bodies and Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Moebner, R."],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Bartkowiak, A."],["dc.contributor.author","Schmidt, D."],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Westphal, G."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T11:04:23Z"],["dc.date.available","2018-11-07T11:04:23Z"],["dc.date.issued","2007"],["dc.format.extent","206"],["dc.identifier.isi","000244056600045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51833"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","34th Annual Meeting of the Arbeitsgemeinschaft-Dermatologische-Forschung"],["dc.relation.eventlocation","Freiburg, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Analysis of a functional serotonin transporter polymorphism in psoriasis vulgaris"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1419"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","British Journal of Dermatology"],["dc.bibliographiccitation.lastpage","1420"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Stiens, G."],["dc.contributor.author","Platzer, Anja"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Moessner, R."],["dc.date.accessioned","2018-11-07T11:08:22Z"],["dc.date.available","2018-11-07T11:08:22Z"],["dc.date.issued","2008"],["dc.identifier.isi","000261134100133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52763"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","5th International Congress on Psoriasis - From Gene to Clinic"],["dc.relation.eventlocation","Royal Coll Phys, London, ENGLAND"],["dc.relation.issn","0007-0963"],["dc.title","Psychosocial distress in psoriatic outpatients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]