Ahsen, Nicolas von

[["dc.bibliographiccitation.firstpage","306"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","SLAS TECHNOLOGY Translating Life Sciences Innovation"],["dc.bibliographiccitation.lastpage","327"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Eckardstein, Arnold von"],["dc.contributor.author","Roth, Hans Jürgen"],["dc.contributor.author","Jones, Graham"],["dc.contributor.author","Preston, Sharon"],["dc.contributor.author","Szekeres, Thomas"],["dc.contributor.author","Imdahl, Roland"],["dc.contributor.author","Conti, Marc"],["dc.contributor.author","Blanckaert, Norbert"],["dc.contributor.author","Jose, Darren"],["dc.contributor.author","Thiery, Joachim"],["dc.contributor.author","Feldmann, Lisa"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Locatelli, Massimo"],["dc.contributor.author","Kremastinou, Jenni"],["dc.contributor.author","Kunst, Albert"],["dc.contributor.author","Hubbuch, Arnulf"],["dc.contributor.author","McGovern, Margaret"],["dc.date.accessioned","2018-11-07T09:21:38Z"],["dc.date.available","2018-11-07T09:21:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Clinical laboratories need to test patient samples precisely, accurately, and efficiently. The latest member of the Roche cobas modular platform family, the cobas 8000 modular analyzer series allows compact and convenient consolidation of clinical chemistry and immunochemistry assays in high-workload laboratories with a throughput of 3 to 15 million tests annually. Here we present the results of studies designed to test the overall system performance under routine-like conditions that were conducted at 14 laboratories over 2 y. Experiments that test analytical performance of the new module were integrated with overall system functionality testing of all modules in different configurations. More than two million results were generated and evaluated for similar to 100 applications using serum/plasma, urine, or EDTA blood samples. During the workflow studies, eight configurations of the possible 38 combinations were used, covering all available analytical modules. The versatility of the module combinations makes the system customizable to fit the needs of diverse laboratories, allowing precise and accurate analysis of a broad spectrum of clinical chemistry and immunochemistry parameters with short turnaround times. This new system will contribute to the ability of clinical laboratories to offer better service to their customers and support vital clinical decision making."],["dc.description.sponsorship","Roche"],["dc.identifier.doi","10.1177/2211068212472183"],["dc.identifier.isi","000326448100007"],["dc.identifier.pmid","23321915"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29156"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1540-2452"],["dc.relation.issn","2211-0682"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","cobas 8000 Modular Analyzer Series Evaluated under Routine-like Conditions at 14 Sites in Australia, Europe, and the United States"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","41"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Guerchet, Maelenn"],["dc.contributor.author","Houinato, Dismand"],["dc.contributor.author","Paraiso, Moussiliou Noel"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Nubukpo, Philippe"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Clement, Jean-Pierre"],["dc.contributor.author","Preux, Pierre-Marie"],["dc.contributor.author","Dartigues, Jean-Francos"],["dc.date.accessioned","2018-11-07T08:34:21Z"],["dc.date.available","2018-11-07T08:34:21Z"],["dc.date.issued","2009"],["dc.description.abstract","Background/Aims: Dementia is increasing as a priority public health problem because of the ageing of the world population. Our goal was to estimate dementia and cognitive impairment prevalence in an elderly population of rural Benin. Methods: In a door-to-door survey, elderly people aged 65 years and above were screened using the Community Screening Interview for Dementia and the Five-Word Test. Results: The prevalence of cognitive impairment was 10.4% and that of dementia was 2.6%. Age, current depressive disorder and absence of the APOE epsilon 2 allele were significantly associated with cognitive impairment. Conclusion: Prevalence of dementia and cognitive impairment appears to be lower in this study than in developed countries. Copyright (c) 2009 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000188661"],["dc.identifier.isi","000262899200005"],["dc.identifier.pmid","19136831"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17790"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cognitive Impairment and Dementia in Elderly People Living in Rural Benin, West Africa"],["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","371"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","378"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Redyk, Katharina"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krack, Lennart A."],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:47:31Z"],["dc.date.available","2018-11-07T08:47:31Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: To characterize clinical features, CSF biomarkers and genetic polymorphisms of patients suffering from a rapidly progressing subtype of Alzheimer's dementia (rpAD). Methods: Retrospective analyses of 32 neuropathologically confirmed cases differentially diagnosed as AD out of a group with rapidly progressive dementia. CSF biomarkers (14-3-3, tau, beta-amyloid 1-42) and genetic markers (PRNP codon 129, apolipoprotein E, ApoE, polymorphism) were determined. Results: Median survival was 26 months, age at onset 73 years. Biomarkers: mean beta-amyloid 1-42: 266 pg/ml, median tau: 491 pg/ml, 14-3-3 positive: 31%. Genetic polymorphisms showed a predominance of methionine homozygosity at PRNP codon 129 and a low frequency of ApoE4 (38%, no homozygous patients). Thirty-five symptoms were studied. Frequent symptoms were myoclonus (75%), disturbed gait (66%) and rigidity (50%). Discussion: rpAD is associated with a diversity of neurological signs even able to mimic Creutz feldt-Jakob disease. Biomarkers and genetic profile differ from those seen in classical AD. The findings on biomarkers, symptomatology and genetics may aid the differential diagnostic process. Copyright (C) 2010 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000278692"],["dc.identifier.isi","000278130700012"],["dc.identifier.pmid","20453509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Clinical Features of Rapidly Progressive Alzheimer's Disease"],["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","2517"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2530"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Cotte, S."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Huber, B."],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Starck, Michaela"],["dc.contributor.author","Koenig, N."],["dc.contributor.author","Tellez, N."],["dc.contributor.author","Doerr, J."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Koepsell, Hermann"],["dc.contributor.author","Pannek, H."],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, A."],["dc.date.accessioned","2018-11-07T11:24:34Z"],["dc.date.available","2018-11-07T11:24:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Escalation therapy with mitoxantrone (MX) in highly active multiple sclerosis is limited by partially dose-dependent side-effects. Predictors of therapeutic response may result in individualized risk stratification and MX dosing. ATP-binding cassette-transporters ABCB1 and ABCG2 represent multi-drug resistance mechanisms involved in active cellular MX efflux. Here, we investigated the role of ABC-gene single nucleotide polymorphisms (SNPs) for clinical MX response, corroborated by experimental in vitro and in vivo data. Frequencies of ABCB1 2677GT, 3435CT and five ABCG2-SNPs were analysed in 832 multiple sclerosis patients (Germany, Spain) and 264 healthy donors. Using a flow-cytometry-based in vitro assay, MX efflux in leukocytes from individuals with variant alleles in both ABC-genes (designated genotype ABCB1/ABCG2-L(ow), 22.2 of patients) was 37.7 lower than from individuals homozygous for common alleles (ABCB1/ABCG2-H(igh), P 0.05, 14.8 of patients), resulting in genotype-dependent MX accumulation and cell death. Addition of glucocorticosteroids (GCs) inhibited MX efflux in vitro. ABC-transporters were highly expressed in leukocyte subsets, glial and neuronal cells as well as myocardium, i.e. cells/tissues potentially affected by MX therapy. In vivo significance was further corroborated in experimental autoimmune encephalomyelitis in Abcg2(/) animals. Using a MX dose titrated to be ineffective in wild-type animals, disease course and histopathology in Abcg2(/) mice were strongly ameliorated. Retrospective clinical analysis in MX monotherapy patients (n 155) used expanded disability status scale, relapse rate and multiple sclerosis functional composite as major outcome parameters. The clinical response rate [overall 121 of 155 patients (78.1)] increased significantly with genotypes associated with decreasing ABCB1/ABCG2-function [ABCB1/ABCG2-H 15/24 (62.5) responders, ABCB1/ABCG2-I(ntermediate) 78/98 (79.6), ABCB1/ABCG2-L 28/33 (84.8), exact Cochran-Armitage test P 0.039]. The odds ratio for response was 1.9 (95 CI 1.03.5) with each increase in ABCB1/ABCG2 score (from ABCB1/ABCG2-H to I-, and I to L). In 36 patients with severe cardiac or haematological side effects no statistically relevant difference in genotype frequency was observed. However, one patient with biopsy proven cardiomyopathy only after 24 mg/m(2) MX exhibited a rare genotype with variant, partly homozygous alleles in 3 ABC-transporter genes. In conclusion, SNPs in ABC-transporter genes may serve as pharmacogenetic markers associated with clinical response to MX therapy in multiple sclerosis. Combined MX/GC-treatment warrants further investigation."],["dc.description.sponsorship","Merck Serono, Germany"],["dc.identifier.doi","10.1093/brain/awp164"],["dc.identifier.isi","000269963600021"],["dc.identifier.pmid","19605531"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56436"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","ABC-transporter gene-polymorphisms are potential pharmacogenetic markers for mitoxantrone response in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Ophthalmic Research"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Roedl, J. B."],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Schloetzer-Schrehardt, Ursula"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Naumann, G. O. H."],["dc.contributor.author","Kruse, F. E."],["dc.contributor.author","Juenemann, A. G. M."],["dc.date.accessioned","2018-11-07T11:20:31Z"],["dc.date.available","2018-11-07T11:20:31Z"],["dc.date.issued","2008"],["dc.description.abstract","Aims: We assessed homocysteine (Hcy) levels in tear fluid and plasma of patients with primary open-angle glaucoma (POAG). We determined the association between Hcy levels, dry eye syndrome and B vitamin status. Methods: This prospective case-control study included 36 patients with POAG and 36 controls. Hcy concentrations were measured by high-performance liquid chromatography. Results: Patients with POAG had significantly higher mean Hcy levels both in tear fluid (205 +/- 84 nmol/l; p < 0.001, t test) and in plasma (13.43 +/- 3.53 mu mol/l; p = 0.001, t test) than control subjects (130 +/- 53 nmol/l and 10.50 +/- 3.33 mu mol/l, respectively). Hcy in tear fluid was significantly correlated with plasma Hcy in POAG patients (r = 0.459; p = 0.005, Pearson's correlation), but not in controls (r = 0.068; p = 0.695). POAG patients with dry eye disease had significantly higher Hcy levels both in tear fluid and plasma than POAG patients without dry eye disease. There was no association between Hcy levels and B vitamin status in subjects with POAG. Conclusions: The study suggests increased Hcy levels in tear fluid and plasma of patients with POAG. Elevated Hcy levels might be a risk factor for POAG and dry eye syndrome in subjects with glaucoma. Copyright (C) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000127832"],["dc.identifier.isi","000258318600006"],["dc.identifier.pmid","18437035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9359"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55551"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0030-3747"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Increased homocysteine levels in tear fluid of patients with primary open-angle glaucoma"],["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","310"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International journal of molecular epidemiology and genetics"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Karunajeewa, Harin A."],["dc.contributor.author","Gomorrai, Servina"],["dc.contributor.author","Ura, Alice"],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Davis, Timothy M. E."],["dc.contributor.author","Mueller, Ivo"],["dc.contributor.author","Ilett, Kenneth F."],["dc.contributor.author","Oellerich, Michael"],["dc.date.accessioned","2019-07-10T08:13:37Z"],["dc.date.available","2019-07-10T08:13:37Z"],["dc.date.issued","2010"],["dc.description.abstract","PURPOSE: A high frequency of previously unknown CYP2D6 alleles have been reported in Oceania populations. Genetic and functional properties of these alleles remain unknown. METHODS: We performed analyses of the genetic variability of CYP2D6 and CYP2C19 genes using AmpliChip genotyping in cohorts from two distinct Papua New Guinea (PNG) populations (Kunjingini, n=88; Alexishafen, n=84) focussing on the genetic characterisation of PNG-specific alleles by re-sequencing. RESULTS: Previously unknown CYP2D6 alleles have population frequencies of 24% (Kunjingini) and 12% (Alexishafen). An allele similar to CYP2D6 1, but carrying the 1661G>C substitution, was the second most frequent CYP2D6 allele (20% Kunjingini and 10% Alexishafen population frequency). Sequencing suggests the CYP2D6 1661G>C allele originated from a cross-over between CYP2D6 1 and 2 and thus is predicted to confer fully active CYP2D6 enzyme. Two additional predicted full activity alleles [1661G>C;4180G>C] and 31G>A were found in the Kunjingini cohort (frequencies 3 c/c and 1%, respectively) and a novel predicted reduced activity allele [100C>T;1039C>T] was found in the Alexishafen cohort (frequency 2%). A high frequency of ultra-rapid (15%) and notably low frequencies of intermediate and poor CYP2D6 metabolizers (<5%) and a high frequency of poor CYP2C19 metabolizers were observed in PNG. Both CYP2D6 and CYP2C19 showed heterozygote excess that may be explained by exogamy and recent introduction of alleles by migration that are yet to reach HWE in relatively isolated populations. CONCLUSION: The CYP2D6 1661 allele common in Oceania may be regarded as functionally equivalent to the full activity CYP2D6 1 allele."],["dc.identifier.fs","576822"],["dc.identifier.pmid","21532842"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61291"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1948-1756"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","CYP2D6 and CYP2C19 in Papua New Guinea: High frequency of previously uncharacterized CYP2D6 alleles and heterozygote excess."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1625"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","International Journal of Colorectal Disease"],["dc.bibliographiccitation.lastpage","1627"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Ertmer, Christian"],["dc.contributor.author","Mardin, Wolf Arif"],["dc.contributor.author","Brüwer, Matthias"],["dc.contributor.author","Schiller, Meinhard"],["dc.contributor.author","Kemper, Stefanie"],["dc.contributor.author","Ahsen, Nicolas"],["dc.contributor.author","Hahnenkamp, Klaus"],["dc.date.accessioned","2019-07-09T11:53:48Z"],["dc.date.available","2019-07-09T11:53:48Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1007/s00384-011-1183-y"],["dc.identifier.fs","583857"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60496"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Severe immunosuppression in inflammatory bowel disease: opening the floodgates to opportunists?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3325"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","3329"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Brandhorst, Gunnar"],["dc.contributor.author","Petrova, Darinka Todorova"],["dc.contributor.author","Weigand, Sebastian"],["dc.contributor.author","Eberle, Christoph"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Schmitz, Jessica"],["dc.contributor.author","Schultze, Frank Christian"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Karaus, Michael"],["dc.contributor.author","Oellerich, Michael"],["dc.contributor.author","Walson, Philip D."],["dc.date.accessioned","2018-11-07T09:59:29Z"],["dc.date.available","2018-11-07T09:59:29Z"],["dc.date.issued","2015"],["dc.description.abstract","AIM: To compare the number of regulatory T-cells (Tregs) measured by flow cytometry with those obtained using a real-time quantitative PCR (qPCR) method in patients suffering from inflammatory bowel disease (IBD). METHODS: Tregs percentages obtained by both flow cytometry and qPCR methods in 35 adult IBD patients, 18 out of them with Crohn's disease (CD) and 17 with ulcerative colitis (UC) were compared to each other as well as to scores on two IBD activity questionnaires using the Harvey Bradshaw Index (HBI) for CD patients and the Simple Colitis Clinical Activity Index (SCCAI) for UC patients. The Treg percentages by flow cytometry were defined as CD4(+)CD25(high)CD127(low)FOXP3(+) cells in peripheral blood mononuclear cells, whereas the Treg percentages by qPCR method were determined as FOXP3 promoter demethylation in genomic DNA. RESULTS: We found an average of 1.56% +/- 0.78% Tregs by using flow cytometry, compared to 1.07% +/- 0.53% Tregs by using qPCR in adult IBD patients. There were no significant correlations between either the percentages of Tregs measured by flow cytometry or qPCR and the HBI or SCCAI questionnaire scores in CD or UC patients, respectively. In addition, there was no correlation between Treg percentages measured by qPCR and those measured by flow cytometry (r = -0.06, P = 0.73; Spearman Rho). These data suggest that, either Treg-related immune function or the clinical scores in these IBD patients did not accurately reflect actual disease activity. Until the cause(s) for these differences are more clearly defined, the results suggest caution in interpreting studies of Tregs in various inflammatory disorders. CONCLUSION: The two methods did not produce equivalent measures of the percentage of total Tregs in the IBD patients studied which is consistent with the conclusion that Tregs subtypes are not equally detected by these two assays."],["dc.description.sponsorship","Medical Faculty of the University of Goettingen, Germany"],["dc.identifier.doi","10.3748/wjg.v21.i11.3325"],["dc.identifier.isi","000351165100021"],["dc.identifier.pmid","25805940"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11750"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37598"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Baishideng Publishing Group Inc"],["dc.relation.issn","2219-2840"],["dc.relation.issn","1007-9327"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Lack of correlation between Treg quantification assays in inflammatory bowel disease patients"],["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","371"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Journal of Clinical Pharmacology"],["dc.bibliographiccitation.lastpage","381"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Geisen, Christof"],["dc.contributor.author","Luxembourg, Beate"],["dc.contributor.author","Watzka, Matthias"],["dc.contributor.author","Toennes, Stefan W."],["dc.contributor.author","Sittinger, Katja"],["dc.contributor.author","Marinova, Milka"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Lindhoff-Last, Edelgard"],["dc.contributor.author","Seifried, Erhard"],["dc.contributor.author","Oldenburg, Johannes"],["dc.date.accessioned","2018-11-07T08:57:47Z"],["dc.date.available","2018-11-07T08:57:47Z"],["dc.date.issued","2011"],["dc.description.abstract","The anticoagulation response to vitamin K antagonists is characterised by high inter-individual variability. The impact of single nucleotide polymorphisms (SNPs) in several genes of enzymes involved in the vitamin K cycle on phenprocoumon dose variability and phenprocoumon plasma concentrations is still under investigation. We assessed the influence of VKORC1 c.-1639G > A, CYP2C9 2, CYP2C9 3, CYP4F2 c.1297G > A, CALU c. 4A > G, EPHX1 c.337T > C, GGCX c.214+597G > A, F7 c.-402G > A, F7 c.-401G > T, PROC c.-228C > T and PROC c.-215G > A along with clinical and demographic parameters on steady-state phenprocoumon therapy in 75 patients. A prediction model was developed for total phenprocoumon plasma concentrations and daily phenprocoumon doses required for therapeutic anticoagulation. The VKORC1 c.-1639 genotype was the main predictor of the phenprocoumon daily dose (adjusted R(2) = 37.6%) and the total phenprocoumon concentration (adjusted R(2) = 38.3%). CYP2C9 affected the phenprocoumon concentration, but not the dose requirements. SNPs in the other genes of the vitamin K cycle, concomitant medication, nicotine use and alcohol consumption did not predict phenprocoumon concentrations and phenprocoumon dose requirements in a multiple linear regression model. Phenprocoumon concentrations were predicted by VKORC1 c.-1639, CYP2C9 genotype, age and BMI. The final prediction model for the daily phenprocoumon dose requirements comprised VKORC1 c.-1639 genotype, age and height accounting for 48.6% of the inter-individual variability. A rough prediction of phenprocoumon maintenance doses can be achieved by a limited set of parameters (VKORC1, age, height). The investigated SNPs in CYP4F2, CALU, EPHX1, GGCX, F7, and PROC did not improve the predictive value of a pharmacogenetic-based dosing equation for phenprocoumon."],["dc.identifier.doi","10.1007/s00228-010-0950-y"],["dc.identifier.isi","000288399800006"],["dc.identifier.pmid","21110013"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23483"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0031-6970"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Prediction of phenprocoumon maintenance dose and phenprocoumon plasma concentration by genetic and non-genetic parameters"],["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","84"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Wolff, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:15:14Z"],["dc.date.available","2018-11-07T09:15:14Z"],["dc.date.issued","2012"],["dc.description.abstract","Background/Aim: To investigate the influence of established genetic risk factors for Alzheimer's disease on the speed of disease progression. Methods: Polymorphisms (in ACE, ApoE, BIN1, CLU, CR1, CST3, EXOC3L2, GWA14q32.13, IL8, LDLR, PICALM, TNK1) of 40 Alzheimer's disease patients from a longitudinal study were analyzed. A standardized loss of Mini-Mental State Examination points was used as the progression parameter. Results: Polymorphisms in CST3 and EXOC3L2 as well as the absence of APOE4 were associated with more aggressive disease courses. A trend was observed for BIN1. Conclusion: In addition to being a risk factor for disease development, some of the polymorphisms investigated here are associated with higher rates of decline and disease progression and thus might act as prognostic disease markers. This effect needs to be considered in future treatment strategies. Copyright (C) 2012 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000336790"],["dc.identifier.isi","000305654800002"],["dc.identifier.pmid","22414550"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27631"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Alzheimer's Disease: Genetic Polymorphisms and Rate of Decline"],["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"]]