Ahsen, Nicolas von

[["dc.bibliographiccitation.firstpage","1432"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of the European Academy of Dermatology and Venereology"],["dc.bibliographiccitation.lastpage","1439"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Zutt, Markus"],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kretschmer, Lutz"],["dc.date.accessioned","2018-11-07T08:49:13Z"],["dc.date.available","2018-11-07T08:49:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Background Chronic venous leg ulcers (CVU) cause considerable burden of disease for the patients as well as enormous costs for health care systems. The pathophysiology of CVU is complex and not entirely understood. So far reliable pathogenic and/or prognostic parameters have not been identified. Objectives We studied the role of thrombophilia in patients referred to a University dermatology department for treatment of CVU. Patients and methods A cohort of 310 patients with active chronic venous leg ulcers (CEAP 6) was stratified into two comparably large groups according to the presence or absence of post- thrombotic syndrome (PTS+; PTS-) as determined using duplex scan and/or phlebography. In addition, several thrombophilia parameters were assessed. Results The prevalence of protein S deficiency and factor V Leiden mutation was significantly higher in PTS+ patients compared with the PTS- group. However, patients in both subgroups revealed high prevalences of thrombophilia (antithrombin deficiency, protein C deficiency, protein S deficiency, activated protein C resistance, factor V mutation or elevated homocysteine). Conclusion Based on these data, it is conceivable that thrombophilia contributes to the pathogenesis of CVU, possibly through induction of microcirculatory dysregulations."],["dc.identifier.doi","10.1111/j.1468-3083.2011.04001.x"],["dc.identifier.isi","000297952800011"],["dc.identifier.pmid","21392126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21406"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0926-9959"],["dc.title","Thrombophilia in patients with chronic venous leg ulcers-a study on patients with or without post-thrombotic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","427"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","430"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Heyer, Andrea"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Häfner, Heinz"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Gender differences in neuropsychiatric disease are recognized but not well understood. Investigating the survival of primary rat hippocampal neurons in culture, we found significant and inverted gender differences on normoxia versus hypoxia. Male cells were more resistant under normoxia but more vulnerable under hypoxia than female cells. Male vulnerability pattern was acquired in cells from neonatally testosterone-primed females. Estrogens, acting via membrane receptors, had a higher neuroprotective power in male neurons, explained at least in part by the pronounced increase in estrogen receptor beta/alpha ratio during hypoxia in male cells only."],["dc.identifier.doi","10.1038/sj.jcbfm.9600056"],["dc.identifier.gro","3150469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7237"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.subject","aromatase; estrogen receptor alpha; estrogen receptor beta; hippocampus; sex; testosterone"],["dc.title","In vitro gender differences in neuronal survival on hypoxia and in 17 beta-estradiol-mediated neuroprotection"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1170"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","1173"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Decard, Bernhard F."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Grunwald, Thomas"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Stroet, Anke"],["dc.contributor.author","Niggemeier, Petra"],["dc.contributor.author","Schottstedt, Volkmar"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2018-11-07T09:02:57Z"],["dc.date.available","2018-11-07T09:02:57Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective Vitamin D deficiency and Epstein-Barr virus (EBV) infection may be associated with the development of multiple sclerosis (MS). We investigated serum 25-hydroxyvitamin D (25-OH-D) levels and anti-EBV immunoreactivity in 25 individuals before the first clinical manifestation of MS. Patients and methods 56 serum samples of 25 individuals who had donated blood prior to the first clinical MS manifestation (clinically isolated syndrome (CIS)) (four male subjects, 21 female subjects, mean age 31.5 years at time of pre-CIS blood sampling; mean age at disease onset 33.4 years) were available, covering an interval of 7.3 years-2 months (mean 31.5 months) before CIS. In 18 of 25 patients serum samples were also obtained after established diagnosis of MS. Longitudinal age- and gender-matched healthy blood donors (four male subjects, 21 female subjects, 39 samples, mean age 32.5 years) served as controls. Serum 25-OH-D was measured by isotope dilution-liquid chromatography-tandem mass spectrometry. 25-OH-D levels were deconvoluted using published seasonal coefficients from a German population. Immunoglobulin G (IgG) against Epstein-Barr virus nuclear antigen-1 (EBNA1) were assessed using commercially available ELISA. Results Low 25-OH-D levels were observed during the 24-month pre-CIS interval (47.8 (32.5-77.2) nmol/l, median (IQR); healthy controls: 81.6 (57.7-98.5), p=0.004, however, still higher than after established diagnosis (24.5 (13.7-47.7), p<0.0001 compared with controls). IgG against EBNA1 during the 36-month pre-CIS interval was increased (185.9 (91.2-460.0) IU/ml, median (IQR); healthy controls 63.7 (29.5-121.6), p=0.002). Conclusions Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years."],["dc.identifier.doi","10.1136/jnnp-2012-303068"],["dc.identifier.isi","000311097700012"],["dc.identifier.pmid","22888143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24794"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Low vitamin D and elevated immunoreactivity against Epsteine-Barr virus before first clinical manifestation of 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","156"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","161"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Schutz, Ekkehard"],["dc.date.accessioned","2018-11-07T10:16:50Z"],["dc.date.available","2018-11-07T10:16:50Z"],["dc.date.issued","2000"],["dc.description.abstract","Background: alpha(1)-Antitrypsin is the major plasma serine protease inhibitor. Its deficiency is mainly associated with the alleles PI S and PI Z and can lead to obstructive lung disease in adults and to liver cirrhosis during childhood. Methods: A multiplex PCR method has been established that uses two sets of primers to amplify the gene regions covering the PI S or PI Z mutations sites. Mutation detection was performed on the LightCycler by melting curve analysis of detection probes labeled with two different fluorescent dyes, LC-Red640 and LC-Red705. Results: Unequivocal genotyping results were obtained for all investigated samples in an assay time of similar to 30 min. The color compensation procedure greatly improved the readability of the resulting diagnostic melting curves. Conclusions: To our knowledge, this is the first report of simultaneous detection of two mutations in a single tube by PCR of genomic DNA and the use of two different reporter dyes with the LightCycler color compensation feature. This approach is a rapid, convenient, and economic alternative to other methods described to date for the detection of alpha(1)-antitrypsin deficiency alleles. (C) 2000 American Association for Clinical Chemistry."],["dc.identifier.isi","000085288500004"],["dc.identifier.pmid","10657370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41113"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.publisher.place","Washington"],["dc.relation.conference","Meeting of the Deutsche-Gesellschaft-fur-Klinische-Chemie / Deutsche-Gesellschaft-fur-Laboratoriumsmedizin"],["dc.relation.eventlocation","REGENSBURG, GERMANY"],["dc.relation.issn","0009-9147"],["dc.title","Use of two reporter dyes without interference in a single-tube rapid-cycle PCR: alpha(1)-antitrypsin genotyping by multiplex real-time fluorescence PCR with the LightCycler"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:04Z"],["dc.date.available","2018-11-07T10:33:04Z"],["dc.date.issued","2006"],["dc.description.abstract","Measurement of tau-protein and beta-amyloid(1-42) (A beta 42) in cerebrospinal fluid (CSF) has gained increasing acceptance in the differential diagnosis of Alzheimer's disease. We investigated CSF tau-protein and A beta 42 concentrations in 73 patients with advanced idiopathic Parkinson's disease with dementia (PDD) and 23 patients with idiopathic Parkinson's disease without dementia (PD) and in a comparison group of 41 non-demented neurological patients (CG) using commercially available enzyme-linked-immunoabsorbant- assay ( ELISA). tau-Protein levels were statistically significantly higher and A beta 42 lower in the PDD patients compared to PD patients and the CG. This observation was most marked ( p < 0.05) in a subgroup of patients with PDD carrying the apolipoprotein genotype epsilon 3/epsilon 3. The distribution of the apolipoprotein genotypes in PDD and PD patients was similar to that of the CG. Although a significant difference in tau-protein values was observed between PDD and CG, no diagnostic cut-off value was established. These findings suggest that such protein CSF changes may help to support the clinical diagnosis of cognitive decline in PD and that there may be apolipoprotein-E-isoform- specific differences in CSF protein regulation in advanced PDD. Copyright (C) 2006 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000094871"],["dc.identifier.isi","000242167100003"],["dc.identifier.pmid","16899997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1173"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Clinical Biochemistry"],["dc.bibliographiccitation.lastpage","1180"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Metzker, Maria"],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Andag, Rainer"],["dc.contributor.author","Abe, Manabu"],["dc.contributor.author","Canzler, Ortrun"],["dc.contributor.author","Klett, Corinne"],["dc.contributor.author","Leicht, Simone"],["dc.contributor.author","Olbricht, Christoph"],["dc.contributor.author","Wieland, Eberhard"],["dc.date.accessioned","2020-12-10T14:23:06Z"],["dc.date.available","2020-12-10T14:23:06Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.clinbiochem.2016.05.019"],["dc.identifier.issn","0009-9120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71838"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Analytical evaluation of a real-time PCR-based DNA demethylation assay to assess the frequency of naturally occurring regulatory T cells in peripheral blood"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","154"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cellular Signalling"],["dc.bibliographiccitation.lastpage","162"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Samoylenko, Anatoly"],["dc.contributor.author","Byts, Nadiya"],["dc.contributor.author","Rajalingam, Krishnaraj"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Rapp, Ulf R."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:16Z"],["dc.date.available","2017-09-07T11:46:16Z"],["dc.date.issued","2008-01"],["dc.description.abstract","Thrombopoietin (TPO), a hematopoietic growth factor regulating platelet production, and its receptor (TPOR) were recently shown to be expressed in the brain where they exert proapoptotic activity. Here we used PC12 cells, an established model of neuronal differentiation, to investigate the effects of TPO on neuronal survival and differentiation. These cells expressed TPOR mRNA. TPO increased cell death in neuronally differentiated PC12 cells but had no effect in undifferentiated cells. Surprisingly, TPO inhibited nerve growth factor (NGF)-induced differentiation of PC12 cells in a dose- and time-dependent manner. This inhibition was dependent on the activity of Janus kinase-2 (JAK2). Using phospho-kinase arrays and Western blot we found downregulation of the NGF-stimulated phosphorylation of the extracellular signal-regulated kinase p42ERK by TPO with no effect on phosphorylation of Akt or stress kinases. NGF-induced phosphorylation of ERK-activating kinases, MEK1/2 and C-RAF was also reduced by TPO while NGF-induced RAS activation was not attenuated by TPO treatment. In contrast to its inhibitory effects on NGF signalling, TPO had no effect on epidermal growth factor (EGF)-stimulated ERK phosphorylation or proliferation of PC12 cells. Our data indicate that TPO via activation of its receptor-bound JAK2 delays the NGF-dependent acquisition of neuronal phenotype and decreases neuronal survival by suppressing NGF-induced ERK activity."],["dc.identifier.doi","10.1016/j.cellsig.2007.10.006"],["dc.identifier.gro","3150475"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7244"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","TPO; NGF; EGF; PC12; RAS; Mitogen-activated protein kinase; Cell death; Neurite outgrowth"],["dc.title","Thrombopoietin inhibits nerve growth factor-induced neuronal differentiation and ERK signalling"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","835"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal for Parasitology"],["dc.bibliographiccitation.lastpage","841"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Lin, San San"],["dc.contributor.author","Blume, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Gross, Uwe"],["dc.contributor.author","Bohne, Wolfgang"],["dc.date.accessioned","2018-11-07T08:54:48Z"],["dc.date.available","2018-11-07T08:54:48Z"],["dc.date.issued","2011"],["dc.description.abstract","Apicomplexan parasites undergo metabolic shifts in adaptation to environmental changes. Here, we investigate the metabolic requirements which are responsible for ATP homeostasis in the extracellular stage of Toxoplasma gondii. Surprisingly, we found that freshly released tachyzoites are able to maintain a constant ATP level during the first hour of extracellular incubation without the acquisition of external carbon sources. We further demonstrated that the extent of gliding motility and that of host cell invasion is independent from the availability of external carbon sources during this one hour extracellular period. The ATP level and the invasion efficiency of extracellular parasites were severely decreased by treatment with the glycolysis inhibitor, 2-deoxy-D-glucose, but not by the F(0)F(1)-ATPase inhibitor, oligomycin. This suggests that although the uptake of glucose itself is not required during the 1 h incubation period, extracellular parasites depend on the activity of the glycolytic pathway for ATP homeostasis. Furthermore, active glycolysis was evident by the secretion of lactate into the culture medium, even in the absence of external carbon sources. Together, our studies suggest that tachyzoites are independent from external carbon sources within the first hour of their extracellular life, which is the most relevant time span for finding a new host cell, but rely on the glycolytic metabolisation of internal carbon sources for ATP maintenance, gliding motility and host cell invasion. (C) 2011 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijpara.2011.03.005"],["dc.identifier.isi","000292234700004"],["dc.identifier.pmid","21515276"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22753"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","0020-7519"],["dc.title","Extracellular Toxoplasma gondii tachyzoites do not require carbon source uptake for ATP maintenance, gliding motility and invasion in the first hour of their extracellular life"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","991"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","993"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Doerr, J."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Schmailzl, K. J. G."],["dc.contributor.author","Chan, A."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Varon, R."],["dc.contributor.author","Lill, C. M."],["dc.contributor.author","Vogel, H.-P."],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Paul, Friedemann"],["dc.date.accessioned","2018-11-07T11:24:13Z"],["dc.date.available","2018-11-07T11:24:13Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1212/WNL.0b013e3181b878f6"],["dc.identifier.isi","000270035000013"],["dc.identifier.pmid","19770476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","SEVERE CARDIAC FAILURE IN A PATIENT WITH MULTIPLE SCLEROSIS FOLLOWING LOW-DOSE MITOXANTRONE TREATMENT"],["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","22"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","27"],["dc.bibliographiccitation.volume","255"],["dc.contributor.author","Chan, Andrew"],["dc.contributor.author","Stueve, Olaf"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.date.accessioned","2018-11-07T11:08:39Z"],["dc.date.available","2018-11-07T11:08:39Z"],["dc.date.issued","2008"],["dc.description.abstract","Despite novel immunoactive agents, immunosuppressants still play a considerable role in the treatment of MS, especially in rapidly progressive cases. Given the limited tolerability and potentially severe side effects of most immunosuppressive drugs, identification of patients with a favorable benefit-risk profile is essential. A narrow therapeutic index, with sometimes high interindividual variability in terms of response and side effects may partially be explained by genetic factors affecting different metabolic pathways. Here, we will review practical aspects in the clinical use of immunosuppressants in MS and discuss approaches to individualized treatment schemes, including novel pharmacogenetic strategies."],["dc.identifier.doi","10.1007/s00415-008-6005-y"],["dc.identifier.isi","000263166600005"],["dc.identifier.pmid","19300956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52835"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Immunosuppression in clinical practice Approaches to individualized therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]