Dahm, Liane

[["dc.bibliographiccitation.artnumber","181"],["dc.bibliographiccitation.journal","Frontiers in Behavioral Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Lu, Derek"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Ju, Anes"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Chowdhury, Kamal"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2014"],["dc.description.abstract","Autism-spectrum disorders (ASD) are heterogeneous, highly heritable neurodevelopmental conditions affecting around 0.5% of the population across cultures, with a male/female ratio of approximately 4:1. Phenotypically, ASD are characterized by social interaction and communication deficits, restricted interests, repetitive behaviors, and reduced cognitive flexibility. Identified causes converge at the level of the synapse, ranging from mutation of synaptic genes to quantitative alterations in synaptic protein expression, e.g., through compromised transcriptional or translational control. We wondered whether reduced turnover and degradation of synapses, due to deregulated autophagy, would lead to similar phenotypical consequences. Ambra1, strongly expressed in cortex, hippocampus, and striatum, is a positive regulator of Beclin1, a principal player in autophagosome formation. While homozygosity of the Ambra1 null mutation causes embryonic lethality, heterozygous mice with reduced Ambra1 expression are viable, reproduce normally, and lack any immediately obvious phenotype. Surprisingly, comprehensive behavioral characterization of these mice revealed an autism-like phenotype in Ambra1 (+/-) females only, including compromised communication and social interactions, a tendency of enhanced stereotypies/repetitive behaviors, and impaired cognitive flexibility. Reduced ultrasound communication was found in adults as well as pups, which achieved otherwise normal neurodevelopmental milestones. These features were all absent in male Ambra1 (+/-) mice. As a first hint explaining this gender difference, we found a much stronger reduction of Ambra1 protein in the cortex of Ambra1 (+/-) females compared to males. To conclude, Ambra1 deficiency can induce an autism-like phenotype. The restriction to the female gender of autism-generation by a defined genetic trait is unique thus far and warrants further investigation."],["dc.format.extent","19"],["dc.identifier.doi","10.3389/fnbeh.2014.00181"],["dc.identifier.gro","3150538"],["dc.identifier.pmid","24904333"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11695"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7311"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject","Ambra1; autism composite score; autophagy; cognitive rigidity; heterozygous null mutant mice; repetitive behavior; social interaction; ultrasound communication"],["dc.title","Heterozygous Ambra1 deficiency in mice: a genetic trait with autism-like behavior restricted to the female gender"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1233"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","1236"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Heinrich, Ralf"],["dc.contributor.author","Monnheimer, Mathieu"],["dc.contributor.author","Gerhart, Simone"],["dc.contributor.author","Stegmüller, Judith"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:28Z"],["dc.date.available","2017-09-07T11:46:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Traumatic brain injury causes progressive brain atrophy and cognitive decline. Surprisingly, an early treatment with erythropoietin (EPO) prevents these consequences of secondary neurodegeneration, but the mechanisms have remained obscure. Here we show by advanced imaging and innovative analytical tools that recombinant human EPO, a clinically established and neuroprotective growth factor, dampens microglial activity, as visualized also in vivo by a strongly attenuated injury-induced cellular motility."],["dc.identifier.doi","10.1038/jcbfm.2015.100"],["dc.identifier.gro","3150519"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7292"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject","ATP; brain injury; migration; process protrusion; Rac1"],["dc.title","Erythropoietin dampens injury-induced microglial motility"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","579"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cell Biology and Toxicology"],["dc.bibliographiccitation.lastpage","591"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Klugmann, Fanny"],["dc.contributor.author","Gonzalez-Algaba, Angeles"],["dc.contributor.author","Reuss, Bernhard"],["dc.date.accessioned","2018-11-07T08:36:04Z"],["dc.date.available","2018-11-07T08:36:04Z"],["dc.date.issued","2010"],["dc.description.abstract","Gap junctions (GJ) represent a cellular communication system known to influence neuronal differentiation and survival. To assess a putative role of this system for neural effects of tamoxifen (TAM) and raloxifene (RAL), we used the human teratocarcinoma cell line NTera2/D1, retinoic acid (RA)-dependent neuronal differentiation of which is regulated by gap junctions formed of connexin43 (Cx43). As demonstrated by Western blot analysis, concentrations above 1 A mu mol/l for TAM, and 0.1 A mu mol/l for RAL lead to a temporary time- and concentration-dependent increase in Cx43 immunoreactivity, which reached a peak for TAM after 1 day and for RAL after 2 days. Immunocytochemical stainings revealed the increase in Cx43 immunoreactivity to result from an accumulation in intracellular compartments such as the Golgi apparatus or lysosomes. In addition, TAM and RAL were able to prevent the RA-dependent decrease of Cx43 immunoreactivity in NTera2/D1 cells, normally observed during neuronal differentiation. This suggested a suppression of neuronal differentiation to result from these substances. According to this, treatment of NTera2/D1 cells with 10 A mu mol/l TAM or RAL during weeks 1 and 2 of a 6 weeks RA-driven differentiation schedule impaired, whereas treatment during weeks 5 and 6 did not impair, neuronal differentiation of these cells. Modulation of GJ coupling between NTera2/D1 cells by TAM and RAL seems therefore to perturb early neuronal differentiation, whereas differentiated neurons in the mature brain seem to be not affected. These effects could be of importance for actions of TAM and RAL on early embryonic steps of nervous system formation."],["dc.identifier.doi","10.1007/s10565-010-9165-3"],["dc.identifier.isi","000283360100007"],["dc.identifier.pmid","20437090"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18220"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0742-2091"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Tamoxifen and raloxifene modulate gap junction coupling during early phases of retinoic acid-dependent neuronal differentiation of NTera2/D1 cells"],["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","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Saschenbrecker, Sandra"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Borowski, Kathrin"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Lemke, Sandra"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Wienands, Jürgen"],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2014"],["dc.description.abstract","ObjectiveWe previously reported an unexpectedly high seroprevalence (∼10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoantibodies (AB) in healthy and neuropsychiatrically ill subjects (N = 2,817). This finding challenges an unambiguous causal relationship of serum AB with brain disease. To test whether similar results would be obtained for other brain antigen-directed AB previously connected with pathological conditions, we systematically screened serum samples of 4,236 individuals.MethodsSerum samples of healthy (n = 1,703) versus neuropsychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrophic lateral sclerosis, personality disorder; total n = 2,533) were tested. For analysis based on indirect immunofluorescence, we used biochip mosaics of frozen brain sections (rat, monkey) and transfected HEK293 cells expressing respective recombinant target antigens.ResultsSeroprevalence of all screened AB was comparable in healthy and ill individuals. None of them, however, reached the abundance of NMDAR1 AB (again ∼10%; immunoglobulin [Ig] G ∼1%). Appreciable frequency was noted for AB against amphiphysin (2.0%), ARHGAP26 (1.3%), CASPR2 (0.9%), MOG (0.8%), GAD65 (0.5%), Ma2 (0.5%), Yo (0.4%), and Ma1 (0.4%), with titers and Ig class distribution similar among groups. All other AB were found in ≤0.1% of individuals (anti–AMPAR-1/2, AQP4, CV2, Tr/DNER, DPPX-IF1, GABAR-B1/B2, GAD67, GLRA1b, GRM1, GRM5, Hu, LGl1, recoverin, Ri, ZIC4). The predominant Ig class depended on antigen location, with intracellular epitopes predisposing to IgG (chi-square = 218.91, p = 2.8 × 10−48).InterpretationTo conclude, the brain antigen-directed AB tested here are comparably detectable in healthy subjects and the disease groups studied here, thus questioning an upfront pathological role of these serum AB."],["dc.identifier.doi","10.1002/ana.24189"],["dc.identifier.gro","3150539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7312"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Seroprevalence of autoantibodies against brain antigens in health and disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","881"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.lastpage","888"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:27Z"],["dc.date.available","2017-09-07T11:46:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Objectives: Over 12% of patients with bipolar disorder exhibit rapid cycling. The underlying biological mechanisms of this extreme form of bipolar disease are still unknown. This study aimed at replicating and extending findings of our previously published case report, where an involvement of prostaglandin synthesis-related genes in rapid cycling was first proposed. Methods: Psychopathological follow-up of the reported case was performed under cessation of celecoxib treatment. In a prospective observational study, patients with bipolar disorder (n = 47; of these, four had rapid cycling) or with monopolar depression (n = 97) were recruited over a period of three years. Repeated psychopathology measurements were conducted using standard instruments. Peripheral blood mononuclear cells (PBMC) were obtained during as many consecutive episodes as possible and processed for mRNA isolation and quantitative real-time reverse transcriptase polymerase chain reaction for prostaglandin D2 synthase (PTGDS), aldo-ketoreductase family 1, member C3 (AKR1C3), cyclooxygenase-2 (PAN means all splice variants) (COX2PAN), prostaglandin-endoperoxide synthase 2 (PTGS2), and purinergic receptor P2X, ligand-gated ion channel 7 (P2RX7). Results: The follow-up of our original case of a patient with rapid cycling who had shown impressive psychopathological improvement under celecoxib revealed complete loss of this effect upon discontinuation of the COX2 inhibitor. Episode-specific gene expression measurements in PBMC of four newly recruited rapid cycling patients confirmed the higher expression of PTGDS in depressive compared to manic phases. Additionally, higher relative expression of PTGS2/COX2PAN was found. No comparable alterations were observable in samples available from the remaining 43 patients with bipolar disorder and the 97 monopolar depressed patients, emphasizing the advantages of the rapid cycling condition with its rapid and frequent shifts for identification of gene expression changes.Conclusions: This study supports a role for prostaglandins in rapid cycling and advocates the cyclooxygenase cascade as a treatment target in this condition."],["dc.identifier.doi","10.1111/bdi.12223"],["dc.identifier.gro","3150518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7291"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","A role for prostaglandins in rapid cycling suggested by episode-specific gene expression shifts in peripheral blood mononuclear cells: a preliminary report"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1180"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","1186"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Zerche, M."],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Ott, C."],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Worthmann, Hans"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Rentzsch, Katrin"],["dc.contributor.author","Tryc, A. B."],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Ehrenreich, Hanhelore"],["dc.date.accessioned","2017-09-07T11:44:23Z"],["dc.date.available","2017-09-07T11:44:23Z"],["dc.date.issued","2015"],["dc.description.abstract","Background and Purpose—Recently, we reported high seroprevalence (age-dependent up to >19%) of N-methyl-d-aspartate-receptor subunit NR1 (NMDAR1) autoantibodies in both healthy and neuropsychiatrically ill subjects (N=4236). Neuropsychiatric syndrome relevance was restricted to individuals with compromised blood–brain barrier, for example, apolipoprotein E4 (APOE4) carrier status, both clinically and experimentally. We now hypothesized that these autoantibodies may upon stroke be protective in individuals with hitherto intact blood–brain barrier, but harmful for subjects with chronically compromised blood–brain barrier.Methods—Of 464 patients admitted with acute ischemic stroke in the middle cerebral artery territory, blood for NMDAR1 autoantibody measurements and APOE4 carrier status as indicator of a preexisting leaky blood–brain barrier was collected within 3 to 5 hours after stroke. Evolution of lesion size (delta day 7–1) in diffusion-weighted magnetic resonance imaging was primary outcome parameter. In subgroups, NMDAR1 autoantibody measurements were repeated on days 2 and 7.Results—Of all 464 patients, 21.6% were NMDAR1 autoantibody–positive (immunoglobulin M, A, or G) and 21% were APOE4 carriers. Patients with magnetic resonance imaging data available on days 1 and 7 (N=384) were divided into 4 groups according to NMDAR1 autoantibody and APOE4 status. Groups were comparable in all stroke-relevant presenting characteristics. The autoantibody+/APOE4− group had a smaller mean delta lesion size compared with the autoantibody−/APOE4- group, suggesting a protective effect of circulating NMDAR1 autoantibodies. In contrast, the autoantibody+/APOE4+ group had the largest mean delta lesion area. NMDAR1 autoantibody serum titers dropped on day 2 and remounted by day 7.Conclusions—Dependent on blood–brain barrier integrity before an acute ischemic brain injury, preexisting NMDAR1 autoantibodies seem to be beneficial or detrimental."],["dc.identifier.doi","10.1161/strokeaha.114.008323"],["dc.identifier.gro","3151637"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8453"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0039-2499"],["dc.title","Preexisting Serum Autoantibodies Against the NMDAR Subunit NR1 Modulate Evolution of Lesion Size in Acute Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","468"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Vasa"],["dc.bibliographiccitation.lastpage","473"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Dahm, J. B."],["dc.contributor.author","van Buuren, F."],["dc.contributor.author","Hansen, C."],["dc.contributor.author","Becker, J."],["dc.contributor.author","Wolpers, H.-G."],["dc.date.accessioned","2021-06-01T10:50:31Z"],["dc.date.available","2021-06-01T10:50:31Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: Carotid artery stenting (CAS) from the femoral approach can be anatomically very difficult and the incidence of complications is higher in patients with anatomical variations of the aortic arch, difficulties related to peripheral vascular disease and/or with access site complications. Because the typical morphology in patients with a bovine- or type-III aortic arch applies for an arterial access from the right upper extremity (e.g. radial, brachial) we evaluated success rates and safety of the right transradial access in a prospective study. Patients and methods: Between June 2009 and October 2010, seventeen patients (mean age 74,4 ± 9 years, 10 male) with a bovine- (n = 4) or type-III aortic arch (n = 12) underwent CAS with a planned transradial- (n = 3) or after problematic transfemoral access (n = 14). In patients with a type-III aortic arch (n = 13), the right target common carotid artery (CCA) was cannulated from the right radial artery with a 5F IMA diagnostic catheter-, in patients with a bovine aortic arch (n = 4), the left CCA was accessed from the right radial artery with a 5F Amplatz- or Judkins left catheter. In all patients a 6F- (n = 14) or 5F- (n = 3) shuttle sheath was inserted via the diagnostic catheter and a 0.035 extra-stiff guidewire. All interventions were carried out with the use of a peripheral embolization protection device (EPD). Primary study endpoints were procedural success and major adverse cardiac and cerebrovascular events (MACCE), secondary endpoints were access site complications and the mean intervention time. Results: Procedural success could be achieved in all patients (100 %), MACCE and access site complications did not occur in any patient. Mean interventional time was 48 ± 18 min. Conclusions: CAS using the right transradial approach for left CAS in bovine-type aortic arch or the right transradial approach in type-III aortic arch for right CAS appears to be safe and technically feasible."],["dc.description.abstract","Hintergrund: Die Carotisangioplastie mit Stentimplantation (CAS) mit einem femoral-arteriellen Zugang kann aufgrund anatomischer Besonderheiten des Aortenbogens sehr schwierig sein. Da die typische bovine- bzw. Typ-III-Aortenbogenanatomie morphologisch geradezu zu einem Zugangsweg von der oberen Extremität einlädt (z.B. von radial oder brachial), haben wir den transradialen Zugang in Patienten mit dieser Morphologie in einer prospektiven Studie evaluiert. Patienten und Methoden: Zwischen Juni 2009 und Oktober 2010, erfolgte die CAS bei siebzehn Patienten (mittleres Alter 74,4 ± 9 Jahre, 10 Männer) mit bovinem- (n = 4) bzw. Typ-III Aortenbogen (n = 12) geplant transradial- (n = 3) oder nach interventionellen Problemen beim transfemoral-arteriellem Zugang (n = 14). Bei Patienten mit Typ-III Aortenbogen (n = 13), erfolgte der Zugang in die A. carotis communis (CCA) von der rechten A. radialis mit einem 5F IMA Diagnostikkatheter-, bei Patienten mit boviner Anatomie (n = 4), wurde die linke CCA ebenfalls von der rechten A. radialis mit einem 5F Amplatz- oder linken Judkins Katheter kanüliert. Bei allen Patienten konnte anschließend eine 6F- (n = 14) bzw. 5F- (n = 3) Shuttle-Schleuse über den Diagnostikkatheter und einem 0.035 extra-stiff Führungsdraht eingewechselt werden. Sämtliche Interventionen erfolgten mit einem distalen Embolieschutzsystem. Primäre Endpunkte waren prozeduraler Erfolg und das Auftreten kardialer bzw. zereobrovaskulärer Komplikationen (MACCE), sekundäre Endpunkte waren arterielle Zugangskomplikationen und die mittlere Interventionszeit. Ergebnisse: Ein prozeduraler Erfolg konnte in 100 % der Patienten erreicht werden, MACCE bzw. arterielle Zugangskomplikationen traten in keinem Patienten auf (0 %). Die mittlere Interventionszeit betrug 48 ± 18 min. Schlussfolgerungen: CAS über einen rechten radialen Zugang zur Behandlung der linken A. carotis bei bovinem Aortenbogen, bzw. zur Behandlung der rechten A. carotis bei Typ-III Aortenbogen ist sicher und technisch gut machbar."],["dc.identifier.doi","10.1024/0301-1526/a000150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86689"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1664-2872"],["dc.relation.issn","0301-1526"],["dc.title","The concept of an anatomy related individual arterial access: lowering technical and clinical complications with transradial access in bovine- and type-III aortic arch carotid artery stenting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","662"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","684"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Bodda, Chiranjeevi"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Castillo Venzor, Aracely"],["dc.contributor.author","Konte, Bettina"],["dc.contributor.author","Erbaba, Begun"],["dc.contributor.author","Hartmann, Annette M."],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Mannan, Ashraf U."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2014"],["dc.description.abstract","The X-chromosomal MECP2/Mecp2 gene encodes methyl-CpG-binding protein 2, a transcriptional activator and repressor regulating many other genes. We discovered in male FVB/N mice that mild (~50%) transgenic overexpression of Mecp2 enhances aggression. Surprisingly, when the same transgene was expressed in C57BL/6N mice, transgenics showed reduced aggression and social interaction. This suggests that Mecp2 modulates aggressive social behavior. To test this hypothesis in humans, we performed a phenotype-based genetic association study (PGAS) in >1000 schizophrenic individuals. We found MECP2 SNPs rs2239464 (G/A) and rs2734647 (C/T; 3'UTR) associated with aggression, with the G and C carriers, respectively, being more aggressive. This finding was replicated in an independent schizophrenia cohort. Allele-specific MECP2 mRNA expression differs in peripheral blood mononuclear cells by ~50% (rs2734647: C > T). Notably, the brain-expressed, species-conserved miR-511 binds to MECP2 3'UTR only in T carriers, thereby suppressing gene expression. To conclude, subtle MECP2/Mecp2 expression alterations impact aggression. While the mouse data provides evidence of an interaction between genetic background and mild Mecp2 overexpression, the human data convey means by which genetic variation affects MECP2 expression and behavior."],["dc.identifier.doi","10.1002/emmm.201303744"],["dc.identifier.gro","3150551"],["dc.identifier.pmid","24648499"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7325"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Mild expression differences of MECP2 influencing aggressive social behavior"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]