Hasenfuß, Gerd P.

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Knierim, Maria"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Holzamer, Andreas"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2020-12-10T14:10:25Z"],["dc.date.available","2020-12-10T14:10:25Z"],["dc.date.issued","2020"],["dc.description.abstract","Pharmacologic approaches for the treatment of atrial arrhythmias are limited due to side effects and low efficacy. Thus, the identification of new antiarrhythmic targets is of clinical interest. Recent genome studies suggested an involvement of SCN10A sodium channels (NaV1.8) in atrial electrophysiology. This study investigated the role and involvement of NaV1.8 (SCN10A) in arrhythmia generation in the human atria and in mice lacking NaV1.8. NaV1.8 mRNA and protein were detected in human atrial myocardium at a significant higher level compared to ventricular myocardium. Expression of NaV1.8 and NaV1.5 did not differ between myocardium from patients with atrial fibrillation and sinus rhythm. To determine the electrophysiological role of NaV1.8, we investigated isolated human atrial cardiomyocytes from patients with sinus rhythm stimulated with isoproterenol. Inhibition of NaV1.8 by A-803467 or PF-01247324 showed no effects on the human atrial action potential. However, we found that NaV1.8 significantly contributes to late Na+ current and consequently to an increased proarrhythmogenic diastolic sarcoplasmic reticulum Ca2+ leak in human atrial cardiomyocytes. Selective pharmacological inhibition of NaV1.8 potently reduced late Na+ current, proarrhythmic diastolic Ca2+ release, delayed afterdepolarizations as well as spontaneous action potentials. These findings could be confirmed in murine atrial cardiomyocytes from wild-type mice and also compared to SCN10A−/− mice (genetic ablation of NaV1.8). Pharmacological NaV1.8 inhibition showed no effects in SCN10A−/− mice. Importantly, in vivo experiments in SCN10A−/− mice showed that genetic ablation of NaV1.8 protects against atrial fibrillation induction. This study demonstrates that NaV1.8 is expressed in the murine and human atria and contributes to late Na+ current generation and cellular arrhythmogenesis. Blocking NaV1.8 selectively counteracts this pathomechanism and protects against atrial arrhythmias. Thus, our translational study reveals a new selective therapeutic target for treating atrial arrhythmias."],["dc.identifier.doi","10.1007/s00395-020-0780-8"],["dc.identifier.pmid","32078054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70756"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/349"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.rights","CC BY 4.0"],["dc.title","Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","P4479"],["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","suppl_1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Iyer, L. M."],["dc.contributor.author","Noack, C."],["dc.contributor.author","Nagarajan, S."],["dc.contributor.author","Woelfer, M."],["dc.contributor.author","Schoger, E."],["dc.contributor.author","Pang, S. T."],["dc.contributor.author","Kari, V."],["dc.contributor.author","Zafeiriou, M. P."],["dc.contributor.author","Toischer, K."],["dc.contributor.author","Hasenfuss, G."],["dc.contributor.author","Johnsen, S. A."],["dc.contributor.author","Zelarayan, L. C."],["dc.date.accessioned","2019-02-19T13:47:43Z"],["dc.date.available","2019-02-19T13:47:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/eurheartj/ehx504.P4479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57586"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/177"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.issn","0195-668X"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","B-catenin/TCF7L2 signaling orchestrates initiation of pathological hypertrophic cardiac remodeling by inducing chromatin modifications"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Keweloh, B."],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Wehling, M."],["dc.contributor.author","Domeier, E."],["dc.contributor.author","Janssen, PML"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T09:30:10Z"],["dc.date.available","2018-11-07T09:30:10Z"],["dc.date.issued","2001"],["dc.format.extent","583A"],["dc.identifier.isi","000166692202658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31236"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.publisher.place","Bethesda"],["dc.relation.issn","0006-3495"],["dc.title","Influence of amino-pyruvate on contractility and cardiac energy metabolism in isolated rabbit myocardial trabeculae"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","286"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","EuroIntervention"],["dc.bibliographiccitation.lastpage","293"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Korte, Kerstin Pia"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Danner, Bernhard"],["dc.contributor.author","Schoendube, Friedrich"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.date.accessioned","2021-06-01T10:48:55Z"],["dc.date.available","2021-06-01T10:48:55Z"],["dc.date.issued","2017"],["dc.description.abstract","AIMS: The objective of this study was to examine the impact of guideline-defined subtypes of severe aortic stenosis (AS) on long-term outcomes after TAVI. METHODS AND RESULTS: Four hundred (400) consecutive patients who underwent TAVI (203 transapical, 197 transfemoral) at our institution 8/2008-3/2013 were followed systematically (for up to seven years). One hundred and forty-seven (147) individuals suffered from NEF-HG AS (LV-EF ≥50%, high Pmean ≥40 mmHg), 63 from LEF-HG AS (LV-EF <50%, high gradient), 77 from PLF-LG AS (LV-EF ≥50%, low gradient, stroke volume index [SVI] <35 ml/m²), and 81 from LEF-LG AS (LV-EF <50%, low gradient). LEF-LG status was associated with the highest all-cause and cardiovascular mortality and MACCE rate, whereas NEF-HG patients exhibited the best outcome (i.e., median survival 5.1 years in NEF-HG vs. 1.3 years in LEF-LG, p=0.0006; or vs. 3.3 years in PLF-LG, p=0.02). In multivariate analysis, LEF-LG status emerged as the outcome predictor with the highest hazard ratio for all-cause mortality (HR 2.86, p=0.003), cardiovascular mortality (HR 6.53, p<0.0001), and MACCE (HR 2.44, p=0.007), whereas neither baseline EF nor SVI <35 ml/m² independently predicted these endpoints. CONCLUSIONS: These findings suggest that an assessment of LV-EF alone for outcome prediction after TAVI is inadequate; it is the guideline-defined subtype of AS that determines outcome."],["dc.identifier.doi","10.4244/EIJ-D-16-00801"],["dc.identifier.gro","3142338"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86102"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.relation.issn","1774-024X"],["dc.title","Long-term outcomes after TAVI in patients with different types of aortic stenosis: the conundrum of low flow, low gradient and low ejection fraction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","149"],["dc.bibliographiccitation.journal","Journal of Translational Medicine"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Qasim, Mohamed"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2017-09-07T11:44:53Z"],["dc.date.available","2017-09-07T11:44:53Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Hemodynamic load leads to cardiac hypertrophy and heart failure. While afterload (pressure overload) induces concentric hypertrophy, elevation of preload (volume overload) yields eccentric hypertrophy and is associated with a better outcome. Here we analysed the proteomic pattern of mice subjected to short-term preload. Methods and Results: Female FVB/N mice were subjected to aortocaval shunt-induced volume overload that leads to an eccentric hypertrophy (left ventricular weight/tibia length +31 %) with sustained systolic heart function at 1 week after operation. Two-dimensional gel electrophoresis (2-DE) followed by mass spectrometric analysis showed alteration in the expression of 25 protein spots representing 21 different proteins. 64 % of these protein spots were up-regulated and 36 % of the protein spots were consistently down-regulated. Interestingly, alpha-1-antitrypsin was down-regulated, indicating higher elastin degradation and possibly contributing to the early dilatation. In addition to contractile and mitochondrial proteins, polymerase I and transcript release factor protein (PTRF) was also up-regulated, possibly contributing to the preload-induced signal transduction. Conclusions: Our findings reveal the proteomic changes of early-stage eccentric myocardial remodeling after volume overload. Induced expression of some of the respiratory chain enzymes suggests a metabolic shift towards an oxidative phosphorylation that might contribute to the favorable remodeling seen in early VO. Down-regulation of alpha-1-antitrypsin might contribute to extracellular matrix remodeling and left ventricular dilatation. We also identified PTRF as a potential signaling regulator of volume overload-induced cardiac hypertrophy."],["dc.identifier.doi","10.1186/s12967-016-0898-5"],["dc.identifier.gro","3141681"],["dc.identifier.isi","000377182700001"],["dc.identifier.pmid","27234427"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8784"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation [SFB1002]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1479-5876"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Proteomic analysis of short-term preload-induced eccentric cardiac hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","16"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cardiac Failure"],["dc.bibliographiccitation.lastpage","23"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Abraham, William T."],["dc.contributor.author","Lindenfeld, Joann"],["dc.contributor.author","Reddy, Vivek Y."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Kuck, Karl-Heinz"],["dc.contributor.author","Boscardin, John"],["dc.contributor.author","Gibbons, Robert"],["dc.contributor.author","Burkhoff, Daniel"],["dc.date.accessioned","2017-09-07T11:44:46Z"],["dc.date.available","2017-09-07T11:44:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Cardiac contractility modulation (CCM) signals are nonexcitatory electrical signals delivered during the cardiac absolute refractory period that enhance the strength of cardiac muscular contraction. The FIX-HF-5 study was a prospective randomized study comparing. CCM plus optimal medical therapy (OMT) to OMT alone that included 428 New York Heart Association (NYHA) functional class III or IV heart failure patients with ejection fraction (EF) <= 45% according to core laboratory assessment. The study met its primary safety end point, but did not reach its primary efficacy end point: a responders analysis of changes in ventilatory anaerobic threshold (VAT). However, in a prespecified subgroup analysis, significant improvements in primary and secondary end points, including the responder VAT end point, were observed in patients with EFs ranging from 25% to 45%, who constituted about one-half of the study subjects. We therefore designed a new study to prospectively confirm the efficacy of CCM in this population. A hierarchic bayesian statistical analysis plan was developed to take advantage of the data already available from the first study. In addition, based on technical difficulties encountered in reliably quantifying VAT and the relatively large amount of nonquantifiable studies, the primary efficacy end point was changed to peak VO2, with significant measures incorporated to minimize the influence of placebo effect. In this paper, we provide the details and rationale of the FIX-HF-5C study design to study CCM plus OMT compared with OMT alone in subjects with normal QRS duration, NYHA functional class III or IV, and EF 25%-45%. This study is registered on www.clinicaltrials.gov with identifier no. NCT01381172."],["dc.identifier.doi","10.1016/j.cardfail.2014.09.011"],["dc.identifier.gro","3141989"],["dc.identifier.isi","000347869300004"],["dc.identifier.pmid","25285748"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3312"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Impulse Dynamics"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Churchill Livingstone Inc Medical Publishers"],["dc.relation.eissn","1532-8414"],["dc.relation.issn","1071-9164"],["dc.title","A Randomized Controlled Trial to Evaluate the Safety and Efficacy of Cardiac Contractility Modulation in Patients With Moderately Reduced Left Ventricular Ejection Fraction and a Narrow QRS Duration: Study Rationale and Design"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0224453"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Hellenkamp, Kristian"],["dc.contributor.author","Unsöld, Bernhard"],["dc.contributor.author","Mushemi-Blake, Sitali"],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.editor","Ehrman, Robert"],["dc.date.accessioned","2020-12-10T18:42:11Z"],["dc.date.available","2020-12-10T18:42:11Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1371/journal.pone.0224453"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77837"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A machine learning approach for the prediction of pulmonary hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","955"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","963"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Drexler, H."],["dc.contributor.author","Kastner, S."],["dc.contributor.author","Strobel, A."],["dc.contributor.author","Studer, R."],["dc.contributor.author","Brodde, Otto E."],["dc.contributor.author","Hasenfuß, G."],["dc.date.accessioned","2017-09-07T11:48:06Z"],["dc.date.available","2017-09-07T11:48:06Z"],["dc.date.issued","1998"],["dc.description.abstract","Objectives. The study was designed to evaluate the functional impact of nitric oxide (NO) generation within the myocardium on cardiac contraction in the failing human heart. Background. Heart failure is associated with activation of cytokines and expression of inducible nitric oxide synthase (NOS II), which generates NO from L-arginine. Nitric oxide has been shown to modulate myocardial performance, raising the possibility that cardiac generation of NO by NOS II modulates cardiac contraction in the failing human heart. Methods. Left ventricular (LV) tissue of 24 patients with end-stage heart failure was obtained during cardiac transplantation. Gene expression of NOS II and endothelial NO-synthase (NOS III) was quantified by competitive reverse transcription-polymerase chain reaction and compared to tissues of five non-failing donor hearts. Nitric oxide synthase II activity was determined by citrulline assay and related to changes in force of contraction induced by the beta-adrenergic agonist isoproterenol, NO-donors and/or N-mono-methyl-L-arginine (L-NMMA), an inhibitor of NOS. Results. While NOS III mRNA was reduced in failing hearts, NOS II mRNA was increased in failing LV tissue and correlated with NOS II activity. High NOS II activity was associated with early relaxation and impaired responsiveness to beta-adrenergic stimulation, that is, the inotropic response to isoproterenol in failing hearts was inversely related to NOS II activity (r = 0.61, p < 0.005). Nitric oxide donors or L-NMMA did not affect myocardial performance in failing hearts at baseline. However, L-NMMA enhanced the positive inotropic response to beta-adrenergic stimulation in failing hearts with high NOS II activity. Nitric oxide donors attenuated the isoproterenol-induced increase in force of contraction of failing hearts. Conclusions. Cardiac production of NO by NOS II attenuates the positive inotropic effects of beta-adrenergic stimulation and hastens relaxation in failing human hearts. (C) 1998 by the American College of Cardiology."],["dc.identifier.doi","10.1016/S0735-1097(98)00336-2"],["dc.identifier.gro","3144518"],["dc.identifier.isi","000076214000014"],["dc.identifier.pmid","9768717"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2151"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1558-3597"],["dc.relation.issn","0735-1097"],["dc.title","Expression, activity and functional significance of inducible nitric oxide synthase in the failing human heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","191"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:59Z"],["dc.date.available","2017-09-07T11:51:59Z"],["dc.date.issued","1989"],["dc.identifier.doi","10.1007/BF02650359"],["dc.identifier.gro","3144839"],["dc.identifier.isi","A1989CB18400020"],["dc.identifier.pmid","2573341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2507"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0300-8428"],["dc.title","CLINICAL RELEVANCE OF LONG-TERM THERAPY WITH LEVODOPA AND ORALLY ACTIVE DOPAMINE ANALOGS IN PATIENTS WITH CHRONIC CONGESTIVE HEART-FAILURE"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wagenhäuser, Markus U."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Yoshino, Takuya"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Guenther, Sabina P."],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Mulorz, Joscha"],["dc.contributor.author","Mulorz, Pireyatharsheny"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Ibing, Wiebke"],["dc.contributor.author","Elvers, Margitta"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Ramasubramanian, Anand K."],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Schelzig, Hubert"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2020-12-10T18:44:37Z"],["dc.date.available","2020-12-10T18:44:37Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fphys.2018.01459"],["dc.identifier.eissn","1664-042X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78531"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chronic Nicotine Exposure Induces Murine Aortic Remodeling and Stiffness Segmentation—Implications for Abdominal Aortic Aneurysm Susceptibility"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]