Now showing 1 - 10 of 17
  • 2011Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","528"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Aims The calcineurin and nuclear factor of activated T cells (NFAT) pathway can mediate pro-hypertrophic signalling in the heart. Recently, it has been shown that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) phosphorylates NFAT, which limits calcineurin/NFAT signal transduction in T cells and hypertrophy in cultured cardiomyocytes. The hypothesis tested in this study was that DYRK1A prevents calcineurin/NFAT-mediated cardiac hypertrophy in vivo. Methods and results In cultured rat cardiomyocytes, adenovirus-mediated overexpression of DYRK1A antagonized calcineurin-mediated nuclear NFAT translocation and the phenylephrine-induced hypertrophic growth response. To test the ability of DYRK1A to reduce hypertrophic cardiac growth in vivo, we created tetracycline-repressible Dyrk1a transgenic mice to avoid the cardiac developmental defects associated with embryonic DYRK1A expression. However, in the mouse model, histological determination of myocyte diameter, heart weight/body weight ratio, and echocardiographic measurements revealed that myocardial expression of DYRK1A failed to reduce hypertrophy induced via aortic banding or co-expression of calcineurin. This discrepancy is explained, at least in part, by insufficient long-term inhibition of NFAT and the activation of DYRK1A-resistant maladaptive genes in vivo. Conclusion Isolated augmentation of DYRK1A can be compensated for in vivo, and this may significantly limit anti-hypertrophic interventions aimed at enhancing DYRK1A activity."],["dc.identifier.doi","10.1093/cvr/cvr023"],["dc.identifier.gro","3142722"],["dc.identifier.isi","000290820200018"],["dc.identifier.pmid","21273244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/157"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","267"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","276"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Pelster, Theresa"],["dc.contributor.author","Pax, Anja"],["dc.contributor.author","Horn, Wiebke"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Wagner, Stephan"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2010"],["dc.description.abstract","Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We analyzed hemodynamic data from 200 cardiac arrest survivors during the hypothermia period. The initial LVEF was 32.6 +/- A 1.2% indicating a significantly impaired LV function. During hypothermia induction, the infusion rate of epinephrine could be significantly reduced from 9.1 +/- A 1.3 mu g/min [arrival intensive care unit (ICU) 35.4A degrees C] to 4.6 +/- A 1.0 mu g/min (34A degrees C) and 2.8 +/- A 0.5 mu g/min (33A degrees C). The dobutamine and norepinephrine application rates were not changed significantly. The mean arterial blood pressure remained stable. The mean heart rate significantly decreased from 91.8 +/- A 1.7 bpm (arrival ICU) to 77.3 +/- A 1.5 bpm (34A degrees C) and 70.3 +/- A 1.4 bpm (33A degrees C). In vitro we investigated the effect of hypothermia on isolated ventricular muscle strips from explanted failing human hearts. With decreasing temperature, the contractility increased to a maximum of 168 +/- A 23% at 27A degrees C (n = 16, P < 0.05). Positive inotropic response to hypothermia was accompanied by moderately increased rapid cooling contractures as a measure of sarcoplasmic reticulum (SR) Ca(2+) content, but can be elicited even when the SR Ca(2+) release is blocked in the presence of ryanodine. Contraction and relaxation kinetics are prolonged with hypothermia, indicating increased Ca(2+) sensitivity as the main mechanism responsible for inotropy. In conclusion, mild hypothermia stabilizes hemodynamics in cardiac arrest survivors which might contribute to improved survival rates in these patients. Mechanistically, we demonstrate that hypothermia improves contractility in failing human myocardium most likely by increasing Ca(2+)-sensitivity."],["dc.identifier.doi","10.1007/s00392-010-0113-2"],["dc.identifier.gro","3142931"],["dc.identifier.isi","000277014600001"],["dc.identifier.pmid","20130890"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4240"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/389"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium"],["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"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schuster, Manfred"],["dc.contributor.author","Loibner, Hans"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kuba, Keiji"],["dc.contributor.author","Imai, Yumiko"],["dc.contributor.author","Penninger, Josef"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T11:09:55Z"],["dc.date.available","2018-11-07T11:09:55Z"],["dc.date.issued","2008"],["dc.format.extent","S947"],["dc.identifier.isi","000262104503504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53105"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Angiotensin-Converting-Enzyme 2 (rhACE2) Potently Attenuates the Negative Hemodynamic Effects of Angiotensin II (ATII) and Improves Post-Myocardial Infarction (MI) Remodeling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T11:11:18Z"],["dc.date.available","2018-11-07T11:11:18Z"],["dc.date.issued","2008"],["dc.format.extent","265"],["dc.identifier.isi","000208702501245"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53401"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Large volume, ice-cold intravenous fluid for therapeutic hypothermia does not compromise the respiratory situation in patients after cardiac arrest"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","744"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T08:52:46Z"],["dc.date.available","2018-11-07T08:52:46Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1093/cvr/cvr193"],["dc.identifier.isi","000294069300024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22252"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Letter concerning: 'Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo': reply"],["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"]]
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  • 2015Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Therapeutics"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2017-09-07T11:44:39Z"],["dc.date.available","2017-09-07T11:44:39Z"],["dc.date.issued","2015"],["dc.description.abstract","BackgroundPantoprazole has been shown to exert a negative inotropic effect in isolated myocardium. The purpose of this study was to evaluate the hemodynamic effects of pantoprazole in vivo in healthy myocardium and in the setting of heart failure. Methods and ResultsHealthy mice and mice with heart failure 4weeks after myocardial infarction induced by permanent LAD ligation were instrumented with a Millar Mikrotip conductance catheter to record pressure-volume loops. Pantoprazole was infused at rates of 3 and 10mg/kg/min intravenously, and hemodynamic parameters were recorded. Infusion of pantoprazole at increasing rates lead to a significant decline of end systolic LV pressure by decreasing heart rate, myocardial contractility and arterial elastance. These effects were quick, beginning immediately with the infusion and usually reaching a plateau after 2 or 3min of infusion. The effects on blood pressure and heart rate were of comparable size in healthy mice and mice with MI. However, in sham-operated mice, there was a compensatory increase in stroke volume that sufficed to maintain cardiac output at a constant level, which was missing in mice with MI. In 4 of 13 mice with MI infusion of 10mg/kg/min pantoprazole lead to pump failure, which was lethal in 2 of these animals. ConclusionAt higher infusion rates, pantoprazole is able to induce negative hemodynamic responses. In particular, in the setting of heart failure, these effects can lead to significant impairment of cardiac function. Therefore, high infusion rates of pantoprazole should be avoided especially in heart failure patients."],["dc.identifier.doi","10.1111/1755-5922.12102"],["dc.identifier.gro","3141966"],["dc.identifier.isi","000348660500004"],["dc.identifier.pmid","25529757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3057"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.eissn","1755-5922"],["dc.relation.issn","1755-5914"],["dc.title","Negative Hemodynamic Effects of Pantoprazole at High Infusion Rates in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2011Conference Abstract
    [["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Pelster, Theresa"],["dc.contributor.author","Pax, Anja"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Maier, Lars. S."],["dc.date.accessioned","2018-11-07T08:49:42Z"],["dc.date.available","2018-11-07T08:49:42Z"],["dc.date.issued","2011"],["dc.identifier.isi","000299738700061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21528"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Trends in Postresuscitation Care: A 7-Year Experience After Implementation of Therapeutic Hypothermia"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article
    [["dc.bibliographiccitation.firstpage","e241"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cardiovascular Pathology"],["dc.bibliographiccitation.lastpage","e250"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Köhler, Jürgen"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:52:37Z"],["dc.date.available","2017-09-07T11:52:37Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.carpath.2009.11.005"],["dc.identifier.gro","3144974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2659"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Elsevier BV"],["dc.relation.issn","1054-8807"],["dc.title","Proteome changes in CaMKIIδC-overexpressing cardiac myocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.date.accessioned","2018-11-07T10:10:31Z"],["dc.date.available","2018-11-07T10:10:31Z"],["dc.date.issued","2016"],["dc.format.extent","945"],["dc.identifier.isi","000383869504531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39871"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Rome, ITALY"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Outcome of interventional treatment for access site complications in transfemoral aortic valve implantation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2020Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","46"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Magnetic Resonance"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Backhaus, Sören Jan"],["dc.contributor.author","Lange, Torben"],["dc.contributor.author","Beuthner, Bo Eric"],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Wang, Xiaoqing"],["dc.contributor.author","Kowallick, Johannes Tammo"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Uecker, Martin"],["dc.contributor.author","Hasenfuß, Gerd P."],["dc.contributor.author","Schuster, Andreas"],["dc.date.accessioned","2021-03-08T07:13:57Z"],["dc.date.available","2021-03-08T07:13:57Z"],["dc.date.issued","2020"],["dc.description.abstract","Myocardial fibrosis is a major determinant of outcome in aortic stenosis (AS). Novel fast real-time (RT) cardiovascular magnetic resonance (CMR) mapping techniques allow comprehensive quantification of fibrosis but have not yet been compared against standard techniques and histology."],["dc.identifier.doi","10.1186/s12968-020-00632-0"],["dc.identifier.pmid","32564773"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17418"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80477"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/50"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/359"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.issn","1532-429X"],["dc.relation.workinggroup","RG Hasenfuß"],["dc.relation.workinggroup","RG Uecker"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Backhaus"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Real-time cardiovascular magnetic resonance T1 and extracellular volume fraction mapping for tissue characterisation in aortic stenosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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