Dellas, Claudia

[["dc.bibliographiccitation.issue","48"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T11:08:55Z"],["dc.date.available","2018-11-07T11:08:55Z"],["dc.date.issued","2008"],["dc.format.extent","2511"],["dc.identifier.doi","10.1055/s-0028-1100948"],["dc.identifier.isi","000261573800005"],["dc.identifier.pmid","19021083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52899"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0012-0472"],["dc.title","Operative treatment in pelvic vein thrombose contra"],["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","220"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","227"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Schremmer, Carmen"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:49:27Z"],["dc.date.available","2017-09-07T11:49:27Z"],["dc.date.issued","2007"],["dc.description.abstract","Urokinase plasminogen activator (uPA) is strongly expressed in atherosclerotic lesions, but the overall effect of the protease on plaque composition and growth remains controversial. In the present study, apolipoprotein E-deficient (apoE(-/-)) mice were intercrossed with mice which were lacking the uPA gene (double-knockout; DKO). In ferric chloride-induced carotid artery lesions in chow-fed mice, uPA deficiency increased neointimal size (P=0.015) and luminal stenosis (P=0.014), while reducing media thickness (P=0.002). A lack of uPA also increased the size of and the luminal obstruction from atherosclerotic plaques at the coronary and brachiocephalic arteries of apoE(-/-) mice. Plaques were characterised by a higher fibrinogen/fibrin content and a decrease in cellularity and collagen content. When apoE(-/-) and DKO mice were analysed as a single group, a significant-correlation was found between the (x-actin (smooth muscle cell) and collagen content of atherosclerotic lesions (r = 0.554; P < 0.05), and a negative correlation existed between the a-actin and fibrin/fibrinogen immunopositive area (r = -0.79 1; P < 0.001). Further analysis of brachiocephalic atherosclerosis, a predilection site for plaque rupture in the apoE(-/-) mouse, revealed signs of plaque vulnerability, including a reduced cap-to-intima ratio (0.21 +/- 0.04 vs. 0.37 +/- 0.05; P=0.03) and more frequent detection of intraplaque haemorrhage (56% vs. 13%; P < 0.01) and buried fibrous caps (1.8 +/- 0.5 vs. 0.5 +/- 0.2; P=0.02) in DKO compared to apoE(-/-) mice. These results indicate that, at least at (patho) physiologic concentrations, uPA is essential for maintaining the cellularity and collagen content and, possibly, the stability of lesions, both by preventing excessive intramural fibrin accumulation and by facilitating cell migration and invasion."],["dc.identifier.doi","10.1160/TH06-09-0508"],["dc.identifier.gro","3143478"],["dc.identifier.isi","000248180700037"],["dc.identifier.pmid","17598016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/996"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0340-6245"],["dc.title","Lack of urokinase plasminogen activator promotes progression and instability of atherosclerotic lesions in apolipoprotein E-knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1402"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","New England Journal of Medicine"],["dc.bibliographiccitation.lastpage","1411"],["dc.bibliographiccitation.volume","370"],["dc.contributor.author","Meyer, Guy"],["dc.contributor.author","Vicaut, Eric"],["dc.contributor.author","Danays, Thierry"],["dc.contributor.author","Agnelli, Giancarlo"],["dc.contributor.author","Becattini, Cecilia"],["dc.contributor.author","Beyer-Westendorf, Jan"],["dc.contributor.author","Bluhmki, Erich"],["dc.contributor.author","Bouvaist, Helene"],["dc.contributor.author","Brenner, Benjamin"],["dc.contributor.author","Couturaud, Francis"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Empen, Klaus"],["dc.contributor.author","Franca, Ana"],["dc.contributor.author","Galie, Nazzareno"],["dc.contributor.author","Geibel, Annette"],["dc.contributor.author","Goldhaber, Samuel Z."],["dc.contributor.author","Jimenez, David"],["dc.contributor.author","Kozak, Matija"],["dc.contributor.author","Kupatt, Christian"],["dc.contributor.author","Kucher, Nils"],["dc.contributor.author","Lang, Irene M."],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Meneveau, Nicolas"],["dc.contributor.author","Pacouret, Gerard"],["dc.contributor.author","Palazzini, Massimiliano"],["dc.contributor.author","Petris, Antoniu"],["dc.contributor.author","Pruszczyk, Piotr"],["dc.contributor.author","Rugolotto, Matteo"],["dc.contributor.author","Salvi, Aldo"],["dc.contributor.author","Schellong, Sebastian"],["dc.contributor.author","Sebbane, Mustapha"],["dc.contributor.author","Sobkowicz, Bozena"],["dc.contributor.author","Stefanovic, Branislav S."],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Torbicki, Adam"],["dc.contributor.author","Verschuren, Franck"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T09:41:18Z"],["dc.date.available","2018-11-07T09:41:18Z"],["dc.date.issued","2014"],["dc.description.abstract","BackgroundThe role of fibrinolytic therapy in patients with intermediate-risk pulmonary embolism is controversial. MethodsIn a randomized, double-blind trial, we compared tenecteplase plus heparin with placebo plus heparin in normotensive patients with intermediate-risk pulmonary embolism. Eligible patients had right ventricular dysfunction on echocardiography or computed tomography, as well as myocardial injury as indicated by a positive test for cardiac troponin I or troponin T. The primary outcome was death or hemodynamic decompensation (or collapse) within 7 days after randomization. The main safety outcomes were major extracranial bleeding and ischemic or hemorrhagic stroke within 7 days after randomization. ResultsOf 1006 patients who underwent randomization, 1005 were included in the intention-to-treat analysis. Death or hemodynamic decompensation occurred in 13 of 506 patients (2.6%) in the tenecteplase group as compared with 28 of 499 (5.6%) in the placebo group (odds ratio, 0.44; 95% confidence interval, 0.23 to 0.87; P=0.02). Between randomization and day 7, a total of 6 patients (1.2%) in the tenecteplase group and 9 (1.8%) in the placebo group died (P=0.42). Extracranial bleeding occurred in 32 patients (6.3%) in the tenecteplase group and 6 patients (1.2%) in the placebo group (P<0.001). Stroke occurred in 12 patients (2.4%) in the tenecteplase group and was hemorrhagic in 10 patients; 1 patient (0.2%) in the placebo group had a stroke, which was hemorrhagic (P=0.003). By day 30, a total of 12 patients (2.4%) in the tenecteplase group and 16 patients (3.2%) in the placebo group had died (P=0.42). ConclusionsIn patients with intermediate-risk pulmonary embolism, fibrinolytic therapy prevented hemodynamic decompensation but increased the risk of major hemorrhage and stroke. (Funded by the Programme Hospitalier de Recherche Clinique in France and others; PEITHO EudraCT number, 2006-005328-18; ClinicalTrials.gov number, NCT00639743.) In a randomized trial, 1006 patients with intermediate-risk pulmonary embolism were assigned to tenecteplase or placebo in addition to standard heparin therapy. The tenecteplase group had a lower rate of hemodynamic decompensation but more frequent major hemorrhage and stroke. Acute pulmonary embolism occurs frequently and may cause death or serious disability.(1) Case fatality rates vary widely,(2),(3) but approximately 10% of all patients with acute pulmonary embolism die within 3 months after the diagnosis.(4),(5) Acute right ventricular pressure overload at diagnosis is an important determinant of the severity and early clinical outcome of pulmonary embolism.(6) High-risk pulmonary embolism(7) is characterized by overt hemodynamic instability and warrants immediate advanced therapy, including consideration of fibrinolysis. In contrast, for patients presenting without systemic hypotension or hemodynamic compromise, standard anticoagulation is generally considered adequate treatment.(8) However, patients who have acute right ventricular ..."],["dc.identifier.doi","10.1056/NEJMoa1302097"],["dc.identifier.isi","000334095200008"],["dc.identifier.pmid","24716681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33698"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Massachusetts Medical Soc"],["dc.relation.issn","1533-4406"],["dc.relation.issn","0028-4793"],["dc.title","Fibrinolysis for Patients with Intermediate-Risk Pulmonary Embolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Kuhnert, K."],["dc.contributor.author","Stuebing, M."],["dc.contributor.author","Schaefer, K."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Dellas, Claudia"],["dc.date.accessioned","2018-11-07T09:07:23Z"],["dc.date.available","2018-11-07T09:07:23Z"],["dc.date.issued","2012"],["dc.format.extent","412"],["dc.identifier.isi","000308012403272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25785"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Munchen, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","Risk stratification of non-high-risk pulmonary embolism by the use of a novel rapid immunoturbidimetric H-FABP assay"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2196"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Arteriosclerosis Thrombosis and Vascular Biology"],["dc.bibliographiccitation.lastpage","2201"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schafer, K."],["dc.contributor.author","Neels, J. G."],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Loskutoff, D. J."],["dc.date.accessioned","2018-11-07T10:44:04Z"],["dc.date.available","2018-11-07T10:44:04Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective - Human obesity is associated with an increased risk for arterial and venous thrombosis and with elevated levels of leptin in the blood. Leptin administration promotes arterial thrombosis in mice, and leptin-deficient ob/ob mice have an attenuated thrombotic response to injury. Thus, endogenous leptin may regulate arterial and venous thrombosis in vivo. Experiments were performed to test this hypothesis. Methods and Results - A leptin-neutralizing antibody was administered intravenously into wild-type mice 15 minutes before carotid artery injury with ferric chloride. The antibody-treated mice demonstrated prolonged times to thrombotic occlusion and formed unstable, embolizing thrombi. Thus, inhibiting leptin converted the thrombotic phenotype of wild-type mice into one that closely resembled that of ob/ob mice. The effect of leptin inhibition on venous thrombosis and pulmonary embolism was also investigated. Injection of a mixture of collagen and epinephrine into the jugular vein induced fatal pulmonary embolism in > 90% of the control wild-type mice but in < 40% of their antibody-treated counterparts. Histological analysis revealed that the antibody significantly reduced the number of occlusive thrombi in the pulmonary vessels. Conclusions - Inhibition of circulating leptin protects against arterial and venous thrombosis in mice and possibly in hyperleptinemic obese individuals."],["dc.description.sponsorship","NHLBI NIH HHS [HL75736, HL47819]"],["dc.identifier.doi","10.1161/01.ATV.0000146531.79402.9a"],["dc.identifier.isi","000224900300035"],["dc.identifier.pmid","15458978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47189"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1079-5642"],["dc.title","Inhibition of endogenous leptin protects mice from arterial and venous thrombosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1063"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","1071"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Rohm, Ilonka"],["dc.contributor.author","Lankeit, Mareike"],["dc.contributor.author","Leifheit, Maren"],["dc.contributor.author","Loskutoff, David J."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2017-09-07T11:49:24Z"],["dc.date.available","2017-09-07T11:49:24Z"],["dc.date.issued","2007"],["dc.description.abstract","Leptin enhances agonist-induced platelet aggregation, and human platelets have been reported to express the leptin receptor. However, the pathways and mediators lying downstream of leptin binding to platelets remain, with few exceptions, unknown. In the present study, we sought to gain further insight into the possible role of leptin as a platelet agonist. Stimulation of platelets with leptin promoted thromboxane generation and activation of alpha(IIb)beta(3), as demonstrated by PAC-I binding. Furthermore, it increased the adhesion to immobilised fibrinogen (p < 0.001) and induced cytoskeletal rearrangement of both platelets and Meg01 cells. Leptin time- and dose-dependently phosphorylated the intracellular signalling molecules JAK2 and STAT3, although the importance of STAT3 for leptin-induced platelet activation remains to be determined. Important intracellular mediators and pathways activated by leptin downstream of JAK2 were found to include phosphaticlylinositol-3 kinase, phospholipase C gamma 2 and protein kinase C,as well as the p38 MAP kinase-phospholipase A(2) axis. Accordingly, incubation with the specific inhibitors AG490, Ly294002, U73122, and SB203580 prevented leptin-mediated platelet activation. These results help delineate biologically relevant leptin signalling pathways in platelets and may improve our understanding of the mechanisms linking hyperleptinaemia to the increased thrombosis risk in human obesity."],["dc.identifier.doi","10.1160/TH07-03-0213"],["dc.identifier.gro","3143420"],["dc.identifier.isi","000251064400021"],["dc.identifier.pmid","18000612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/932"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NCRR NIH HHS [M01 RR00833]; NHLBI NIH HHS [HL75736]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0340-6245"],["dc.title","Leptin signalling and leptin-mediated activation of human platelets: Importance of JAK2 and the phospholipases C gamma 2 and A(2)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","112"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Arteriosclerosis Thrombosis and Vascular Biology"],["dc.bibliographiccitation.lastpage","117"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Schafer, K."],["dc.contributor.author","Halle, Martin"],["dc.contributor.author","Goeschen, C."],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Pynn, M."],["dc.contributor.author","Loskutoff, D. J."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T10:52:03Z"],["dc.date.available","2018-11-07T10:52:03Z"],["dc.date.issued","2004"],["dc.description.abstract","Objectives-Human obesity is associated with elevated leptin levels and a high risk of death from cardiovascular disease. In the present study, we investigated the effects of leptin on vascular wound healing and arterial lesion growth in mice. Methods and Results-Wild-type mice placed on an atherogenic, high-fat diet had elevated (9-fold) leptin levels compared with their counterparts maintained on normal chow, and the former demonstrated significantly enhanced neointimal thickening after carotid artery injury with ferric chloride. The lesions forming in response to injury strongly expressed leptin receptor mRNA and protein. Unexpectedly, the atherogenic diet had no effect on injured vessels from leptin-deficient ob/ob mice despite aggravating obesity, diabetes, and hyperlipidemia in these animals. Daily administration of leptin to ob/ob mice during the 3-week period after injury reversed this phenotype, dramatically increasing neointimal thickness and the severity of luminal stenosis. Exogenous leptin also enhanced lesion growth and increased cellular proliferation in injured arteries from wild-type mice but had no effect on vessels from leptin receptor-deficient db/db mice. Conclusions-Our results raise the possibility that there might be a direct, leptin receptor-mediated link between the hyperleptinemia in human obesity and the increased risk for cardiovascular complications associated with this condition."],["dc.description.sponsorship","NHLBI NIH HHS [HL 47819]"],["dc.identifier.doi","10.1161/01.ATV.0000105904.02142.e7"],["dc.identifier.isi","000187791600018"],["dc.identifier.pmid","14615386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49030"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1079-5642"],["dc.title","Leptin promotes vascular remodeling and neointimal growth in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Friesen, D."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Dellas, Claudia"],["dc.date.accessioned","2018-11-07T08:39:21Z"],["dc.date.available","2018-11-07T08:39:21Z"],["dc.date.issued","2010"],["dc.format.extent","627"],["dc.identifier.isi","000281531904141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","0195-668X"],["dc.title","Bedside testing for H-FABP is a useful tool for immediate risk stratification of normotensive patients with acute pulmonary embolism"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1254"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","1259"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Weiss, Elisabeth"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2017-09-07T11:52:41Z"],["dc.date.available","2017-09-07T11:52:41Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective - To investigate the ability of bone marrow ( BM) - derived cells to modulate neointimal growth after injury by expressing plasminogen activator inhibitor-1 ( PAI-1). Methods and Results - We performed BM transplantation ( BMT) in lethally irradiated wild- type ( WT) and PAI-1-/- mice. Three weeks after carotid injury with ferric chloride, analysis of Y-chromosome DNA expression in the vessel wall of female hosts revealed that 20.8 +/- 6.0% of the cells in the neointima and 37.6 +/- 5.7% of those in the media were of BM origin. Lack of PAI-1 in either the host or the donor cells did not affect recruitment of BM-derived cells into sites of vascular injury. The neointima consisted predominantly of smooth muscle cells, and a proportion of these cells expressed PAI-1. Overall, lack of PAI-1 was associated with enhanced neointimal formation. However, importantly, BMTWT -> PAI-1-/- mice exhibited reduced neointimal area ( P = 0.05) and luminal stenosis ( P = 0.04) compared with BMTPAI-1-/--> PAI-1-/- mice. Although PAI-1-expressing cells were shown to be present in BMTWT -> PAI-1-/- lesions, these mice did not exhibit detectable levels of the inhibitor in the circulation, suggesting that local production of PAI-1 by cells in the neointima and media was sufficient to reduce luminal stenosis. Conclusions - PAI-1 from BM-derived cells appears capable of suppressing neointimal growth after vascular injury."],["dc.identifier.doi","10.1161/01.ATV.0000215982.14003.b7"],["dc.identifier.gro","3143681"],["dc.identifier.isi","000237644000012"],["dc.identifier.pmid","16514083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1221"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1079-5642"],["dc.title","Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Benz, V."],["dc.contributor.author","Schaefer, K."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Dellas, Claudia"],["dc.date.accessioned","2018-11-07T08:53:56Z"],["dc.date.available","2018-11-07T08:53:56Z"],["dc.date.issued","2011"],["dc.format.extent","979"],["dc.identifier.isi","000208702707156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22545"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","The predictive value of heart-type fatty acid-binding protein is independent from the duration of symptoms in normotensive patients with acute pulmonary embolism"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]