Schroeter, Marco Robin

[["dc.bibliographiccitation.firstpage","423"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Stroke"],["dc.bibliographiccitation.lastpage","429"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Schnieder, Marlena"],["dc.contributor.author","Siddiqui, Tariq"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schroeter, Marco R"],["dc.contributor.author","Liman, Jan"],["dc.date.accessioned","2020-12-10T18:38:36Z"],["dc.date.available","2020-12-10T18:38:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1177/1747493018816511"],["dc.identifier.eissn","1747-4949"],["dc.identifier.issn","1747-4930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77384"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Low flow in the left atrial appendage assessed by transesophageal echocardiography is associated with increased stroke severity—Results of a single-center cross-sectional study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Leifheit, Maren"],["dc.contributor.author","Conrad, Gaby"],["dc.contributor.author","Heide, Nana-Maria"],["dc.contributor.author","Schroeter, Marco"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T11:22:15Z"],["dc.date.available","2018-11-07T11:22:15Z"],["dc.date.issued","2009"],["dc.format.extent","S1151"],["dc.identifier.isi","000271831504246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55953"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","82nd Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0009-7322"],["dc.title","Overexpression of Integrin Beta5 Enhances the Paracrine Angiogenic Properties of Early Outgrowth Endothelial Progenitor Cells via Sire Kinase-Mediated Activation of STAT3"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","111"],["dc.bibliographiccitation.volume","220"],["dc.contributor.author","Tichelbäcker, Tobias"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Schroeter, Marco Robin"],["dc.date.accessioned","2017-09-07T11:44:37Z"],["dc.date.available","2017-09-07T11:44:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Percutaneous mitral valve repair using MitraClip (R) (MC) is a well-established method for a subset of patients with severe mitral regurgitation (MR) and high risk for surgical intervention. Amplatzer (R) Cardiac Plug (ACP) occludes left atrial appendage and allows the discontinuation of oral anticoagulation and prevention of thromboembolic stroke. Due to the need for femoral and transseptal access in both procedures, a single approach could lead to minor risk of further complications and shorter cumulative intervention time. Methods: We systematically analysed all four patients who underwent a combined procedure with MC and ACP in our heart-centre. All procedures were performed under fluoroscopic as well as echocardiographic guidance, and follow-up controls in a midterm period were carried out. Results: In all patients (2 male/female; age 73-88 years), MC (1-2 Clips) and ACP (size 18-28mm) were successfully implanted in one procedure (mean total time: 114 +/- 17 min). At least moderate MR was achieved and two patients had no complications and therefore were discharged early. In a third patient, a dislocation of ACP occurred 2 h after the implantation. The oldest patient developed a respiratory insufficiency due to cardiac decompensation and further complications. Conclusion: A combination of MC and ACP in a single procedure was feasible in this first case series of patients without a significant extension of procedure time. However, it might be important to select patients carefully. The location of optimal transseptal puncture may be challenging in regard to ACP placement, even in experienced hands and subsequent complications can occur. (C) 2016 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2016.06.170"],["dc.identifier.gro","3141615"],["dc.identifier.isi","000381582000019"],["dc.identifier.pmid","27389439"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1456"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Abbott Vascular; St. Jude Medical"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.eissn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","MitraClip (R) and Amplatzer (R) cardiac plug implantation in a single procedure: A reasonable approach?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","216"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Bochenek, Magdalena L."],["dc.contributor.author","Hubert, Astrid"],["dc.contributor.author","Muenzel, Thomas"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:44:47Z"],["dc.date.available","2017-09-07T11:44:47Z"],["dc.date.issued","2016"],["dc.description.abstract","Cardiac angiogenesis is an important determinant of heart failure. We examined the hypothesis that protein tyrosine phosphatase (PTP)-1B, a negative regulator of vascular endothelial growth factor (VEGF) receptor-2 activation, is causally involved in the cardiac microvasculature rarefaction during hypertrophy and that deletion of PTP1B in endothelial cells prevents the development of heart failure. Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in mice with endothelial-specific deletion of PTP1B (End.PTP1B-KO) and controls (End.PTP1B-WT). Survival up to 20 weeks after TAC was significantly improved in mice lacking endothelial PTP1B. Serial echocardiography revealed a better systolic pump function, less pronounced cardiac hypertrophy, and left ventricular dilation compared with End.PTP1B-WT controls. Histologically, banded hearts from End.PTP1B-KO mice exhibited increased numbers of PCNA-positive, proliferating endothelial cells resulting in preserved cardiac capillary density and improved perfusion as well as reduced hypoxia, apoptotic cell death, and fibrosis. Increased relative VEGFR2 and ERK1/2 phosphorylation and greater eNOS expression were present in the hearts of End.PTP1B-KO mice. The absence of PTP1B in endothelial cells also promoted neovascularization following peripheral ischaemia, and bone marrow transplantation excluded a major contribution of Tie2-positive haematopoietic cells to the improved angiogenesis in End.PTP1B-KO mice. Increased expression of caveolin-1 as well as reduced NADPH oxidase-4 expression, ROS generation and TGF beta signalling were observed and may have mediated the cardioprotective effects of endothelial PTP1B deletion. Endothelial PTP1B deletion improves cardiac VEGF signalling and angiogenesis and protects against chronic afterload-induced heart failure. PTP1B may represent a useful target to preserve cardiac function during hypertrophy."],["dc.identifier.doi","10.1093/cvr/cvw101"],["dc.identifier.gro","3141642"],["dc.identifier.isi","000383197000008"],["dc.identifier.pmid","27207947"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4455"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/296"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C06: Mechanismen und Regulation der koronaren Gefäßneubildung"],["dc.relation.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Schäfer (Translationale Vaskuläre Biologie)"],["dc.title","Endothelial deletion of protein tyrosine phosphatase-1B protects against pressure overload-induced heart failure in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Heart Journal - Case Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Schroeter, Marco R"],["dc.contributor.author","Klingel, Karin"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.editor","De Potter, Tom"],["dc.contributor.editor","Vidal-Perez, Rafael"],["dc.contributor.editor","Nistor, Dan Octavian"],["dc.contributor.editor","Agarwal, Megha"],["dc.contributor.editor","Sunjaya, Antony Paulo"],["dc.date.accessioned","2022-04-01T10:01:50Z"],["dc.date.available","2022-04-01T10:01:50Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Background Lyme disease is a tick-borne multisystem infection. The most common cardiac manifestation is an acute presentation of Lyme carditis, which often manifests as conduction disorder and rarely as myocarditis. Case summary We report the case of a 37-year-old male with a history of microscopic polyangiitis receiving immunosuppressive therapy. He was admitted for severe dyspnoea secondary to acute heart failure. Echocardiography and cardiac magnetic resonance imaging indicated a severely reduced left ventricular ejection fraction (LVEF) with global hypokinesia. Coronary heart disease was excluded, and endomyocardial biopsies (EMB) were performed. The left ventricular EMB revealed a rare case of fulminant Lyme carditis with evidence of typical lymphocytic myocarditis. Borrelia afzelii-DNA was detected without any relevant atrioventricular blockage or systemic signs of Lyme disease. The patient had no clinically apparent tick-borne infection or self-reported history of a tick bite. Immunological testing revealed a positive ELISA and Immunoblot for anti-Borrelia immunoglobulin G antibodies. After specific intravenous antibiotic therapy and optimized medical therapy for heart failure, the LVEF recovered, and the patient could be discharged in an improved condition. Repeat EMB a few months later revealed a dramatic regression of the cardiac inflammation and absence of Borrelia DNA in the myocardium. Discussion A severely reduced LVEF can be the primary manifestation of Lyme disease even without typical systemic findings and can have a favourable prognosis with antibiotic treatment. A thorough workup for Lyme carditis is required in patients with unexplained heart failure, particularly with EMB, especially in immunosuppressed patients."],["dc.identifier.doi","10.1093/ehjcr/ytac062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105759"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2514-2119"],["dc.title","Fulminant Lyme myocarditis without any other signs of Lyme disease in a 37-year-old male patient with microscopic polyangiitis—a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","473"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","476"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Vollmann, Dirk"],["dc.date.accessioned","2017-09-07T11:47:41Z"],["dc.date.available","2017-09-07T11:47:41Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1007/s00392-013-0557-2"],["dc.identifier.gro","3142348"],["dc.identifier.isi","000319081700008"],["dc.identifier.pmid","23529655"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7286"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1861-0684"],["dc.title","Atrial standstill in a patient with progressive severe heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Schroeter, M. R."],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantindes, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2018-11-07T10:57:45Z"],["dc.date.available","2018-11-07T10:57:45Z"],["dc.date.issued","2007"],["dc.format.extent","839"],["dc.identifier.isi","000250394303788"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50323"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","80th Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0009-7322"],["dc.title","Effects of obesity and weight loss on the functional properties of endothelial progenitor cells"],["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.firstpage","264"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Schnieder, Marlena"],["dc.contributor.author","Siddiqui, Tariq"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2018-04-23T11:49:25Z"],["dc.date.available","2018-04-23T11:49:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: A significant proportion of ischemic strokes are cryptogenic. In this context, the clinical pertinence of patent foramen ovale (PFO) with and without atrial septum aneurysm (ASA) remains controversial. The aim of this study was to identify how PFO +/–ASA and cryptogenic stroke are associated in a representative sample of stroke patients. Methods: We enrolled all patients (n = 909) with ischemic stroke or transient ischemic attack admitted to the certified stroke unit or neurological intensive care unit of our university medical center who underwent transesophageal echocardiography (TEE) between 2012 and 2014. The baseline characteristics, cardio-/neurovascular risk factors, clinical parameters and TEE findings were analyzed. Results: PFO was present in 26.2%, and PFO was combined with an ASA in 9.9%. In cryptogenic stroke, the prevalence of PFO was higher compared to other etiologies (30.9 vs. 21.9%; p < 0.002). Patients with PFO had lower National Institute of Health Stroke Score (NIHSS) values at admission than those without (2 [0–5] vs. 3 [1–7]; p = 0.001; 95% CI [0.62–0.88]). No difference was found in NIHSS values of PFO patients with or without ASA (2 [0–5] vs. 2 [0–5]; p = 0.683; 95% CI 0.94 [0.68–1.28]). Conclusions: Our study indicates that a detected PFO +/–ASA could exhibit a stroke-relevant finding, if classical risk factors for the stroke were lacking."],["dc.identifier.doi","10.1159/000479962"],["dc.identifier.gro","3142067"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13691"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0014-3022"],["dc.title","Clinical Relevance of Patent Foramen Ovale and Atrial Septum Aneurysm in Stroke: Findings of a Single-Center Cross-Sectional Study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","206"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Henkel, Sarah"],["dc.contributor.author","Limbourg, Anne"],["dc.contributor.author","Limbourg, Florian P."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Quigley, James P."],["dc.contributor.author","Ruggeri, Zaverio M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:10Z"],["dc.date.available","2017-09-07T11:46:10Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective-To investigate the capacity of the adipokine leptin to promote angiogenesis by modulating the function of circulating angiogenic cells (CACs). Methods and Results-In vitro, leptin specifically promoted CAC adhesion to tubular endothelial structures and migration along outgrowing sprouts of endothelial cells. In vivo, stimulation of CACs with leptin increased their capacity to promote new vessel formation in the chorioallantoic membrane of chicken embryos and to improve neovascularization of ischemic murine hind limbs. These effects required the phosphorylation of alpha v beta 5 integrins, which depended on the interaction of leptin with its receptor ObR, and on Janus kinase (JAK) 2- and phospholipase C (PLC) gamma-mediated activation of Src kinase. Protein tyrosine phosphatase 1B, a negative regulator of leptin signaling, was overexpressed in CACs from obese, hyperleptinemic individuals, and this was associated with insensitivity of CACs to the angiogenic effects of leptin. Weight loss (by 30 +/- 15 kg) normalized protein tyrosine phosphatase 1B expression in CACs and restored their responsiveness to leptin. A similar dose- dependent response was found after incubation of CACs from obese subjects with a protein tyrosine phosphatase 1B inhibitor ex vivo. Conclusion-Our results point to the ObR-Src kinase-alpha v beta 5 cross talk as a distinct novel component of the network of specific interactions between integrins and cytokine receptors in angiogenesis. (Arterioscler Thromb Vasc Biol. 2010; 30: 200-206.)"],["dc.identifier.doi","10.1161/ATVBAHA.109.192807"],["dc.identifier.gro","3142969"],["dc.identifier.isi","000273799900014"],["dc.identifier.pmid","19910644"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/431"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: National Institutes of Health [NIH HL-75736]"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1079-5642"],["dc.title","Leptin Enhances the Potency of Circulating Angiogenic Cells Via Src Kinase and Integrin alpha v beta 5 Implications for Angiogenesis in Human Obesity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]