Riggert, Joachim

[["dc.bibliographiccitation.firstpage","700"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Microcirculation"],["dc.bibliographiccitation.lastpage","710"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Vogler, Melanie"],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Meier, Julia"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:43:27Z"],["dc.date.available","2017-09-07T11:43:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: The zinc finger transcription factor KLF4 is known to control diverse EC functions. Methods: The functional role of KLF4 for angiogenesis and its association with CAD was examined in HUVECs and human CECs. Results: In two different angiogenesis assays, siRNA-mediated KLF4 downregulation impaired HUVEC sprouting and network formation. Conversely, KLF4 overexpression increased HUVEC sprouting and network formation. Similar findings were observed after incubation of HUVECs with CdM from KLF4 cDNA-transfected cells, suggesting a role of paracrine factors for mediating angiogenic KLF4 effects. In this regard, VEGF expression was increased in KLF4-overexpressing HUVECs, whereas its expression was reduced in HUVECs transfected with KLF4 siRNA. To examine the relevance of our in vitro findings for human endothelial dysfunction, we analyzed the expression of KLF4 in CECs of patients with stable CAD. Flow cytometry analyses revealed decreased numbers of KLF4-positive CECs in peripheral blood from CAD patients compared to healthy controls. Conclusions: Our findings suggest that KLF4 may represent a potential biomarker for EC dysfunction. In the future, (therapeutic) modulation of KLF4 may be useful in regulating EC function during vascular disease processes."],["dc.identifier.doi","10.1111/micc.12226"],["dc.identifier.gro","3141793"],["dc.identifier.isi","000365387200003"],["dc.identifier.pmid","26214161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1135"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1549-8719"],["dc.relation.issn","1073-9688"],["dc.title","Circulating Endothelial Cells Expressing the Angiogenic Transcription Factor Kruppel-Like Factor 4 are Decreased in Patients with Coronary Artery Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","144"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Internal Medicine"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","BackgroundMonocytes and platelets are important cellular mediators of atherosclerosis. Human monocytes can be divided into CD14(++)CD16(-), CD14(++)CD16(+) and CD14(+)CD16(++) cells, which differ in their functional properties. The aim of this study was to examine monocyte subset distribution, monocyte-platelet aggregate (MPA) formation and expression of CCR5, the receptor of the platelet-derived chemokine CCL5, and to determine whether these parameters are altered in individuals with coronary atherosclerosis. MethodsPeripheral blood cells from 64 healthy blood donors (HBDs) and 60 patients with stable coronary artery disease (CAD) were stained with antibodies against CD14, CD16, CD42b and CCR5 and analysed by flow cytometry. Circulating CCL5 levels were determined using an enzyme-linked immunosorbent assay. ResultsIn patients with CAD, the relative proportion of the CD14(++)CD16(-) monocyte subset was elevated (P<0.05) and of the CD14(+)CD16(++) subset was reduced (P<0.001) compared with the HBD group. Furthermore, MPA formation significantly increased in patients with CAD in all three monocyte subsets. In both study groups, the majority of CCR5(+) cells was detected in CD14(++)CD16(+) monocytes (P<0.001 versus CD14(++)CD16(-) and CD14(+)CD16(++)), although the CCR5(+) monocyte number was reduced in patients with CAD (CD14(++)CD16(-)/CD14(+)CD16(++), P<0.001; CD14(++)CD16(+), P<0.05) compared with the HBD group, particularly in those who were not taking statins. Ex vivo incubation of monocytes from HBDs with plasma from patients with CAD also decreased CCR5(+) expression (P<0.05 versus plasma from HBDs). Serum CCL5 levels were similar in both groups. ConclusionsThe increased monocyte-platelet cross-talk in patients with CAD might have contributed to atherosclerosis progression. The decreased CCR5(+) monocyte numbers in patients with CAD could have resulted from CCR5(+) cell recruitment into atherosclerotic lesions or CCR5 downregulation in response to circulating factors."],["dc.identifier.doi","10.1111/joim.12145"],["dc.identifier.gro","3142194"],["dc.identifier.isi","000329764500006"],["dc.identifier.pmid","24118494"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5577"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: University Medical Center Gottingen"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1365-2796"],["dc.relation.issn","0954-6820"],["dc.title","Increased proatherogenic monocyte-platelet cross-talk in monocyte subpopulations of patients with stable coronary artery disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1080"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","1082"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:47:04Z"],["dc.date.available","2017-09-07T11:47:04Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1160/TH13-05-0367"],["dc.identifier.gro","3142259"],["dc.identifier.isi","000326991900026"],["dc.identifier.pmid","23884216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6298"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Schattauer Gmbh-verlag Medizin Naturwissenschaften"],["dc.relation.issn","0340-6245"],["dc.title","Atheroprotective Kruppel-like factor 4 is downregulated in monocyte subsets of patients with coronary artery disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","357"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","367"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Heida, Nana-Maria"],["dc.contributor.author","Mueller, Jan-Peter"],["dc.contributor.author","Cheng, I-Fen"],["dc.contributor.author","Leifheit-Nestler, Maren"],["dc.contributor.author","Faustin, Vivien"],["dc.contributor.author","Riggert, Joachim"],["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","Objectives The purpose of this study was to examine the impact of obesity and weight loss on the angiogenic and regenerative capacity of endothelial progenitor cells (EPCs). Background EPCs participate in angiogenesis and tissue repair. Several cardiovascular risk factors are associated with EPC dysfunction. Methods Early outgrowth EPCs were isolated from 49 obese (age 42 +/- 14 years; body mass index 42 +/- 7 kg/m(2)) normo-glycemic participants in a professional weight reduction program and compared with those from 49 age-matched lean controls. EPC function was tested both in vitro and in vivo. Results EPCs expanded from the obese possessed reduced adhesive, migratory, and angiogenic capacity, and mice treated with obese EPCs exhibited reduced EPC homing in ischemic hind limbs in vivo. EPCs from the obese subjects failed to respond to conditioned medium of lean controls or to potent angiogenic factors such as vascular endothelial growth factor. Although no differences existed between lean and obese EPCs regarding the surface expression of vascular endothelial growth factor or chemokine receptors, basal p38 mitogen-activated protein kinase (MAPK) phosphorylation was elevated in obese EPCs (3.7 +/- 2.1-fold increase; p = 0.006). These cells also showed reduced secretion of the angiogenic chemokines interleukin-8 (p = 0.047) and monocyte chemoattractant protein-1 (p = 0.012). By inhibiting p38 MAPK, we could restore chemokine levels to those of lean control EPCs and also improve the angiogenic properties of obese EPCs. Accordingly, 6-month follow-up of 26 obese persons who achieved significant weight reduction revealed normalization of p38 MAPK phosphorylation levels and improved EPC function. Conclusions Obesity is associated with a reversible functional impairment of EPCs. This involves reduced secretion of angiogenic chemokines and increased basal phosphorylation of signaling molecules, notably p38 MAPK. (J Am Coll Cardiol 2010; 55: 357-67) (C) 2010 by the American College of Cardiology Foundation"],["dc.identifier.doi","10.1016/j.jacc.2009.09.031"],["dc.identifier.gro","3142979"],["dc.identifier.isi","000273802200013"],["dc.identifier.pmid","20117442"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6292"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/442"],["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","Elsevier Science Inc"],["dc.relation.issn","0735-1097"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Effects of Obesity and Weight Loss on the Functional Properties of Early Outgrowth Endothelial Progenitor Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Microcirculation"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Bernhardt, Markus"],["dc.contributor.author","Kuschicke, Hendrik"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:46:33Z"],["dc.date.available","2017-09-07T11:46:33Z"],["dc.date.issued","2014"],["dc.description.abstract","ObjectiveHuman monocytes can be divided into CD16(-) monocytes and CD16(+) monocytes. Studies in mice suggested differential effects of monocyte subsets during new vessel formation. MethodsThe functional role of human monocyte subsets in neovascularization processes was investigated. For in vivo experiments, nude mice underwent unilateral hindlimb ischemia surgery before being injected with either total monocytes, CD16(-) monocytes or CD16(+) monocytes isolated from healthy individuals. ResultsIn vitro, cytokine array analysis demonstrated that monocytes release numerous angiogenic cytokines, some of which were differentially expressed in monocyte subsets. Sprout length was enhanced in EC spheroids being cultured in conditioned medium obtained from total monocytes and, to a lesser extent, also in supernatants of CD16(-) monocytes. Laser Doppler perfusion imaging up to day 28 after surgery revealed a trend toward improved revascularization in mice treated with monocytes, but no significant differences between monocyte subsets. Histological analyses four weeks after surgery showed an increased arteriole size in mice having received CD16(+) monocytes, whereas the number of capillaries did not significantly differ between groups. ConclusionsOur findings suggest additive and differential effects of monocyte subsets during neovascularization processes, possibly due to an altered secretion of angiogenic factors and their paracrine capacity to stimulate new vessel formation."],["dc.identifier.doi","10.1111/micc.12100"],["dc.identifier.gro","3142188"],["dc.identifier.isi","000331339000007"],["dc.identifier.pmid","24125396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5510"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: University Medical Center Gottingen"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1549-8719"],["dc.relation.issn","1073-9688"],["dc.title","In Vitro and In Vivo Effects of Human Monocytes and their Subsets on New Vessel Formation"],["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","33"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Kuschicke, H."],["dc.contributor.author","Schlegel, Mathias"],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Bernhardt, M."],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, K."],["dc.date.accessioned","2018-11-07T09:07:30Z"],["dc.date.available","2018-11-07T09:07:30Z"],["dc.date.issued","2012"],["dc.format.extent","750"],["dc.identifier.isi","000308012405357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25808"],["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","Krueppel-like factor 4 is downregulated in circulating monocyte subsets of patients with Coronary Artery Disease"],["dc.type","conference_abstract"],["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","34"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Vogler, Melanie"],["dc.contributor.author","Kuschicke, H."],["dc.contributor.author","Meier, J. Fabian"],["dc.contributor.author","Gogiraju, R."],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, K."],["dc.date.accessioned","2018-11-07T09:21:36Z"],["dc.date.available","2018-11-07T09:21:36Z"],["dc.date.issued","2013"],["dc.format.extent","1052"],["dc.identifier.isi","000327744606386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29147"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","The transcription factor Krueppel-like factor 4 is a positive regulator of angiogenic properties in endothelial cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","461"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Obesity"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Wagner, Nana-Maria"],["dc.contributor.author","Brandhorst, Gunnar"],["dc.contributor.author","Czepluch, Frauke S."],["dc.contributor.author","Lankeit, Mareike"],["dc.contributor.author","Eberle, Christoph"],["dc.contributor.author","Herzberg, Sebastian"],["dc.contributor.author","Faustin, Vivien"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Oellerich, Michael"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:47:46Z"],["dc.date.available","2017-09-07T11:47:46Z"],["dc.date.issued","2013"],["dc.description.abstract","Objective: Reduced numbers of regulatory T (T-reg) cells have been observed in visceral adipose tissue of obese mice and humans. However, it is unknown whether human obesity affects circulating Treg cells and whether their number is associated with markers of systemic inflammation or glucose intolerance. Design and Methods: Peripheral blood mononuclear cells were isolated from venous blood of obese (BMI >= 27 kg/m(2); n = 30) and nonobese (BMI >= 27 kg/m(2); n = 13) individuals and analyzed using flow cytometry for the expression of CD4, CD25, and Foxp3. Results: Reduced circulating T-reg-cell numbers were detected in obese compared with nonobese study participants (P = 0.038). Circulating CD4(+)CD25(+)CD127(-)Foxp3 T-reg cells inversely correlated with body weight (P = 0.009), BMI (P = 0.004) and plasma leptin levels (P = 0.004) and were reduced in subjects with hsCRP >= 3.0 mg/L (P = 0.034) or HbA1c >= 5.5% (P < 0.005). Receiver operating characteristic curve analysis revealed a cutoff of circulating Treg cells < 1.06% to be predictive for hsCRP levels >= 3.0 mg/L, and logistic regression showed that the risk of having hsCRP levels >= 3.0 mg/L was increased 9.6-fold (P = 0.008), if T-reg cells were below this threshold. The T-reg cutoff for HbA1c levels >= 5.5% was 0.73%, and this cutoff also predicted an increased risk of having elevated levels of both hsCRP and HbA1c, if only obese subjects were examined. Conclusion: Our findings thus reveal an association between circulating T-reg cells and measures of adiposity, inflammation, and glucose intolerance. Although further prospective studies are needed, we present data suggesting that the determination of T-reg cells might be useful to identify obese subjects at increased risk of developing cardiovascular and/or metabolic complications."],["dc.identifier.doi","10.1002/oby.20087"],["dc.identifier.gro","3142378"],["dc.identifier.isi","000322087600030"],["dc.identifier.pmid","23592653"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7619"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1930-7381"],["dc.title","Circulating Regulatory T Cells Are Reduced in Obesity and May Identify Subjects at Increased Metabolic and Cardiovascular Risk"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1123"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","1129"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Rohm, Ilonka"],["dc.contributor.author","Lankeit, Mareike"],["dc.contributor.author","Ellrott, Thomas"],["dc.contributor.author","Faustin, Vivien"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros"],["dc.date.accessioned","2017-09-07T11:48:08Z"],["dc.date.available","2017-09-07T11:48:08Z"],["dc.date.issued","2008"],["dc.description.abstract","Clinical studies have shown that elevated leptin levels are an independent cardiovascular risk factor. However, little is known about the existence of platelet resistance to leptin in the setting of obesity. We examined the effects of leptin on platelet aggregation in morbidly obese subjects (n=40; BMI, 41.6 +/- 1.1 kg/m(2); leptin, 49.7 +/- 3.4 ng/ml) in comparison to normal-weight controls (n=36 BMI, 23.3 +/- 0.4 kg/m(2); leptin, 6.5 +/- 0.7 ng/ml).The aggregatory response to increasing concentrations of adenosine diphosphate (ADP) (2, 3,4,and 5 mu M) was significantly increased in platelets from obese compared to lean donors, reflecting a left shift in the dose-response curve. Plasma leptin levels, but not BMI, were significantly higher in subjects with stronger (above the median) compared to weaker (below the median) platelet aggregation at all ADP concentrations tested. In further experiments, stimulation (preincubation) with leptin (500 ng/ml) promotedADP-induced platelet aggregation by approximately 25%, and there was no difference between platelets from obese and those from lean donors regarding the responsiveness to leptin (p=0.99). Western blotting revealed that leptin induced phosphorylation of JAK2 and STAT3 to a similar extent in platelets from both groups. Expression of potential mediators of leptin resistance (SOCS3 and PTP IB) also did not differ in platelets from obese and control subjects. In conclusion,our data indicate that platelets from obese donors show increased aggregatory response to ADP, and that this might partly be the consequence of increased circulating leptin levels. Platelets from obese donors are not resistant to the enhancing effects of leptin on ADP-induced platelet aggregation."],["dc.identifier.doi","10.1160/TH08-05-0314"],["dc.identifier.gro","3143206"],["dc.identifier.isi","000261880900030"],["dc.identifier.pmid","19132239"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6290"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/695"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation; University of Goettingen"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Schattauer Gmbh-verlag Medizin Naturwissenschaften"],["dc.relation.issn","0340-6245"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Absence of leptin resistance in platelets from morbidly obese individuals may contribute to the increased thrombosis risk in obesity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]