Lankeit, Mareike

[["dc.bibliographiccitation.firstpage","916"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","CHEST Journal"],["dc.bibliographiccitation.lastpage","922"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Gomez, Vicente"],["dc.contributor.author","Wagner, Carolin"],["dc.contributor.author","Aujesky, Drahomir"],["dc.contributor.author","Recio, Monica"],["dc.contributor.author","Briongos, Sem"],["dc.contributor.author","Moores, Lisa K."],["dc.contributor.author","Yusen, Roger D."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Jimenez, David"],["dc.date.accessioned","2018-11-07T09:11:34Z"],["dc.date.available","2018-11-07T09:11:34Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: This study aimed to assess the performance of two prognostic models-the European Society of Cardiology (ESC) model and the simplified Pulmonary Embolism Severity Index (sPESI)-in predicting short-term mortality in patients with pulmonary embolism (PE). Methods: We compared the test characteristics of the ESC model and the sPESI for predicting 30-day outcomes in a cohort of 526 patients with objectively confirmed PE. The primary end point of the study was all-cause mortality. The secondary end point included all-cause mortality, nonfatal symptomatic recurrent VTE, or nonfatal major bleeding. Results: Overall, 40 of 526 patients died (7.6%; 95% CI, 5.3%-9.9%) during the first month of follow-up. The sPESI classified fewer patients as low risk (31% [165 of 526], 95% CI, 27%-35%) compared with the ESC model (39% [207 of 526], 95% CI, 35% to 44%; P < .01). Importantly however, low-risk patients based on the sPESI had no 30-day mortality compared with 3.4% (95% CI, 0.9-5.8) in low-risk patients by the ESC model. The secondary end point occurred in 1.8% of patients in the sPESI low-risk and 5.8% in the ESC low-risk group (difference, 4.0 percentage points; 95% CI, 0.2-7.8). The prognostic ability of the ESC model remained significant in the subgroup of patients at high-risk according to the sPESI model (OR 1.95, 95% CI, 1.41 to 2.71, P < .001). Conclusions: Both the sPESI and the ESC model successfully predict 30-day mortality after acute symptomatic PE, but exclusion of an adverse early outcome does not appear to require routine imaging procedures or laboratory biomarker testing. CHEST 2012; 141(4):916-922"],["dc.identifier.doi","10.1378/chest.11-1355"],["dc.identifier.isi","000302592700015"],["dc.identifier.pmid","21852296"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26749"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Coll Chest Physicians"],["dc.relation.issn","0012-3692"],["dc.title","A Strategy Combining Imaging and Laboratory Biomarkers in Comparison With a Simplified Clinical Score for Risk Stratification of Patients With Acute Pulmonary Embolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","379"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Best Practice & Research Clinical Haematology"],["dc.bibliographiccitation.lastpage","389"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T09:06:16Z"],["dc.date.available","2018-11-07T09:06:16Z"],["dc.date.issued","2012"],["dc.description.abstract","Approximately 10% of all patients with acute pulmonary embolism (PE) die within the first three months after diagnosis. However, PE is not universally life-threatening, but covers a wide spectrum of clinical severity and death risk. Thrombolytic treatment is indicated patients with acute massive PE who are at high risk for early death, i.e. those patients who present with arterial hypotension and shock. On the other hand, low molecular-weight heparin or fondaparinux is adequate treatment for most normotensive patients with PE. Recombinant tissue plasminogen activator, given as 100 mg infusion over 2 h, is the treatment of choice for patients with PE, although older regimens using urokinase or streptokinase are also efficacious. Beyond the relatively small numbers of patients with massive, high-risk PE as a target population for thrombolysis, there is increasing awareness of the need for risk stratification of normotensive patients and the search for an intermediate-risk group (also called submassive PE). Recent meta-analyses of cohort studies suggest that imaging of the right ventricle or biomarkers of myocardial injury alone may be insufficient for guiding therapeutic decisions. Instead, accumulating evidence appears to support strategies which combine the information provided by an imaging procedure with a biomarker test. These data provide the rationale for a large multinational randomized trial which has set out to determine whether normotensive patients with right ventricular dysfunction, detected by echocardiography or computed tomography, plus evidence of myocardial injury as indicated by a positive troponin test, may benefit from early thrombolytic treatment. This study, which is underway in 13 European countries, will enroll a total of 1000 patients and will be completed in 2012. Together with a parallel trial currently being conducted in the United States, it will hopefully answer the question whether thrombolysis is indicated in submassive PE, thus terminating a 40-year-old debate and filling an important gap in our management concept for acute pulmonary embolism. (c) 2012 Elsevier Ltd. All rights reserved."],["dc.description.sponsorship","Boehringer Ingelheim"],["dc.identifier.doi","10.1016/j.beha.2012.06.005"],["dc.identifier.isi","000309571100015"],["dc.identifier.pmid","22959553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25515"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","1521-6926"],["dc.title","Thrombolytic therapy for submassive pulmonary embolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Dallas, Claudia"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T11:09:52Z"],["dc.date.available","2018-11-07T11:09:52Z"],["dc.date.issued","2008"],["dc.format.extent","S621"],["dc.identifier.isi","000262104501728"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53094"],["dc.notes.status","zu prüfen"],["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","Heart-Type Fatty Acid-Binding Protein Predicts Outcome In Normotensive Patients With 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","877"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","883"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T08:43:54Z"],["dc.date.available","2018-11-07T08:43:54Z"],["dc.date.issued","2010"],["dc.description.abstract","Patients with high-risk pulmonary embolism (PE), i.e. those with shock or hypotension at presentation, are at high risk of in-hospital death, particularly during the first hours after admission. A meta-analysis of trials which included haemodynamically compromised patients indicated that thrombolytic treatment significantly reduces the rate of in-hospital death or PE recurrence. Therefore, thrombolysis should be administered to patients with high-risk PE unless there are absolute contraindications to its use. Uncontrolled data further suggest that thrombolysis may be a safe and effective alternative to surgery in patients with PE and free-floating thrombi in the right heart. On the other hand, normotensive patients generally have a favourable short-term prognosis if heparin anticoagulation is instituted promptly, and they are thus considered to have non-high-risk PE. Generally, the bleeding risk of thrombolysis appears to outweigh the clinical benefits of this treatment in patients without haemodynamic compromise. However, within the group of normotensive patients with PE, some may have evidence of right ventricular dysfunction on echocardiography or computed tomography, or of myocardial injury based on elevated cardiac biomarkers (troponin I or T, heart-type fatty acid-binding protein). These patients have an intermediate risk of an adverse outcome in the acute phase of PE. Existing data suggest that selected patients with intermediate-risk PE may benefit from early thrombolytic treatment, particularly if they have a low bleeding risk. However, controversy will continue to surround the optimal treatment for this group until the results of a large ongoing thrombolysis trial are available in a few years."],["dc.identifier.doi","10.1160/TH10-01-0005"],["dc.identifier.isi","000278020000002"],["dc.identifier.pmid","20216979"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20084"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Schattauer Gmbh-verlag Medizin Naturwissenschaften"],["dc.relation.issn","0340-6245"],["dc.title","Thrombolysis for pulmonary embolism: Past, present and future"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","759"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinics in Chest Medicine"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T08:36:06Z"],["dc.date.available","2018-11-07T08:36:06Z"],["dc.date.issued","2010"],["dc.description.abstract","Acute venous thromboembolism remains a frequent disease, with an incidence ranging between 23 and 69 cases per 100,000 population per year. Of these patients, approximately one-third present with clinical symptoms of acute pulmonary embolism (PE) and two-thirds with deep venous thrombosis (DVT). Recent registries and cohort studies suggest that approximately 10% of all patients with acute PE die during the first 1 to 3 months after diagnosis. Overall, 1% of all patients admitted to hospitals die of acute PE, and 10% of all hospital deaths are PE-related. These facts emphasize the need to better implement our knowledge on the pathophysiology of the disease, recognize the determinants of death or major adverse events in the early phase of acute PE, and most importantly, identify those patients who necessitate prompt medical, surgical, or interventional treatment to restore the patency of the pulmonary vasculature."],["dc.identifier.doi","10.1016/j.ccm.2010.06.007"],["dc.identifier.isi","000284507800012"],["dc.identifier.pmid","21047581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18231"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","0272-5231"],["dc.title","Mortality Risk Assessment and the Role of Thrombolysis in Pulmonary Embolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E407"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Thrombosis Research"],["dc.bibliographiccitation.lastpage","E408"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Lankeit, Mareike K."],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2018-11-07T08:36:35Z"],["dc.date.available","2018-11-07T08:36:35Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.thromres.2009.10.010"],["dc.identifier.isi","000284830100001"],["dc.identifier.pmid","19896704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18348"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0049-3848"],["dc.title","Tenecteplase can be given to patients with intermediate-risk pulmonary embolism - But should it?"],["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.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","1332"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Thrombosis and Haemostasis"],["dc.bibliographiccitation.lastpage","1346"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Kölmel, Sebastian"],["dc.contributor.author","Hobohm, Lukas"],["dc.contributor.author","Käberich, Anja"],["dc.contributor.author","Krieg, Valentin J."],["dc.contributor.author","Bochenek, Magdalena L."],["dc.contributor.author","Wenzel, Philip"],["dc.contributor.author","Wiedenroth, Christoph B."],["dc.contributor.author","Liebetrau, Christoph"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Mayer, Eckhard"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Guth, Stefan"],["dc.contributor.author","Lankeit, Mareike"],["dc.date.accessioned","2019-08-06T12:12:56Z"],["dc.date.available","2019-08-06T12:12:56Z"],["dc.date.issued","2019"],["dc.description.abstract"," Inflammation and incomplete thrombus resolution leading to obstructive fibrotic remodelling are considered critical mechanisms for the development of chronic thromboembolic pulmonary hypertension (CTEPH) after pulmonary embolism (PE). Osteopontin (OPN) is involved in a variety of biological processes including inflammation and tissue fibrosis."],["dc.identifier.doi","10.1055/s-0039-1692174"],["dc.identifier.pmid","31183846"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62313"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","2567-689X"],["dc.relation.issn","0340-6245"],["dc.relation.issn","2567-689X"],["dc.title","Potential Involvement of Osteopontin in Inflammatory and Fibrotic Processes in Pulmonary Embolism and Chronic Thromboembolic Pulmonary Hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]