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  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; Germany ; VITRO ; DISEASE ; MICE ; TIME ; MACROPHAGES ; SERA ; REDUCTION ; animals ; bone marrow ; BONE-MARROW ; DELETION ; NO ; LESIONS ; DIFFERENCE ; inactivation ; MUSCLE ; ATHEROSCLEROSIS ; DIET ; MOUSE MODEL ; VASCULATURE ; glucocorticoid receptor ; CALCIUM ; BEHAVIOR ; SMOOTH-MUSCLE ; inflammation ; SERUM ; PRODUCTS ; INCREASE ; DEFICIENT MICE ; GC ; methods ; dexamethasone ; USA ; BONE ; animal ; SMOOTH-MUSCLE-CELLS ; smooth muscle cells ; MEDIA ; RANKL ; VASCULAR CALCIFICATION ; MUSCLE-CELLS ; MARROW ; in vitro ; CRUCIAL ROLE ; DRIVEN ; ARTERIAL CALCIFICATION ; CHOLESTEROL-FED RABBITS ; CORONARY ANGIOPLASTY ; KAPPA-B LIGAND ; OSTEOPROTEGERIN ; RECEPTOR ACTIVATOR
    Abstract: Objective - Macrophage-derived products are known to play a crucial role during atherogenesis and vascular calcification. Glucocorticoids (GC) are important modulators of immune cell functions, but their specific effects on macrophages behavior during plaque formation are not defined. The present study was therefore designed to investigate the effects of macrophage-specific deletion of the glucocorticoid receptor (GR(LysMCre)) on atherogenesis and vascular calcification in a hyperlipidemic mouse-model. Methods and Results - Bone marrow was isolated from GRLysMCre mice and wild-type controls (GR(flox)) and subsequently transplanted into lethally irradiated LDL-receptor -deficient mice. Animals were fed a Western-type diet for 15 or 24 weeks, and atherosclerotic lesions within the aortic sinus were evaluated. At both time points, no significant difference in serum lipid and corticosterone concentrations, atherosclerotic lesion size and macrophage-content within the lesions could be observed. However, GRLysMCre mice showed less calcification as well as a significant reduction of RANKL, BMP2, and Msx2 expression within the vasculature. In vitro studies using conditioned media from macrophages which had been stimulated with dexamethasone demonstrated a dose-dependent increase in calcium deposition by vascular smooth muscle cells. Conclusion - This study demonstrates that macrophage-specific glucocorticoid receptor inactivation reduces vascular calcification without affecting atherosclerotic lesion size in LDL receptor -deficient mice. (Arterioscler Thromb Vasc Biol. 2008;28:2158-2164.)
    Type of Publication: Journal article published
    PubMed ID: 18787189
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  • 2
    Publication Date: 2018-09-28
    Description: Rivaroxaban is an effective and safe alternative to warfarin in patients with atrial fibrillation and venous thromboembolism. We tested the efficacy and safety of rivaroxaban compared with warfarin in high-risk patients with thrombotic antiphospholipid syndrome. This is a randomized open-label multicenter noninferiority study with blinded end point adjudication. Rivaroxaban, 20 mg once daily (15 mg once daily based on kidney function) was compared with warfarin (international normalized ratio target 2.5) for the prevention of thromboembolic events, major bleeding, and vascular death in patients with antiphospholipid syndrome. Only high-risk patients triple positive for lupus anticoagulant, anti-cardiolipin, and anti–β2-glycoprotein I antibodies of the same isotype (triple positivity) were included in the study. The trial was terminated prematurely after the enrollment of 120 patients (59 randomized to rivaroxaban and 61 to warfarin) because of an excess of events among patients in the rivaroxaban arm. Mean follow-up was 569 days. There were 11 (19%) events in the rivaroxaban group, and 2 (3%) events in the warfarin group. Thromboembolic events occurred in 7 (12%) patients randomized to rivaroxaban (4 ischemic stroke and 3 myocardial infarction), whereas no event was recorded in those randomized to warfarin. Major bleeding occurred in 6 patients: 4 (7%) in the rivaroxaban group and 2 (3%) in the warfarin group. No death was reported. The use of rivaroxaban in high-risk patients with antiphospholipid syndrome was associated with an increased rate of events compared with warfarin, thus showing no benefit and excess risk. This trial was registered at www.clinicaltrials.gov as #NCT02157272.
    Keywords: Plenary Papers, Thrombosis and Hemostasis, Clinical Trials and Observations
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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