1,721,043 research outputs found
Update on the Cardiovascular Risk in Obesity: Endocrine and Paracrine Role of the Adipose Tissue
No full textUpdate on the Cardiovascular Risk in Obesity: Endocrine and Paracrine Role of the Adipose Tissue
No full textAdipokines and thrombosis
No full text1. Obesity is a major risk factor for cardiovascular disease. An increased body mass index (BMI) is associated with venous thromboembolism, myocardial infarction, stroke and stent thrombosis after percutaneous interventions. Studies in mouse models of obesity and induced arterial or venous thrombosis have provided insights into the mechanisms involved
Rosuvastatin reduces atherosclerotic lesions and promotes progenitor cell mobilisation and recruitment in apolipoprotein E knockout mice
No full textStatins enhance incorporation of bone marrow-derived cells into experimental neointimal lesions. However, the contribution of progenitor cells to progression of spontaneous atherosclerotic plaques, and the possible modulatory role of statins in this process, remain poorly understood. We compared the effects of rosuvastatin (1 and 10 mg/kg BW) and pravastatin (10 mg/kg) on progenitor cell mobilisation, recruitment into atherosclerotic plaques, and lesion growth. Statins were administered over 8 weeks to apolipoprotein E knockout mice on atherogenic diet. In addition, mice were lethally irradiated, followed by transplantation of bone marrow from LacZ transgenic mice. Rosuvastatin reduced lesion area and intima-to-media ratio at the brachiocephalic artery compared to vehicle. while both parameters were not significantly altered by pravastatin. Rosuvastatin also augmented endothelialisation (P<0.05) and reduced the smooth muscle cells (SMC) content (P= 0.042) of lesions. Numbers of c-kit, sca-1 and flk-1, sca-1 double-positive progenitor cells were significantly increased in rosuvastatin compared to controltreated mice, both in the bone marrow and the peripheral blood. Similarly, the number of spleen-derived acLDL, lectin double-positive progenitor cells (P= 0.001) and colony-forming units (P= 0.0104) was significantly increased in mice treated with rosuvastatin compared to vehicle alone. In the bone marrow, increased Akt and p42/44 MAP kinase phosphorylation and upregulated SDF1 alpha mRNA expression were observed. Importantly, rosuvastatin treatment also increased the plasma levels of c-kit ligand (P = 0.003), and the number of c-kit-positive cells within atherosclerotic lesions (P = 0.041). Our findings suggest that rosuvastatin reduces the size of atherosclerotic plaques, and this effect appears to involve progenitor cell mobilisation and recruitment into vascular lesions. (C) 2008 Elsevier Ireland Ltd. All rights reserved.University of Goettingen; Astra Zeneca Lt
Effect of the Factor Xa Inhibitor Rivaroxaban on Arterial Thrombosis in Wild-Type and Apolipoprotein E-Deficient Mice
No full textRivaroxaban is a potent and specific direct inhibitor of coagulation factor Xa. Recent studies have highlighted its effectiveness in the prevention of venous thrombosis and embolic stroke due to atrial fibrillation. To evaluate the antithrombotic effects of rivaroxaban in an in vivo model of arterial thrombosis, photochemical vascular injury was induced in wild-type mice by intravenous rose bengal (50 mg/kg body weight [BW]) followed by illumination of the left common carotid artery using a 543 nm helium-neon laser beam. Rivaroxaban, injected concomitantly with rose bengal at doses of 1.0, 1.5, 2.0, or 3.0 mg/kg BW, dose-dependently prolonged the times to first thrombotic occlusion and stable thrombosis. Quantitative analysis of carotid flow curves revealed higher blood volumes passing through the injured artery with increasing rivaroxaban doses (p<0.01 and p<0.001 vs. vehicle for 2.0 and 3.0 mg/kg, respectively), suggesting a dose-dependent effect on vascular patency. Consistently, a significantly higher proportion of mice that received 2.0 and 3.0 mg/kg rivaroxaban exhibited patent carotid arteries at the end of the flow monitoring period compared to vehicle alone (p<0.05 and p<0.001, respectively). Histological analysis showed complete thrombotic arterial occlusion in vehicle-treated mice compared to less thrombotic material in mice injected with 3.0 mg/kg rivaroxaban (p<0.05). Rivaroxaban also prolonged the time to cessation of tail bleeding in a dose-dependent manner, starting at 1.5 mg/kg. Similar findings were obtained in apolipoprotein E-knockout mice. Rivaroxaban may exert beneficial effects by preventing arterial thrombosis and vascular occlusion after endothelial injury. (C) 2012 Elsevier Ltd. All rights reserved
Prolactin as a modulator of platelet function and thrombosis: The end of the story, or a new beginning?
No full textGeometric morphometrics of male facial shape in relation to physical strength and perceived attractiveness, dominance, and masculinity
No full textObjectives: Evolutionary psychologists claim that women have adaptive preferences for specific male physical traits. Physical strength may be one of those traits, because recent research suggests that women rate faces of physically strong men as more masculine, dominant, and attractive. Yet, previous research has been limited in its ability to statistically map specific male facial shapes and features to corresponding physical measures (e.g., strength) and ratings (e.g., attractiveness). Methods: The association of handgrip strength (together with measures of shoulder width, body height, and body fat) and women's ratings of male faces (concerning dominance, masculinity, and attractiveness) were studied in a sample of 26 Caucasian men (aged 18-32 years). Geometric morphometrics was used to statistically assess the covariation of male facial shape with these measures. Statistical results were visualized with thin-plate spline deformation grids along with image unwarping and image averaging. Results: Handgrip strength together with shoulder width, body fat, dominance, and masculinity loaded positively on the first dimension of covariation with facial shape (explaining 72.6%, P < 0.05). These measures were related to rounder faces with wider eyebrows and a prominent jaw outline while highly attractive and taller men had longer, narrower jaws and wider/fuller lips. Conclusions: Male physical strength was more strongly associated with changes in face shape that relate to perceived masculinity and dominance than to attractiveness. Our study adds to the growing evidence that attractiveness and dominance/masculinity may reflect different aspects of male mate quality. Am. J. Hum. Biol. 23: 805-814, 2011. (C) 2011 Wiley Periodicals, Inc
Importance of leptin signaling and signal transducer and activator of transcription-3 activation in mediating the cardiac hypertrophy associated with obesity
Full text linkBackground: The adipokine leptin and its receptor are expressed in the heart, and leptin has been shown to promote cardiomyocyte hypertrophy in vitro. Obesity is associated with hyperleptinemia and hypothalamic leptin resistance as well as an increased risk to develop cardiac hypertrophy and heart failure. However, the role of cardiac leptin signaling in mediating the cardiomyopathy associated with increased body weight is unclear, in particular, whether it develops subsequently to cardiac leptin resistance or overactivation of hypertrophic signaling pathways via elevated leptin levels. Methods: The cardiac phenotype of high-fat diet (HFD)-induced obese wildtype (WT) mice was examined and compared to age-matched genetically obese leptin receptor (LepR)-deficient (LepR(db/db)) or lean WT mice. To study the role of leptin-mediated STAT3 activation during obesity-induced cardiac remodeling, mice in which tyrosine residue 1138 within LepR had been replaced with a serine (LepR(S1138)) were also analyzed. Results: Obesity was associated with hyperleptinemia and elevated cardiac leptin expression in both diet-induced and genetically obese mice. Enhanced LepR and STAT3 phosphorylation levels were detected in hearts of obese WT mice, but not in those with LepR mutations. Moreover, exogenous leptin continued to induce cardiac STAT3 activation in diet-induced obese mice. Although echocardiography revealed signs of cardiac hypertrophy in all obese mice, the increase in left ventricular (LV) mass and diameter was significantly more pronounced in LepR(S1138) animals. LepR(S1138) mice also exhibited an increased activation of signaling proteins downstream of LepR, including Jak2 (1.8-fold), Src kinase (1.7-fold), protein kinase B (1.3-fold) or C (1.6-fold). Histological analysis of hearts revealed that the inability of leptin to activate STAT3 in LepR(db/db) and LepR(S1138) mice was associated with reduced cardiac angiogenesis as well as increased apoptosis and fibrosis. Conclusions: Our findings suggest that hearts from obese mice continue to respond to elevated circulating or cardiac leptin, which may mediate cardioprotection via LepR-induced STAT3 activation, whereas signals distinct from LepR-Tyr1138 promote cardiac hypertrophy. On the other hand, the presence of cardiac hypertrophy in obese mice with complete LepR signal disruption indicates that additional pathways also play a role
Generation of cardiovascular progenitors from multipotent adult mouse germline stem cells
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