1,720,971 research outputs found
Early reduction of therapy-resistant hypertension in a patient after single-sided renal denervation approach
No full text17 beta-estradiol inhibition of NADPH oxidase expression in human endothelial cells
No full textWe investigated the hypothesis that the antiatherosclerotic effect of 17 beta -estradiol (E-2) is due to a shift in the nitric oxide (NO)/superoxide (O-2(-)) balance in the vessel wall, thereby increasing the bioavailability of NO. In human umbilical vein cultured endothelial cells, E-2 (1-100 nmol/l), but not 17 alpha -estradiol, caused a time- and concentration-dependent decrease in expression of the NADPH oxidase subunit gp91phox (up to 60% inhibition at both the mRNA and protein level). This effect was prevented by coincubation with the estrogen receptor antagonists tamoxifen and ICI 182,780 (1 mu mol/l each). Within the same concentration range, E-2 also up-regulated endothelial nitric oxide synthase expression (similar to twofold). Moreover, preincubation of the cells with E-2 or a gp91phox antisense oligonucleotide significantly decreased their capacity to generate O-2(-) on phorbol ester stimulation (i.e., assembly of the active NADPH oxidase complex). Blockade of NO synthase activity, on the other hand, had no effect on phorbol ester-stimulated O-2(-) formation. In addition, E-2 (100 nmol/l) inhibited the increase in adhesion molecule and chemokine expression in cells exposed to cyclic strain. Cyclic strain enhanced endothelial O-2(-) formation, thereby offsetting the inhibitory effect of NO on the expression of these gene products. E-2 thus seems to act as an antioxidant at the genomic level which by improving the NO/O-2(-) balance normalizes expression of proatherosclerotic gene products in endothelial cells
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
Uncommon delayed and late complications after percutaneous left atrial appendage closure with Amplatzer(A (R)) Cardiac Plug
No full textAims Percutaneous left atrial appendage closure with Amplatzer(A (R)) Cardiac Plug (St. Jude Medical Inc.) for the prevention of stroke in patients with atrial fibrillation is rapidly propagating. We sought to provide additional safety data. We have screened our database of patients having been treated with Amplatzer(A (R)) Cardiac Plug and found 3 cases with uncommon complications that have not been reported previously. One patient experienced an embolisation of the occluder about 12 months after implantation that potentially resulted from mismatch of occluder size and landing zone. Another patient developed cardiac tamponade 9 days after implantation. This case of delayed effusion was probably not a result of interventional trauma, but might have been provoked by scratching of the inner pericardial membrane. A third patient developed a large thrombus in the left atrium which was considered to be caused by injury of the endothelial wall during implantation. The first two cases could be treated by a percutaneous procedure, the last case by cardiac surgery without any sequelae. Complications after left atrial appendage closure not related to a device-related thrombus can occur later after implantation. With appropriate percutaneous or surgical management these complications can be handled without sequelae
Pro-thrombotic condition in a woman with peripartum cardiomyopathy treated with bromocriptine and an Impella LP 2.5 heart pump
No full textRenal artery ablation instead of pulmonary vein ablation in a hypertensive patient with symptomatic, drug-resistant, persistent atrial fibrillation
No full textDifferential effects of leptin signaling in endothelial or smooth muscle cells on neointima formation following vascular injury in mice
No full textDifferential effects of leptin signaling in endothelial or smooth muscle cells on neointima formation following vascular injury in mice
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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