1,721,022 research outputs found
Emergenze cardiovascolari e respiratorie nell'anziano
No full textRevisione ed aggiornam,ento trattamento emergenze cardiovascolari e respiratorie nell'anziano
Vascular biology of human coronary artery and bypass graft disease
No full textAnalisi fisiopatologica molecolare degli eventi che portano a malattia coronarica e del bypas
Emergenze cardiovascolari e repiratorie nell'anziano
No full textViene descritto l'approccio clinico, diagnostico e terapeutico alle crisi ipertensive, alla insuff. respiratoria acuta ed alla fibrillazione atriale
Bimodal effects of angiotensin II on migration of human and rat smooth muscle cells
No full textAngiotensin II may be an important mediator of neointima formation in vascular disease. This study was designed to examine the mechanisms involved in angiotensin II-stimulated migration of human and rat aortic vascular smooth muscle cells (VSMCs). VSMCs were seeded in one corner of Nunc four-well culture chambers; angiotensin II within filter paper was glued onto the wall of the opposite side. After 48 hours of incubation in serum-free medium containing growth-arresting factor, migrated cells were counted using a light microscope. Angiotensin II (2 x 10(-11) to 2 x 10(-8) mol/L) increased migration of VSMCs in a concentration-dependent manner. Interestingly, at higher concentrations of angiotensin II (up to 2 x 10(-6) mol/L), migration was reduced to levels comparable with control levels. Losartan, an AT1 receptor antagonist, prevented migration, while PD123319, an AT2 receptor antagonist, had no significant inhibitory effect. Transforming growth factor-beta 1 (TGF-beta 1; 0.01 to 10.0 pg/mL) inhibited migration induced by angiotensin II (2 x 10(-8) mol/L) in a concentration-dependent manner. A neutralizing TGF-beta antibody unmasked migratory effects of high concentrations of angiotensin II. Furthermore, angiotensin II (10(-6) mol/L) upregulated TGF-beta 1 mRNA levels fivefold in rat and fourfold in human VSMCs; this effect was prevented by losartan but not by PD123319. Thus, the effects of angiotensin II on migration of VSMCs are bimodal, ie, both migratory and antimigratory pathways are activated. Autocrine release of TGF-beta 1 induced by angiotensin II exerts an antimigratory effect in rat and human VSMCs. The AT1 receptor is involved in regulation of both pathway
[Action of natural estrogens on the vessel wall: molecular mechanisms and clinical implications]. [Article in German]
No full textMyocardial infarction is the major cause of death in the Western world. Men are more prone to develop coronary artery disease than women, who rarely develop coronary disease before menopause. Although epidemiological data has long been available showing a protective effect of estrogen on the vascular system, the underlying mechanisms have been investigated more thoroughly only in recent years. Meta-analysis studies have revealed that only half of the protective effect on estrogen replacement therapy is due to its positive effects on the lipid profile and that a large part of this protection is caused by mechanisms distinct from lipid metabolism. It is now known that estrogens also exert effects on vascular function and structure of the vessel wall involving numerous cellular and molecular mechanisms. Here we review actions of natural estrogens on human vascular cells and arteries. Estrogens can modulate vascular function by increasing nitric oxide production via stimulation of endothelial nitric oxide synthase (eNOS) and decreasing endothelin-1 levels in vivo. Furthermore, 17 beta-estradiol is an inhibitor of vascular smooth muscle cell proliferation and migration, phenomena that play a major role in atherosclerotic vascular disease and in the remodelling process. 17 beta-estradiol can also acutely affect vascular tone in human arteries and attenuates constriction induced by contractile agonists. Finally, clinical studies have shown that 17 beta-estradiol can acutely and chronically ameliorate vascular function in women with and without vascular disease. In conclusion, results from clinical and in vitro studies confirm the positive effects of natural estrogens on vascular function and protection from coronary heart disease. Thus, primary prevention of coronary heart disease by estrogen replacement therapy after the menopause appears to be a new and straightforward approach by which cardiovascular mortality in women can be reduce
17beta-Estradiol and smooth muscle cell proliferation in aortic cells of male and female rats.
No full textThe low incidence of cardiovascular disease in women before menopause or during hormone replacement therapy suggests a protective effect of estrogens. The mechanism(s) are uncertain but may involve effects on lipids, coagulation and the endothelium. Vascular smooth muscle cell (VSMC) proliferation also contributes to atherosclerosis. Hence, we investigated whether 17 beta-estradiol (E2) inhibits VSMC proliferation. VSMC of 6 female and 6 male Wistar Kyoto rats (WKY; age 10-12 weeks) were incubated for 24 h with E2 and/or fetal calf serum (FCS). E2 (10(-9)-10(-5) M) alone reduced [3H]thymidine uptake at 10(-5) (n=8, p<0.05 vs control) in female cells only. In female and male VSMC, FCS (1%) increased [3H]thymidine uptake (4.5-fold, p<0.05 vs. control). When given simultaneously, E2 did not prevent this effect of FCS (1%). However, when cells were preincubated for 24 h with E2 and then stimulated with FCS, [3H]thymidine uptake was reduced by E2 at 10(-5) M in female VSMC (n=7, p<0.05 vs FCS alone), while in male VSMC this effect was minimal (n.s.): Both female and male VSMC expressed estrogen receptors as demonstrated by RT-PCR. Pretreatment of female VSMC cells with the E2 receptor antagonist tamoxifen prevented the antiproliferative effects exerted by E2. In aortic VSMC of female rats, E2 moderately inhibited proliferation on its own and during stimulation with FCS, while this effect was small in VSM of male rats. The expression of the E2 receptor in female and male VSMC and the effects of tamoxifen suggest that this effect is mediated by E2 receptor
Effetti dell’angiotensina II (Ang II) e del peptide natriuretico atriale (ANP) su proliferazione ed espressione genica di adipociti umani in coltura
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
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
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