1,721,327 research outputs found
Nuove acquisizioni sull'aterosclerosi: placca vulnerabile
Full text linkNuove acquisizioni sull’aterosclerosi: la placca vulnerabile
Marina Camera
Dip. Scienze Farmacologiche, Università degli Studi di Milano e Centro Cardiologico Monzino IRCCS Milano.
L'aterosclerosi è una patologia infiammatoria, degenerativa, a lenta progressione, caratterizzata dalla presenza di placche aterosclerotiche che possono andare incontro a rottura. L’evento trombotico conseguente alla rottura della placca è responsabile degli eventi cardiovascolari, quali angina instabile, infarto del miocardio e ictus cerebrale.
Studi anatomo-patologici e clinici hanno ormai chiarito che il rischio di rottura è legato più alle caratteristiche istomorfologiche della placca che alle sue dimensioni e al grado di stenosi luminale che essa provoca. Placche instabili sono caratterizzate da un grosso core lipidico, un cappuccio fibroso sottile, un ricco infiltrato di cellule infiammatorie macrofagiche e scarse cellule muscolari lisce. Negli ultimi due decenni, particolare attenzione è stata rivolta al concetto di "placca vulnerabile" come strumento per migliorare la stratificazione del rischio cardiovascolare e per portare, potenzialmente, a nuove opzioni terapeutiche invasive e non per prevenire e curare la malattia cardiovascolare aterotrombotica. È inoltre ipotizzabile che nei prossimi anni le nuove tecniche di imaging ad alta risoluzione saranno in grado di individuare le caratteristiche fondamentali che definiscono una placca vulnerabile che rischia di rompersi. Per ogni placca aterosclerotica potrebbe quindi essere generato un sistema di valutazione finalizzato a valutare il rischio specifico di instabilità con lo scopo di identificare prospetticamente gli eventi coronarici acuti. Inoltre, l'associazione di specifiche informazioni morfologiche con marcatori sistemici di vulnerabilità potrebbe consentire, in un prossimo futuro, di prevedere il rischio reale di infarto miocardico acuto per ogni singolo paziente
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
Atorvastatin and its metabolite inhibit Tissue Factor expression in TNF-activated human endothelial cells
No full textNF-kB-mediated Tissue Factor induction in human endothelial cells is blocked by Fluvastatin
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Fluvastatin blocks NF-kB-mediated Tissue Factor induction in human endothelial cells
No full textWe have developed a model system to measure quantitatively removal of cholesterol from a well-defined depot in vivo. To that end, lipoproteins were injected into the rectus femoris muscle of small rodents, using a 25 μl Hamilton syringe and a 27-gauge needle. In most experiments, the injected volume was 10 μl containing 200 μg of cholesterol. The lipoproteins tested were native or modified LDL labeled with trace amounts of [3H]free cholesterol ([3H]FC). The amount of label or of cholesterol mass recovered at various time intervals after injection was normalized to that found after 10 min (designated time 0). In mice, the highest recovery of the [3H]cholesterol 24 h after injection was found with cationized LDL, and ranged between 78% and 84%, whereas retention of native LDL did not exceed 24%. Based on results of 9 experiments with cationized LDL, the loss of [3H]FC was mono-exponential between 1 and 14 days and the t(1/2) was about 4 days. The disappearance curve of cholesterol mass showed an initial slow and a later more rapid component, the latter with a t(1/2) of 4 days. The initial lag is most probably due to the presence of cholesteryl ester, which needs to be hydrolyzed prior to egress. This assumption was verified by injection of cat-LDL labeled with [3H]cholesteryl oleate and finding a similar lag as well as evidence of [3H]cholesteryl ester hydrolysis. Histological examination of the injected muscle 1-4 days after injection of cat LDL showed infiltration with mononuclear cells in an area limited to the site of injection. The presently described model system, which mimics to some extent events occurring during atherogenesis, permits quantitative evaluation of egress of deposited cholesterol and may allow to study the role of HDL in such a process
Fluvastatin inhibits TNF- and LPS-induced c-Rel/p65 nuclear translocation and tissue factor expression in human endothelial cell
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