187,637 research outputs found
Sulle tracce di Darwin
No full textIncontro con gli studenti delle Scuole Medie Superiori
Introduzione Paola Catapano
DARWIN L'UOMO
Chi era Darwin
Il viaggio del Beagle
DARWIN GEOFISICO
Filmato
Darwin e il grande terremoto-maremoto cileno del 1835
LA TEORIA DELL'EVOLUZIONE DELLE SPECIE PER SELEZIONE NATURALE
Filmato
L'evoluzione in 5 parole
DNA: sulle tracce dell'evoluzione Marco Passamonti
COLLEGAMENTO EMBL (European Molecular Biology Lab)
DARWIN: SCIENZA E SOCIETÀ
Le teorie dell'evoluzione nella sfera pubblic
Ritmi circadiani ormonali in pazienti con sinndrome ossessivo-compulsiva prima e dopo trattamento con fluoxetina
No full textCorrelati neuroendocrini della sindrome ossessivo-compulsiva: implicazioni per il trattamento
No full textClass II Phosphoinositide 3-Kinases Contribute to Endothelial Cells Morphogenesis
No full textPMCID: PMC3539993This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Differenti disturbi della trasmissione GABAergica in schizofrenici con o senza discinesie tardive.
No full textRecensione di: Maestri perché testimoni. Pensare il futuro con John Henry Newman e Edith Stein. Atti del Convegno Internazionale, Istituto Universitario Salesiano – Venezia, 19-20 gennaio 2017, a cura di P. MANGANARO e M. MARCHETTO, Roma: LAS – Lateran University Press, 2017, pp. 393
No full textRecensione del volume: Maestri perché testimoni. Pensare il futuro con John Henry Newman e Edith Stein. Atti del Convegno Internazionale, Istituto Universitario Salesiano – Venezia, 19-20 gennaio 2017, a cura di P. MANGANARO e M. MARCHETTO, Roma: LAS – Lateran University Press, 2017, pp. 393
Pitavastatin - pharmacological profile from early phase studies
No full textPitavastatin has been designed as a synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor with a novel cyclopropyl moiety that results in several differences compared to other statins. These include effective inhibition of cholesterol synthesis and increased lipoprotein lipase expression at lower doses than other statins, and significant high-density lipoprotein-cholesterol and apolipoprotein A1-elevating activity that persists with time. The safety, tolerability and pharmacokinetics of pitavastatin and its major metabolite, pitavastatin lactone, have been investigated in a variety of patient groups with similar results, which suggests dosage adjustments are not required for gender, age or race. In healthy subjects, pitavastatin is well tolerated at the approved doses with no serious adverse events. The bioavailability of pitavastatin is, at 60%, higher than that of any other statin and the majority of the bioavailable fraction of an oral dose is excreted unchanged in the bile. The entero-hepatic circulation of unchanged drug contributes to the prolonged duration of action and allows once-daily, any-time dosing. Pitavastatin is only slightly metabolised by cytochrome P450 (CYP) 2C9 and not at all by CYP3A4. Neither pitavastatin nor its lactone form, have inhibitory effects on CYP, and CYP3A4 inhibitors have no effect on pitavastatin concentrations. Moreover, P-glycoprotein-mediated transport does not play a major role in the drug's disposition and pitavastatin does not inhibit P-glycoprotein activity. Pitavastatin is transported into the liver by several hepatic transporters but OATP1B1 inhibitors have relatively little effect on plasma concentrations compared with other statins. In general, interactions, except with multi-transporter inhibitors like ciclosporin, are not clinically significant. Consequently, pitavastatin has minimal drug-food and drug-drug interactions making it a treatment option in the large group of dyslipidaemic people that require multidrug therapy
Pitavastatin and HDL: Effects on plasma levels and function(s)
No full textLow high density lipoprotein cholesterol (HDL-C) levels represent an independent risk factor for cardiovascular disease; in addition to the reduced HDL-C levels commonly observed in patients at cardiovascular risk, the presence of dysfunctional HDL, i.e. HDL with reduced atheroprotective properties, has been reported. Despite the established inverse correlation between HDL-C levels and cardiovascular risk, several clinical trials with HDL-C-increasing drugs (such as niacin, CETP inhibitors or fibrate) failed to demonstrate that a significant rise in HDL-C levels translate into a cardiovascular benefit. Statins, that are the most used lipid-lowering drugs, can also increase HDL-C levels, although this effect is highly variable among studies and statins; the most recent developed statin, pitavastatin, beside its role as LDL-C-lowering agent, increases HDL-C levels at a significantly higher extent and progressively upon treatment; such increase was observed also when patients where shifted from another statin to pitavastatin. The stratification by baseline HDL-C levels revealed that only pitavastatin significantly increased HDL-C levels in patients with baseline HDL-C â¤45 mg/dl, while no changes were observed in patients with higher baseline HDL-C levels. In the last years the hypothesis that functional properties of HDL may be more relevant than HDL-C levels has risen from several observations. The treatment with pitavastatin not only increased HDL-C levels, but also increased the phospholipid content of HDL, increased the HDL efflux capacity and their anti-oxidant properties. These observations suggest that, besides its high LDL-C-lowering effect, pitavastatin also exhibits a significantly higher ability to increase HDL-C levels and may also positively affect the quality and functionality of HDL particles
Dual effect of hypochlorite in the modification of high density lipoproteins
No full textHDL-cholesterol levels are inversely correlated to the risk of cardiovascular disease. In recent years the concept that not only the quantity, but also the quality of HDL is related to their atheroprotective function has gained momentum. In fact several studies have showed that HDL can shift their properties from anti-atherogenic to pro-atherogenic upon chemical or enzymatic "modification". However, not all kind of modifications affect the antiatherogenic properties of HDL. For example, tyrosylation of HDL improves its ability to remove cholesterol from cultured cells and inhibits mice atherosclerotic lesion formation; oxidation of HDL(3) with 15-lipoxygenase or with copper ions for short time induce the formation of pre-β-migrating particles that are highly effective as cholesterol acceptors from lipid laden cells. Myeloperoxidase modifies HDL and apoA-I and reduces their ability to promote ABCA1-mediated cholesterol efflux. In the present study we show that modification with low concentration HOCl (a myeloperoxidase product) induces the formation of pre-β-migrating particles, thus improving the function of HDL in the reverse cholesterol transport, without affecting the anti-inflammatory activity. At higher HOCl concentration, pre-β-migrating particles were not detectable and the anti-inflammatory properties of HDL were lost. These findings suggest that during early phases of inflammation, when a low HOCl concentration is generated, changes in HDL occur that increase their ability to remove cholesterol and sparing anti-inflammatory properties; later during acute inflammation, when higher HOCl concentration are present changes in HDL occur that severely decrease their ability to remove cholesterol from macrophages and to protect endothelial cells from pro-inflammatory stimuli
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