University of Milan

About: University of Milan is a education organization based out in Milan, Italy. It is known for research contribution in the topics: Population & Transplantation. The organization has 58413 authors who have published 139784 publications receiving 4636354 citations. The organization is also known as: Università degli Studi di Milano & Statale.

Increasing Oxide Reducibility: The Role of Metal/Oxide Interfaces in the Formation of Oxygen Vacancies

Abstract: Reducibility is an essential characteristic of oxide catalysts in oxidation reactions following the Mars–van Krevelen mechanism. A typical descriptor of the reducibility of an oxide is the cost of formation of an oxygen vacancy, which measures the tendency of the oxide to lose oxygen or to donate it to an adsorbed species with consequent change in the surface composition, from MnOm to MnOm–x. The oxide reducibility, however, can be modified in various ways: for instance, by doping and/or nanostructuring. In this review we consider an additional aspect, related to the formation of a metal/oxide interface. This can be realized when small metal nanoparticles are deposited on the surface of an oxide support or when a nanostructured oxide, either a nanoparticle or a thin film, is grown on a metal. In the past decade, both theory and experiment indicate a particularly high reactivity of the oxygen atoms at the boundary region between a metal and an oxide. Oxygen atoms can be removed from interface sites at much...

Increased MET Gene Copy Number Negatively Affects Survival of Surgically Resected Non–Small-Cell Lung Cancer Patients

Abstract: Purpose To investigate the prognostic role of genomic gain for MET and epidermal growth factor receptor (EGFR) genes in surgically resected non‐small-cell lung cancer (NSCLC).

International Union of Pharmacology. LXIV. Estrogen Receptors

Abstract: Estrogen receptors (ERs[1][1]) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. In the late 1950s, the existence of a receptor molecule that could bind 17β-estradiol was demonstrated by Jensen and Jacobsen ([Jensen and Jordan, 2003][2]). The first

HMG-CoA Reductase Inhibitors Reduce MMP-9 Secretion by Macrophages

Abstract: -Macrophages secrete matrix metalloproteinases (MMPs) that may weaken the fibrous cap of atherosclerotic plaque, predisposing its fissuration. The 92-kDa gelatinase B (MMP-9) has been identified in abdominal aortic aneurysms and in atherosclerotic tissues. Fluvastatin, through the inhibition of the isoprenoid pathway, inhibits major processes of atherogenesis in experimental models (smooth muscle cell migration and proliferation and cholesterol accumulation in macrophages). We studied the effect of fluvastatin on the activity of MMP-9 in mouse and human macrophages in culture. Conditioned media of cells treated for 24 hours with fluvastatin were analyzed by gelatin zymography. In mouse macrophages, fluvastatin (5 to 100 micromol/L) significantly inhibited in a dose-dependent manner MMP-9 activity from 20% to 40% versus control. The drug, at a concentration as low as 5 micromol/L, inhibited MMP-9 activity ( approximately 30%) in human monocyte-derived macrophages as well. Phorbol esters (TPA, 50 ng/mL) stimulated MMP-9 activity by 50%, and fluvastatin inhibited this enhanced activity up to 50% in both mouse and human macrophages. The above results on the secretion of MMP-9 were confirmed by Western blotting and ELISA. The inhibitory effect of fluvastatin was overcome by the simultaneous addition of exogenous mevalonate (100 micromol/L), a precursor of isoprenoids. Fluvastatin's effect was fully reversible, and the drug did not cause any cellular toxicity. The statin did not block directly the in vitro activation of the secreted protease. Similar data were obtained with simvastatin. Altogether, our data indicate an inhibition of MMP-9 secretion by the drug. This effect is mediated by the inhibition of synthesis of mevalonate, a precursor of numerous derivatives essential for several cellular functions.

Selective Potentiation of Peripheral Chemoreflex Sensitivity in Obstructive Sleep Apnea

Abstract: Background—The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. Methods and Results—We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects...