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Dive into the research topics where Alberto Madureri is active.

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Featured researches published by Alberto Madureri.


Heart International | 2007

Nitric oxide and cardiovascular risk factors

Riccardo Raddino; Giorgio Caretta; Melissa Teli; Ivano Bonadei; Debora Robba; Gregoriana Zanini; Alberto Madureri; Savina Nodari; Livio Dei Cas

The endothelium is a dynamic organ with many properties that takes part in the regulation of the principal mechanisms of vascular physiology. Its principal functions include the control of blood-tissue exchange and permeability, the vascular tonus, and the modulation of inflammatory or coagulatory mechanisms. Many vasoactive molecules, produced by the endothelium, are involved in the control of these functions. The most important is nitric oxide (NO), a gaseous molecule electrically neutral with an odd number of electrons that gives the molecule chemically reactive radical properties. Already known in the twentieth century, NO, sometimes considered as a dangerous molecule, recently valued as an important endogenous vasodilator factor. Recently, it was discovered that it is involved in several physiological mechanisms of endothelial protection (Tab. I). In 1992, Science elected it as “molecule of the year”; 6 yrs later three American researchers (Louis Ignarro, Robert Furchgott and Fried Murad) obtained a Nobel Prize for Medicine and Physiology “for their discoveries about NO as signal in the cardiovascular system”. TABLE I EFFECTS OF ENDOTHELIAL NITRIC OXIDE ON THE CARDIOVASCULAR SYSTEM NO is synthesized by endothelial cells from L-argynine and oxygen (Fig. 1). Blood flow and laminar shear stress induce the activation through phosphorilation of NO synthase (NOS), that catalyzes the conversion reaction from L-arginine to citrullin and NO, through two cofactors: calmodulin and pteridin-thetraidrobiopterine (BH4) (Fig. 2). There are at least three isoforms of constitutive NOS: the endothelial form (eNOS), the neuronal form (nNOS) and the inducible form (iNOS); eNOS, the calcium-dependent form of the enzyme, is in many cellular types and it is responsible for NO production in healthy blood vessels. nNOS is a special type of eNOS, expressed in the central nervous system. iNOS, a form induced by immunological stimuli (1), is expressed in the myocytes, in the macrophages and in the endothelial cells. NOS are formed by two distinct catalytic subunits, as terminal C-reductase and terminal N-oxygenase domain. In the presence of sufficient amounts of BH4, these domains work together and synthesize NO. Otherwise in case of increased oxidative stress they cause the production of peroxynitrites. The NO produced induces guanilate cyclase to the synthesis of cGMP from cGTP. The last molecule causes cellular hyperpolarization due to the activation of the potassium canals. These reactions cause the inhibition of the entrance of calcium and, in this way, the vasodilatation in the cardiovascular system (Tab. I). Fig. 1 Fig. 2 1 ENDOTHELIAL DYSFUNCTION AND NO Normal vascular tonus depends on the equilibrium between the vasoconstrictor and vasodilator molecules released from the endothelium. In healthy endothelium, the balance is shifted towards vasodilatation due to NO (Tab. II). Endothelial dysfunction is synonymous with the insufficiency of endothelium dependent vasodilatation and results in the failure of vasoactive, anticoagulant and anti-inflammatory effects of healthy endothelium. The most important mechanism for endothelial dysfunction is the reduction in NO availability. The substrate insufficiency such as the reduction in L-arginine in endothelial cells or any defect in the transport of L-arginine into the cell, the existence of NOS inhibitors such as asymmetrical dimethylarginine (ADMA) and G-monomethyl-L-arginine (L-NM-MA), increase in the reactive oxygen molecules, reduction in the diffusion of NO due to intimal thickening, the mutations in the eNOS gene expression, increase in the catabolism of NO, cofactor insufficiency and increase in the vasoconstrictor molecules released from the endothelium are the other mechanisms that must be considered in endothelial dysfunction. Endothelial dysfunction coexists with many disease states in the cardiovascular system and is known as the first stage of atherosclerosis, which is probably the most important disease of the modern age. In the cardiovascular system, other clinical conditions, which are related with endothelial dysfunction are hypertension, are hyperglycemia-insulin resistance, dyslipidemia, menopause, heart failure, variant angina, cardiac syndrome X and hyperhomocysteinemia. TABLE II EFFECTS OF ENDOTHELIAL NITRIC OXIDE ON THE CARDIOVASCULAR SYSTEM NO oppose the atherogenical stimuli preventing vascular structural modifications; it can inhibit the adhesion of platelets and monocytes, the migration of the smooth muscular cells and the endothelial apoptosys. It was demonstrated that NO, for example, inhibits, through S-nytrosation, key-enzymes of the apoptotic chart (Caspases 6, 7, 8) (2). I. Aging Data obtained in humans and in animal experiments indicate that aging alters the endothelial dependent vasodilatation in the big arteries and in the resistance vessels (3). Moreover, aging is associated with a progressive remodeling of the vascular wall, which includes the thickening of the tunica intima and of the tunica media and the increase in its rigidity (4). With advancing old age, smooth muscular cells migrate progressively from the tunica media and accumulate in the intima (5). This fact is associated with a progressive decline in endothelial functionality, which causes a reduced response to the vasodilating factors, consequent to the alteration of the expression and/or the activity of NOS and with an increased formation of free radicals. Aging is associated with an alteration in the equilibrium between vasoconstrictor and vasodilating factors released by the endothelium, or rather with a progressive reduction in NO and endothelial derived hyperpolarizing factor (EDHF) associated with an increase in oxygen free radicals and prostanoids derived from cycle-oxygenase. In addition, it was recently demonstrated that, with aging, there is an inferior proliferation and migration of the endothelial cells from the sites near the atherosclerotic lesion, preventing the preservation of intimal integrity, which is normally favored by a healthy endothelium (6).


Journal of the American College of Cardiology | 2013

EFFECT OF HIGH DOSE OF ATORVASTATIN VERSUS MODERATE DOSE ON ENDOTHELIAL FUNCTION AND INFLAMMATORY BIOMARKERS IN PATIENTS WITH STEMI

Riccardo Raddino; Paolo Della Pina; Mara Gavazzoni; Elio Gorga; Alberto Madureri; Marco Metra

The use of statins allowed a striking progress in the treatment of coronary artery disease both in chronic and acute phase. Despite these evidences, at this date few data are available about the efficacy of statin therapy in the subgroup of patients with acute coronary syndromes and persistent ST-


Heart International | 2006

Diagnostic value of the head-up tilt test and the R-test in patients with syncope

Riccardo Raddino; Gregoriana Zanini; Debora Robba; Ivano Bonadei; Federica Chieppa; Claudio Pedrinazzi; Giorgio Caretta; Alberto Madureri; Enrico Vizzardi; Livio Dei Cas

The diagnostic value of the head-up tilt test (HUTT) in discovering vasovagal syndrome depends on the pre-test probability. An accurate anamnesis and clinical examination screens the patients indicated for the HUTT. In patients with unexplained syncope, the R-test is an alternative procedure to discover its cause. In our study, we evaluated the diagnostic significance of the HUTT in a group of 211 patients and of the R-test in a subgroup of 45 patients with negative HUTT results and with negative traditional Holter ECG monitoring (24 hr).


European Heart Journal | 1998

Effects of neurohormonal antagonism on symptoms and quality-of-life in heart failure.

Metra M; S. Nodari; A. D'alola; Alberto Madureri; F. Rosselli; Luca Bontempi; Zanini R; L. Dei Cas


Internal and Emergency Medicine | 2009

High sensitivity C-reactive protein: a predictor for recurrence of atrial fibrillation after successful cardioversion

Enrico Vizzardi; Savina Nodari; Gregoriana Zanini; Alessandra Manerba; Silvia Frattini; Alberto Madureri; Riccardo Raddino; Livio Dei Cas


Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo | 2016

Erythropoietin: a new perspective in cardiovascular therapy

Riccardo Raddino; Debora Robba; Giorgio Caretta; Ivano Bonadei; Melissa Teli; Gregoriana Zanini; Alberto Madureri; Enrico Vizzardi; Livio Dei Cas


Recenti progressi in medicina | 2009

Utilità della misurazione dei diametri e del volume atriale sinistro nella valutazione della funzione diastolica del ventricolo sinistro

Enrico Vizzardi; Ivano Bonadei; Melissa Teli; Giorgio Caretta; Cristian Maiandi; Alberto Madureri; T. Bordonali; Ermanna Chiari; Riccardo Raddino; Livio Dei Cas


Nutrafoods | 2012

Efficacy of a combination of natural lipid-lowering and antioxidant agents in hypercholesterolaemic patients

Riccardo Raddino; Paolo Della Pina; Mara Gavazzoni; Elio Gorga; Eleftheria Trikaki; Valentina Regazzoni; Giulio Brambilla; Alberto Madureri


Giornale italiano di cardiologia | 2008

[Diabetes and ischemic heart disease: specific treatment].

Riccardo Raddino; Ivano Bonadei; Melissa Teli; Debora Robba; Giorgio Caretta; Alberto Madureri; Gregoriana Zanini; Claudio Pedrinazzi; Enrico Vizzardi; Livio Dei Cas


Giornale italiano di cardiologia | 2010

Indicazione alla terapia con statine nel paziente con sindrome coronarica acuta ad eziologia ischemica

Riccardo Raddino; Paolo Della Pina; Elio Gorga; Giorgio Caretta; Alberto Madureri; Dei Cas

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