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Biomedical subjects

P Allegrini

Publications and source records attributed to P Allegrini.

11 recordsLinked to original sources
PubMed2004

Non-Poisson dichotomous noise: higher-order correlation functions and aging.

We study a two-state symmetric noise, with a given waiting time distribution psi (tau) , and focus our attention on the connection between the four-time and two-time correlation functions. The transition of psi (tau) from the exponential to the nonexponential condition yields the breakdown of the usual factorization condition of high-order correlation functions, as well as the birth of aging effects. We discuss the subtle connections between these two properties and establish the condition that the Liouville-like approach has to satisfy in order to produce a correct description of the resulting diffusion process.

Journal Article↗
PubMed2003

Long- and short-time analysis of heartbeat sequences: correlation with mortality risk in congestive heart failure patients.

We analyze RR heartbeat sequences with a dynamic model that satisfactorily reproduces both the long- and the short-time statistical properties of heart beating. These properties are expressed quantitatively by means of two significant parameters, the scaling delta concerning the asymptotic effects of long-range correlation, and the quantity 1-pi establishing the amount of uncorrelated fluctuations. We find a correlation between the position in the phase space (delta, pi) of patients with congestive heart failure and their mortality risk.

Biophysics↗
PubMed2002

Scaling breakdown: a signature of aging.

We prove that the Lévy walk is characterized by bilinear scaling. This effect mirrors the existence of a form of aging that does not require the adoption of nonstationary conditions.

Journal Article↗
PubMed2002

Memory beyond memory in heart beating, a sign of a healthy physiological condition.

We describe two types of memory and illustrate each using artificial and actual heartbeat data sets. The first type of memory, yielding anomalous diffusion, implies the inverse power-law nature of the waiting time distribution and the second the correlation among distinct times, and consequently also the occurrence of many pseudoevents, namely, not genuinely random events. Using the method of diffusion entropy analysis, we establish the scaling that would be determined by the real events alone. We prove that the heart beating of healthy patients reveals the existence of many more pseudoevents than in the patients with congestive heart failure.

Computer Simulation↗
PubMed1999

Dynamic entropy as a measure of caging and persistent particle motion in supercooled liquids.

The length-scale dependence of the dynamic entropy is studied in a molecular dynamics simulation of a binary Lennard-Jones liquid above the mode-coupling critical temperature T(c). A number of methods exist for estimating the entropy of dynamical systems, and we utilize an approximation based on calculating the mean first-passage time (MFPT) for particle displacement because of its tractability and its accessibility in real and simulation measurements. The MFPT dynamic entropy S(epsilon) is defined as equal to the inverse of the average first-passage time for a particle to exit a sphere of radius epsilon. This measure of the degree of chaotic motion allows us to identify characteristic time and space scales and to quantify the increasingly correlated particle motion and intermittency occurring in supercooled liquids. In particular, we identify a "cage" size defining the scale at which the particles are transiently localized, and we observe persistent particle motion at intermediate length scales beyond the scale where caging occurs. Furthermore, we find that the dynamic entropy at the scale of one interparticle spacing extrapolates to zero as the mode-coupling temperature T(c) is approached.

Journal Article↗
PubMed1996

Left ventricular wall stress and sarcoplasmic reticulum Ca(2+)-ATPase gene expression in renal hypertensive rats: dose-dependent effects of ACE inhibition and AT1-receptor blockade.

BACKGROUND: Cardiac hypertrophy is associated with altered Ca2+ handling and may predispose to the development of LV dysfunction and cardiac failure. At the cellular level, the re-expression of ANF represents a well-established marker of myocyte hypertrophy while the decreased expression of the sarcoplasmatic reticulum (SR) Ca(2+)-ATPase is thought o play a crucial role in the alterations of Ca2+ handling and LV function. We assessed the dose-dependent effect of chronic ACE inhibition or AT1 receptor blockade on cardiac function in relation to the cardiac expression of the SR Ca(2+)-ATPase and ANF. METHODS AND RESULTS: Renal hypertensive rats (2K-1C) were treated for 12 weeks with three different doses of the ACE inhibitor benazepril, the AT1-receptor antagonist valsartan (each drug 0.3, 3, and 10 mg/kg per day i.p.) or placebo. LV dimensions, hypertrophy and wall stress were determined in vivo by magnetic resonance imaging and the gene expressions of ANF and SR Ca(2+)-ATPase were quantified by Northern blot. Low doses of both drugs did not affect blood pressure, hypertrophy, systolic wall stress and the ANF and SR Ca(2+)-ATPase gene expression. High doses of each drug reduced systolic blood pressure, wall stress, and LV hypertrophy to a similar extent and to values comparable to normotensive, age-matched rats. In addition, high dose treatment reduced LV end-systolic and end-diastolic volume as compared to untreated 2K-1C animals and normalized the mRNA levels of both ANF and SR Ca(2+)-ATPase (as compared to normotensive animals). CONCLUSIONS: We conclude that in this model, high doses of ACE inhibition and AT1-receptor blockade are necessary to normalize systolic blood pressure, LV hypertrophy and systolic LV wall stress which, in turn, is associated with restoration of a normal cardiac phenotype with respect to SR Ca(2+)-ATPase and ANF and normalization of cardiac function.

Angiotensin II↗