10,103 research outputs found
Autocatalytic reaction-diffusion processes in restricted geometries
We study the dynamics of a system made up of particles of two different
species undergoing irreversible quadratic autocatalytic reactions: . We especially focus on the reaction velocity and on the average time at
which the system achieves its inert state. By means of both analytical and
numerical methods, we are also able to highlight the role of topology in the
temporal evolution of the system
Universal features of information spreading efficiency on -dimensional lattices
A model for information spreading in a population of mobile agents is
extended to -dimensional regular lattices. This model, already studied on
two-dimensional lattices, also takes into account the degeneration of
information as it passes from one agent to the other. Here, we find that the
structure of the underlying lattice strongly affects the time at which
the whole population has been reached by information. By comparing numerical
simulations with mean-field calculations, we show that dimension is
marginal for this problem and mean-field calculations become exact for .
Nevertheless, the striking nonmonotonic behavior exhibited by the final degree
of information with respect to and the lattice size appears to be
geometry independent.Comment: 8 pages, 9 figure
Autocatalytic reaction-diffusion processes in restricted geometries
We study the dynamics of a system made up of particles of two different
species undergoing irreversible quadratic autocatalytic reactions: . We especially focus on the reaction velocity and on the average time at
which the system achieves its inert state. By means of both analytical and
numerical methods, we are also able to highlight the role of topology in the
temporal evolution of the system
The meaning of different forms of structural myocardial injury, immune response and timing of infarct necrosis and cardiac repair
Although a decline in the all-cause and cardiac mortality rates following myocardial infarction (MI) during the past 3 decades has been reported, MI is a major cause of death and disability worldwide. From a pathological point of view MI consists in a particular myocardial cell death due to prolonged ischemia. After the onset of myocardial ischemia, cell death is not immediate, but takes a finite period of time to develop. Once complete myocytes’ necrosis has occurred, a process leading to a healed infarction takes place. In fact, MI is a dynamic process that begins with the transition from reversible to irreversible ischemic injury and culminates in the replacement of dead myocardium by a fibrous scar. The pathobiological mechanisms underlying this process are very complex, involving an inflammatory response by several pathways, and pose a major challenge to ability to improve our knowledge. An improved understanding of the pathobiology of cardiac repair after MI and further studies of its underlying mechanisms provide avenues for the development of future strategies directed toward the identification of novel therapies. The chronologic dating of MI is of great importance both to clinical and forensic investigation, that is, the ability to create a theoretical timeline upon which either clinicians or forensic pathologists may increase their ability to estimate the time of MI. Aging of MI has very important practical implications in clinical practice since, based on the chronological dating of MI, attractive alternatives to solve therapeutic strategies in the various phases of MI are developing
Thermal characterization of a multilayer coating for seismic and energy building renovation
Many buildings built in Italy in the 60s and 70s need an energy requalification and at the same time an improvement of the seismic behaviour. A non-invasive method for a joint requalification consists of an anti-seismic plaster layer and a thermal coating. In this work, a multi-layer package of 3 cm of SFRM coating and 8 cm of wood fiber placed on a 20 cm masonry wall is analyzed. Numerical and experimental analysis allowed to characterize the wall, and to determine the influence of the connecting elements
Cardiac oxidative stress and inflammatory cytokines response after myocardial infarction
Oxidative stress in heart failure or during ischemia/reperfusion occurs as a result of the excessive generation or accumulation of free radicals or their oxidation products. Free radicals formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. Oxidative stress is a condition in which oxidant metabolites exert toxic effects because of their increased production or an altered cellular mechanism of protection. In the early phase of acute heart ischemia cytokines have the feature to be functional pleiotropy and redundancy, moreover, several cytokines exert similar and overlapping actions on the same cell type and one cytokine shows a wide range of biological effects on various cell types. Activation of cytokine cascades in the infarcted myocardium was established in numerous studies. In experimental models of myocardial infarction, induction and release of the pro-inflammatory cytokines like TNF-&alpha (Tumor Necrosis Factor &alpha), IL-1&beta (Interleukin- 1&beta) and IL-6 (Interleukin-6) and chemokines are steadily described. The current review examines the role of oxidative stress and pro-inflammatory cytokines response following acute myocardial infarction and explores the inflammatory mechanisms of cardiac injur
Anisotropic renormalized fluctuations in the microwave resistivity in YBCO
We discuss the excess conductivity above Tc due to renormalized
order-parameter fluctuations in YBCO at microwave frequencies. We calculate the
effects of the uniaxial anisotropy on the renormalized fluctuations in the
Hartree approximation, extending the isotropic theory developed by Dorsey
[Phys. Rev. B 43, 7575 (1991)]. Measurements of the real part of the microwave
resistivity at 24 and 48 GHz and of the dc resistivity are performed on
different YBCO films. The onset of the superconducting transition and the
deviation from the linear temperature behavior above Tc can be fully accounted
for by the extended theory. According to the theoretical calculation here
presented, a departure from gaussian toward renormalized fluctuations is
observed. Very consistent values of the fundamental parameters (critical
temperature, coherence lenghts, penetration depth) of the superconducting state
are obtained.Comment: RevTex, 8 pages with 5 figures included, to be published in Physical
Review
Numerical precision radiative corrections to the Dalitz plot of baryon semileptonic decays including the spin-momentum correlation of the decaying and emitted baryons
We calculate the radiative corrections to the angular correlation between the
polarization of the decaying and the direction of the emitted spin one-half
baryons in the semileptonic decay mode. The final results are presented, first,
with the triple integration of the bremsstrahlung photon ready to be performed
numerically and, second, in an analytical form. A third presentation of our
results in the form of numerical arrays of coefficients to be multiplied by the
quadratic products of form factors is discussed. This latter may be the most
practical one to use in Monte Carlo simulations. A series of crosschecks is
performed. Previous results to order (alpha/pi)(q/M_1) for the decays of
unpolarized baryons are reviewed, too, where q is the momentum transfer and M_1
is the mass of the decaying baryon. This paper is self-contained and organized
to make it accessible and reliable in the analysis of the Dalitz plot of
precision experiments involving heavy quarks and is not compromised to fixing
the form factors at predetermined values. It is assumed that the real photons
are kinematically discriminated. Otherwise, our results have a general
model-independent applicability.Comment: 34 pages, 4 tables, no figures. Some sections have been shortened.
Conclusions remain unchange
Confocal laser scanning microscope, raman microscopy and western blotting to evaluate inflammatory response after myocardial infarction
Cardiac muscle necrosis is associated with inflammatory cascade that clears the infarct from dead
cells and matrix debris, and then replaces the damaged tissue with scar, through three overlapping phases: the
inflammatory phase, the proliferative phase and the maturation phase.
Western blotting, laser confocal microscopy, Raman microscopy are valuable tools for studying the inflammatory
response following myocardial infarction both humoral and cellular phase, allowing the identification and
semiquantitative analysis of proteins produced during the inflammatory cascade activation and the topographical distribution
and expression of proteins and cells involved in myocardial inflammation. Confocal laser scanning microscopy
(CLSM) is a relatively new technique for microscopic imaging, that allows greater resolution, optical sectioning of the
sample and three-dimensional reconstruction of the same sample. Western blotting used to detect the presence of a specific
protein with antibody-antigen interaction in the midst of a complex protein mixture extracted from cells, produced
semi-quantitative data quite easy to interpret. Confocal Raman microscopy combines the three-dimensional optical resolution
of confocal microscopy and the sensitivity to molecular vibrations, which characterizes Raman spectroscopy.
The combined use of western blotting and confocal microscope allows detecting the presence of proteins in the sample
and trying to observe the exact location within the tissue, or the topographical distribution of the same. Once demonstrated
the presence of proteins (cytokines, chemokines, etc.) is important to know the topographical distribution, obtaining in this
way additional information regarding the extension of the inflammatory process in function of the time stayed from the
time of myocardial infarction. These methods may be useful to study and define the expression of a wide range of inflammatory
mediators at several different timepoints providing a more detailed analysis of the time course of the infarct
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