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: $A + B \to 2A$. 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

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: $A + B \to 2A$. 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

Very extended cold gas, star formation and outflows in the halo of a bright QSO at z>6

Past observations of QSO host galaxies at z >6 have found cold gas and star formation on compact scales of a few kiloparsecs. We present new high sensitivity IRAM PdBI follow-up observations of the [CII] 158micron emission line and FIR continuum in the host galaxy of SDSS J1148+5152, a luminous QSO at redshift 6.4189. We find that a large fraction of the gas traced by [CII] is at high velocities, up to ~1400 km/s relative to the systemic velocity, confirming the presence of a major quasar-driven outflow indicated by previous observations. The outflow has a complex morphology and reaches a maximum projected radius of ~30 kpc. The extreme spatial extent of the outflow allows us, for the first time in an external galaxy, to estimate mass-loss rate, kinetic power and momentum rate of the outflow as a function of the projected distance from the nucleus and the dynamical time-scale. These trends reveal multiple outflow events during the past 100 Myr, although the bulk of the mass, energy and momentum appear to have been released more recently, within the past ~20 Myr. Surprisingly, we discover that also the quiescent gas at systemic velocity is extremely extended. More specifically, we find that, while 30% of the [CII] within v\in(-200, 200) km/s traces a compact component that is not resolved by our observations, 70% of the [CII] emission in this velocity range is extended, with a projected FWHM size of 17.4+-1.4 kpc. We detect FIR continuum emission associated with both the compact and the extended [CII] components, although the extended FIR emission has a FWHM of 11+-3 kpc, thus smaller than the extended [CII] source. Overall, our results indicate that the cold gas traced by [CII] is distributed up to r~30 kpc. A large fraction of extended [CII] is likely associated with star formation on large scales, but the [CII] source extends well beyond the FIR continuum.Comment: Accepted for publication in A&A, 21 pages, 18 figures, 3 tables (v2: accepted version, discussion expanded in Sect. 3, 4 and in the Appendices, minor changes elsewhere

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