Transitions dans le parcours de vie et construction des inégalités

Tout au long de leur existence, les individus suivent des chemins singuliers dont les trajectoires ne sont pas le simple fait de la seule volonté ou du hasard. Ces cheminements se révèlent souvent générateurs d'inégalités entre individus, notamment au cours des transitions des âges de la vie (enfance, adolescence, âge adulte, grand âge), ou lors de différentes étapes (mariage, divorce, deuil, etc). C'est afin de mieux comprendre les modalités et les combinaisons d'influence à l'origine des inégalités dans les parcours de vie, que les éditeurs de cet ouvrage ont réuni des chercheurs issus des sciences psychologiques, sociales et économiques, afin de croiser leurs regards sur la manière dont ces inégalités se creusent ou se réduisent au fil des trajectoires. Cet ouvrage interdisciplinaire met en relief la richesse d'une approche des inégalités dans la perspective dynamique du parcours de vie.Peer reviewe

Glucose is arrhythmogenic in the anoxic-reoxygenated embryonic chick heart.

Unlike in adult heart, embryonic myocardium works at low PO2 and depends preferentially on glucose. Therefore, activity of the embryonic heart during anoxia and reoxygenation should be particularly affected by changes in glucose availability. Hearts excised from 4-d-old chick embryos were submitted in vitro to strictly controlled anoxia-reoxygenation transitions at glucose concentrations varying from 0 to 20 mmol/L. Spontaneous and regular heart contractions were detected optically as movements of the ventricle wall and instantaneous heart rate, amplitude of contraction, and velocities of contraction and relaxation were determined. Anoxia induced transient tachycardia and rapidly depressed contractile activity, whereas reoxygenation provoked a temporary and complete cardioplegia (oxygen paradox). In the presence of glucose, atrial rhythm became irregular during anoxia and chaotic-periodic during reoxygenation. The incidence of these arrhythmias depended on duration of anoxia, and no ventricular ectopic beats were observed. Removal of glucose or blockade of glycolysis suppressed arrhythmias. These results show similarities but also differences with respect to the adult heart. Indeed, glucose 1) delayed and anoxic contractile failure, shortened the reoxygenation-induced cardiac arrest, and improved the recovery of contractile activity; 2) attenuated stunning at 20 mmol/L but worsened it at 8 mmol/L; and 3) paradoxically, was arrhythmogenic during anoxia and reoxygenation, especially when present at the physiologic concentration of 8 mmol/L. The last named phenomenon seems to be characteristic of the young embryonic heart, and our findings underscore that fluctuations of glycolytic activity may play a role in the reactivity of the embryonic myocardium to anoxiareoxygenation transitions