« Entrer » et « sortir » de l'islam : regards croisés sur les trajectoires, dynamiques et engagements autour de la conversion religieuse Responsable

International audienceHow can the "quest-after-truth" approach lead those who set out to achieve such to varied forms of religious expression in community life? What function do religious considerations have for those individuals who integrate themselves into a new community? How do they redefine their relationship with their body after such a conversion? This workshop proposes looking at religious conversion through the prism of cross trajectories that branch off and communicate and which can include diversions, shifts and rediscovery of the self. The cross views on the ways of "entering" and "leaving" Islam aim to examine how religious considerations mobilise individuals around artistic, learned or militant driving forces.Comment la démarche de « quête de Vérité » peut-elle amener ses aspirants à des formes variées d’expression du religieux dans la cité ? Quelle est la fonction du religieux pour ces individus qui s’insèrent dans une communauté nouvelle ? Comment redéfinissent-ils le rapport à leur corps après cette conversion ? Cet atelier propose d’appréhender la conversion religieuse au prisme de trajectoires croisées, bifurquantes et communiquantes dans lesquelles se rejoignent des mouvements de détour, décentrement et retour vers soi. Les regards croisés sur les « entrées » et « sorties » de l’islam visent à interroger le religieux dans sa capacité à mobiliser les individus autour de dynamiques artistiques, savantes ou militantes

Alterations in the brain adenosine metabolism cause behavioral and neurological impairment in ADA-deficient mice and patients

Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates. Neurological and behavioral abnormalities observed in ADA-SCID patients surviving after stem cell transplantation or gene therapy represent an unresolved enigma in the field. We found significant neurological and cognitive alterations in untreated ADA-SCID patients as well as in two groups of patients after short- and long-term enzyme replacement therapy with PEG-ADA. These included motor dysfunction, EEG alterations, sensorineural hypoacusia, white matter and ventricular alterations in MRI as well as a low mental development index or IQ. Ada-deficient mice were significantly less active and showed anxiety-like behavior. Molecular and metabolic analyses showed that this phenotype coincides with metabolic alterations and aberrant adenosine receptor signaling. PEG-ADA treatment corrected metabolic adenosine-based alterations, but not cellular and signaling defects, indicating an intrinsic nature of the neurological and behavioral phenotype in ADA deficiency