Technologies du risque et technologies de soi : Gouverner les jeunes par la prévention pénale des risques

Les auteurs conceptualisent l’émergence de la notion jeune-à-risque à l’aide des travaux de Castel. Ils utilisent la notion foucaldienne de gouvernement pour explorer la signification d’un sujet jeune-à-risque qu’ils associent aux psychologies humaniste et cognitiviste. Puis, ils illustrent brièvement leurs propos en décrivant une modulation possible des mesures extrajudiciaires de la Loi sur le système de justice pénale pour les adolescents (LSJPA) au Québec. Enfin, à l’aide de cette problématisation, les auteurs veulent aussi souligner les limites concrètes de la notion jeune-à-risque.This text looks at the emergence of the notion of youth-at-risk from the work of Castel. They further conceptualize this notion by referring to Foucault’s government and by linking the youth subject to humanist and psychologist psychology. With this framework, they present one type of modulation of extrajudiciary measures authorized by the recent Youth Criminal Justice Act (YCJA). In the end, the authors also insist on the practical limits of that sort of problematization

Technologies du risque et technologies de soi

Les auteurs conceptualisent l’émergence de la notion jeune-à-risque à l’aide des travaux de Castel. Ils utilisent la notion foucaldienne de gouvernement pour explorer la signification d’un sujet jeune-à-risque qu’ils associent aux psychologies humaniste et cognitiviste. Puis, ils illustrent brièvement leurs propos en décrivant une modulation possible des mesures extrajudiciaires de la Loi sur le système de justice pénale pour les adolescents (LSJPA) au Québec. Enfin, à l’aide de cette problématisation, les auteurs veulent aussi souligner les limites concrètes de la notion jeune-à-risque.This text looks at the emergence of the notion of youth-at-risk from the work of Castel. They further conceptualize this notion by referring to Foucault’s government and by linking the youth subject to humanist and psychologist psychology. With this framework, they present one type of modulation of extrajudiciary measures authorized by the recent Youth Criminal Justice Act (YCJA). In the end, the authors also insist on the practical limits of that sort of problematization

Comparison of spatio-temporal gait parameters between the GAITRite® platinum plus classic and the GAITRite® CIRFACE among older adults: a retrospective observational study.

International audienceThe GAITRite® system is one of the gold standards for gait electronic analysis, especially for older adults. Previous GAITRite® systems were composed of an electronic roll-up walkway. Recently, a new GAITRite® electronic walkway, named CIRFACE, was commercialized. It is composed of a changeable association of stiff plates, unlike previous models. Are the gait parameters measured similar between these two walkways among older adults and according to the cognitive status, the history of falls, and the use of walking aids

FGF21, not GCN2, influences bone morphology due to dietary protein restrictions

BACKGROUND: Dietary protein restriction is emerging as an alternative approach to treat obesity and glucose intolerance because it markedly increases plasma fibroblast growth factor 21 (FGF21) concentrations. Similarly, dietary restriction of methionine is known to mimic metabolic effects of energy and protein restriction with FGF21 as a required mechanism. However, dietary protein has been shown to be required for normal bone growth, though there is conflicting evidence as to the influence of dietary protein restriction on bone remodeling. The purpose of the current study was to evaluate the effect of dietary protein and methionine restriction on bone in lean and obese mice, and clarify whether FGF21 and general control nonderepressible 2 (GCN2) kinase, that are part of a novel endocrine pathway implicated in the detection of protein restriction, influence the effect of dietary protein restriction on bone. METHODS: Adult wild-type (WT) or KO mice were fed a normal protein (18 kcal%; CON) or low protein (4 kcal%; LP) diet for 2 or 27 weeks. In addition, adult WT or KO mice were fed a CON or LP diet for 27 weeks. Young New Zealand obese (NZO) mice were placed on high-fat diets that provided protein at control (16 kcal%; CON), low levels (4 kcal%) in a high-carbohydrate (LP/HC) or high-fat (LP/HF) regimen, or on high-fat diets (protein, 16 kcal%) that provided methionine at control (0.86%; CON-MR) or low levels (0.17%; MR) for up to 9 weeks. Long bones from the hind limbs of these mice were collected and evaluated with micro-computed tomography (μCT) for changes in trabecular and cortical architecture and mass. RESULTS: In WT mice the 27-week LP diet significantly reduced cortical bone, and this effect was enhanced by deletion of but not . This decrease in bone did not appear after 2 weeks on the LP diet. In addition, KO mice had significantly less bone than their WT counterparts. In obese NZO mice dietary protein and methionine restriction altered bone architecture. The changes were mediated by FGF21 due to methionine restriction in the presence of cystine, which did not increase plasma FGF21 levels and did not affect bone architecture. CONCLUSIONS: This study provides direct evidence of a reduction in bone following long-term dietary protein restriction in a mouse model, effects that appear to be mediated by FGF21

Members of the YjgF/YER057c/UK114 Family of Proteins Inhibit Phosphoribosylamine Synthesis in Vitro*

The YjgF/YER057c/UK114 family of proteins is highly conserved across all three domains of life and currently lacks a consensus biochemical function. Analysis of Salmonella enterica strains lacking yjgF has led to a working model in which YjgF functions to remove potentially toxic secondary products of cellular enzymes. Strains lacking yjgF synthesize the thiamine precursor phosphoribosylamine (PRA) by a TrpD-dependent mechanism that is not present in wild-type strains. Here, PRA synthesis was reconstituted in vitro with anthranilate phosphoribosyltransferase (TrpD), threonine dehydratase (IlvA), threonine, and phosphoribosyl pyrophosphate. TrpD-dependent PRA formation in vitro was inhibited by S. enterica YjgF and the human homolog UK114. Thus, the work herein describes the first biochemical assay for diverse members of the highly conserved YjgF/YER057c/UK114 family of proteins and provides a means to dissect the cellular functions of these proteins

Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in similar to 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P=1.1x10(-4)) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70[95%CI 1.3-8.2], P=2.1x10(-4)). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR=19.65[95%CI 2.1-2635.4], P=3.4x10(-3)), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR=4.40[9%CI 2.3-8.4], P=7.7x10(-8)). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years; P=1.68x10(-5)).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old

Correction: Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

International audienc