Suggestion of a classification for urinary calculi in a pediatric population from brittany

International audienc

Pseudohypobicarbonatemia in a patient with a kappa IgA monoclonal gammapathy [Pseudohypobicarbonatémie chez une patiente atteinte d'une gammapathie monoclonale à IgA kappa]

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Prévalence du déficit en vitamine D chez les enfants âgés de 5 a 10 ans en Bretagne Occidentale.

International audienceFrench guidelines do not recommend systematic supplementation of vitamin D in children aged 5-10 years old owing to the lack of data on vitamin D status in this age group. Our objective was to assess the prevalence of vitamin D deficiency in these children. Single-center, prospective, epidemiological study including 358 children aged 0-15 years. The endpoint was the concentration of vitamin D. In all, 316 children were divided into four groups according to age: 0-18 months (n=113); 18 months to 5 years (n=103); 5-10 years (n=62); and 10-15 years (n=38). The median concentration of vitamin D decreased with age (P<0.001): 90.2 nmol/L in the group aged 0-18 months; 56.7 nmol/L in the group aged 18 months to 5 years; 49.05 nmol/L in the group aged 5-10 years; and 42.45 nmol/L in the group aged 10-15 years. This corresponds to an increase in the prevalence of vitamin D deficiency in children aged 5-10 years (51.6% vs. 8.8% in the group aged 0-18 months, P<0.001). For children aged 5-10 years, the prevalence of deficiency was greater in the non-supplementation group (75%) compared with the supplementation group (13%; P<0.001). This study demonstrates the high prevalence of vitamin D deficiency in children aged 5-10 years and the relationship between supplementation and vitamin D status. It provides an argument in favor of supplementation in children aged 5-10 years in this region and a reconsideration of the French recommendations.Les recommandations françaises ne préconisent pas la supplémentation systématique en vitamine D chez les enfants de 5 à 10 ans du faitde l’absence de données sur leur statut en cette vitamine. Méthode. Notre objectif était d’évaluer la prévalence de ce déficit chez ces enfants. Il s’est agi d’une étude épidémiologique, monocentrique, prospective incluant 316 enfants âgés de 0 à 15 ans. Le critère d’évaluation était la concentration sérique en vitamine D. Résultats. Trois cent seize enfants, répartis en 4 classes d'âge, ont été inclus : 0–18 mois (n = 113) ; 18 mois–5 ans (n = 103) ; 5–10 ans (n = 62) ; 10–15 ans (n = 38). La médiane des concentrations de vitamine D diminuait avec l’âge (p < 0,001) : 90,2 nmol/L dans le groupe 0–18 mois ; 56,7 nmol/L dans le groupe 18 mois–5 ans ; 49,05 nmol/L dans le groupe 5–10 ans et 42,45 nmol/L dans le groupe 10–15 ans. Ceci correspond à une augmentation de la prévalence du déficit en vitamine D chez les enfants de 5 a` 10 ans (51,6 % versus 8,8 % dans le groupe 0–18 mois [p < 0,001]). Pour les enfants de ce groupe, la prévalence du déficit était supérieure dans le groupe non supplémente´ (75 %) par rapport au groupesupplémente´ (13 %) (p < 0,001). Conclusion. La prévalence du déficit en vitamine D est importante chez les enfants âgés de 5 a` 10 ans et il existe un lien entre supplémentation et statut en vitamine D. Elle apporte un argument en faveur d’une supplémentation systématique des enfants de 5 a`10 ans dans notre région et d’une reconsidération des recommandationsfranc¸aises

A Fear Memory Engram and Its Plasticity in the Hypothalamic Oxytocin System

International audienceOxytocin (OT) release by axonal terminals onto the central nucleus of the amygdala exerts anxiolysis. To investigate which subpopulation of OT neurons contributes to this effect, we developed a novel method: virus-delivered genetic activity-induced tagging of cell ensembles (vGATE). With the vGATE method, we identified and permanently tagged a small subpopulation of OT cells, which, by optogenetic stimulation, strongly attenuated contextual fear-induced freezing, and pharmacogenetic silencing of tagged OT neurons impaired context-specific fear extinction, demonstrating that the tagged OT neurons are sufficient and necessary, respectively, to control contextual fear. Intriguingly, OT cell terminals of fear-experienced rats displayed enhanced glutamate release in the amygdala. Furthermore, rats exposed to another round of fear conditioning displayed 5-fold more activated magnocellular OT neurons in a novel environment than a familiar one, possibly for a generalized fear response. Thus, our results provide first evidence that hypothalamic OT neurons represent a fear memory engram

Astrocytes mediate the effect of oxytocin in the central amygdala on neuronal activity and affective states in rodents

Oxytocin (OT) orchestrates social and emotional behaviors through modulation of neural circuits. In the central amygdala, the release of OT modulates inhibitory circuits and, thereby, suppresses fear responses and decreases anxiety levels. Using astrocyte-specific gain and loss of function and pharmacological approaches, we demonstrate that a morphologically distinct subpopulation of astrocytes expresses OT receptors and mediates anxiolytic and positive reinforcement effects of OT in the central amygdala of mice and rats. The involvement of astrocytes in OT signaling challenges the long-held dogma that OT acts exclusively on neurons and highlights astrocytes as essential components for modulation of emotional states under normal and chronic pain conditions

Astrocytes mediate the effect of oxytocin in the central amygdala on neuronal activity and affective states in rodents.

Oxytocin (OT) orchestrates social and emotional behaviors through modulation of neural circuits. In the central amygdala, the release of OT modulates inhibitory circuits and, thereby, suppresses fear responses and decreases anxiety levels. Using astrocyte-specific gain and loss of function and pharmacological approaches, we demonstrate that a morphologically distinct subpopulation of astrocytes expresses OT receptors and mediates anxiolytic and positive reinforcement effects of OT in the central amygdala of mice and rats. The involvement of astrocytes in OT signaling challenges the long-held dogma that OT acts exclusively on neurons and highlights astrocytes as essential components for modulation of emotional states under normal and chronic pain conditions

Major Role for TRPV1 and InsP3R in PAR2-Elicited Inflammatory Mediator Production in Differentiated Human Keratinocytes

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