A comparison between different propagative schemes for the simulation of tapered step index slab waveguides

The performance and accuracy of a number of propagative algorithms are compared for the simulation of tapered high contrast step index slab waveguides. The considered methods include paraxial as well as nonparaxial formulations of optical field propagation. In particular attention is paid to the validity of the paraxial approximation. To test the internal consistency of the various methods the property of reciprocity is verified and it is shown that for the paraxial algorithms the reciprocity can only be fulfilled if the paraxial approximation of the power flux expression using the Poynting vector is considered. Finally, modeling results are compared with measured fiber coupling losses for an experimentally realized taper structure

Vezatin is essential for dendritic spine morphogenesis and functional synaptic maturation.

International audienceVezatin is an integral membrane protein associated with cell-cell adhesion complex and actin cytoskeleton. It is expressed in the developing and mature mammalian brain, but its neuronal function is unknown. Here, we show that Vezatin localizes in spines in mature mouse hippocampal neurons and codistributes with PSD95, a major scaffolding protein of the excitatory postsynaptic density. Forebrain-specific conditional ablation of Vezatin induced anxiety-like behavior and impaired cued fear-conditioning memory response. Vezatin knock-down in cultured hippocampal neurons and Vezatin conditional knock-out in mice led to a significantly increased proportion of stubby spines and a reduced proportion of mature dendritic spines. PSD95 remained tethered to presynaptic terminals in Vezatin-deficient hippocampal neurons, suggesting that the reduced expression of Vezatin does not compromise the maintenance of synaptic connections. Accordingly, neither the amplitude nor the frequency of miniature EPSCs was affected in Vezatin-deficient hippocampal neurons. However, the AMPA/NMDA ratio of evoked EPSCs was reduced, suggesting impaired functional maturation of excitatory synapses. These results suggest a role of Vezatin in dendritic spine morphogenesis and functional synaptic maturation

Association of the interferon-β gene with pericentromeric heterochromatin is dynamically regulated during virus infection through a YY1-dependent mechanism

Nuclear architecture as well as gene nuclear positioning can modulate gene expression. In this work, we have analyzed the nuclear position of the interferon-β (IFN-β) locus, responsible for the establishment of the innate antiviral response, with respect to pericentromeric heterochromatin (PCH) in correlation with virus-induced IFN-β gene expression. Experiments were carried out in two different cell types either non-infected (NI) or during the time course of three different viral infections. In NI cells, we showed a monoallelic IFN-β promoter association with PCH that strongly decreased after viral infection. Dissociation of the IFN-β locus away from these repressive regions preceded strong promoter transcriptional activation and was reversible within 12 h after infection. No dissociation was observed after infection with a virus that abnormally maintained the IFN-β gene in a repressed state. Dissociation induced after virus infection specifically targeted the IFN-β locus without affecting the general structure and nuclear distribution of PCH clusters. Using cell lines stably transfected with wild-type or mutated IFN-β promoters, we identified the proximal region of the IFN-β promoter containing YY1 DNA-binding sites as the region regulating IFN-β promoter association with PCH before as well as during virus infection

Placental lactogens induce serotonin biosynthesis in a subset of mouse beta cells during pregnancy

AIMS/HYPOTHESIS: Upregulation of the functional beta cell mass is required to match the physiological demands of mother and fetus during pregnancy. This increase is dependent on placental lactogens (PLs) and prolactin receptors, but the mechanisms underlying these events are only partially understood. We studied the mRNA expression profile of mouse islets during pregnancy to gain a better insight into these changes. METHODS: RNA expression was measured ex vivo via microarrays and quantitative RT-PCR. In vivo observations were extended by in vitro models in which ovine PL was added to cultured mouse islets and MIN6 cells. RESULTS: mRNA encoding both isoforms of the rate-limiting enzyme of serotonin biosynthesis, tryptophan hydroxylase (TPH), i.e. Tph1 and Tph2, were strongly induced (fold change 25- to 200-fold) during pregnancy. This induction was mimicked by exposing islets or MIN6 cells to ovine PLs for 24 h and was dependent on janus kinase 2 and signal transducer and activator of transcription 5. Parallel to Tph1 mRNA and protein induction, islet serotonin content increased to a peak level that was 200-fold higher than basal. Interestingly, only a subpopulation of the beta cells was serotonin-positive in vitro and in vivo. The stored serotonin pool in pregnant islets and PL-treated MIN6 cells was rapidly released (turnover once every 2 h). CONCLUSIONS/INTERPRETATION: A very strong lactogen-dependent upregulation of serotonin biosynthesis occurs in a subpopulation of mouse islet beta cells during pregnancy. Since the newly formed serotonin is rapidly released, this lactogen-induced beta cell function may serve local or endocrine tasks, the nature of which remains to be identified

Fast switching of ferromagnetic single crystals

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Inhibition sélective de l'expression de la tryptophane hydroxylase 2 in vivo (étude de la fonction des neurones sérotoninergiques des noyaux du raphé chez les rongeurs)

La perturbation de la neurotransmission sérotoninergique est associée à des pathologies psychiatriques telles que la dépression et les troubles obsessionnels compulsifs. La détermination du rôle des neurones sérotoninergiques du raphé a été jusqu à présent, essentiellement réalisée suite à des lésions, non spécifiques, toxiques ou détruisant les neurones. Dans le but de disséquer plus précisément le rôle d une structure sérotoninergique particulière, nous avons développé une approche permettant d inactiver une sous population de neurones sérotoninergiques sans les détruire. La stratégie consiste à inhiber l expression de la tryptophane hydroxylase 2 (TPH2), enzyme neuronale de biosynthèse de la sérotonine, de manière sélective dans les neurones d intérêt par la méthode d interférence par l ARN et à analyser les conséquences fonctionnelles de leur inactivation. Nous avons construit et produit un vecteur lentiviral exprimant un shARN, conservé chez le rat et la souris, capable d inhiber efficacement l expression de la TPH2 in vitro. L efficacité de ce vecteur a été validée dans des cultures primaires de neurones sérotoninergiques. L administration de ce vecteur in vivo dans le noyau du raphé dorsal (NRD) de souris et de rat entraîne une baisse importante des niveaux de sérotonine dans les structures cibles : cortex frontal et striatum. Les conséquences d un déficit de synthèse de sérotonine cérébrale sur le comportement de type anxio-dépressif et sur la réponse à un stress ont été analysées dans les deux espèces. Nos premiers résultats suggèrent que l inhibition de l expression de la TPH2 dans le NRD, a un effet sur l activité locomotrice spontanée chez la souris.PARIS-BIUSJ-Biologie recherche (751052107) / SudocSudocFranceF