Les décisions spontanées d’élèves de sixième année dans le contexte d’un projet de développement durable

Les individus influencent la qualité de l’environnement dans leurs rôles de citoyens, d’investisseurs et de membres d’organisations effectuant des choix environnementaux. Or, la prise de décision, en environnement et particulièrement chez les jeunes, est encore peu comprise. La recherche présentée avait pour objectif de décrire le processus décisionnel spontané d’élèves de 10-11 ans, dans le contexte d’un développement résidentiel viable. Les chercheuses voulaient comprendre de quelle façon les élèves représentaient spontanément leur processus décisionnel et les raisons qui motivaient leurs choix. L’approche pédagogique choisie pour le projet en classe a été celle de la simulation globale. Les élèves ont été invités à jouer les rôles des futurs citoyens du développement résidentiel et à prendre des décisions concernant les aménagements à prévoir sur leur propriété. Les outils de collecte de données ont été le journal réflexif des élèves et le journal de la chercheuse. Dans les résultats, on observe que les élèves représentent leur processus décisionnel de façon variée (textes, schémas, listes, tableaux, dessins et plans) et qu’ils ont recours à divers modes décisionnels : la compilation des avantages semblables, le choix par élimination, la liste de comparaison des avantages et inconvénients, le choix par compatibilité des options, le choix basé sur l’argumentation, celui basé sur la description et le choix par visualisation du résultat anticipé. La volonté d’être entouré d’un environnement esthétiquement agréable et aménagé selon ses préférences personnelles sont les principales sources de motivation des élèves dans leurs choix d’aménagement.Individuals influence the quality of the environment through their roles as citizens, investors, and members of organizations making choices that impact the environment. Yet, decision making regarding the environment, especially among young people, is not well understood. This study sought to describe the spontaneous decision-making process of 10-11 years old students, in the context of a sustainable residential neighborhood. The researchers aimed to understand how the students would spontaneously represent their decision-making process and the reasons that motivated their choices. Through their participation in a global simulation, the students were given fictitious identity, representing the future citizens of the residential neighborhood, and had to make decisions concerning the landscaping of their properties. The students’ reflexive journals and the researcher’s journal were the tools used to collect the data. In our results, we observed that the students used a variety of representations of their decision process (texts, schemata, lists, tables, drawings and plans) and a variety of decision modes : the compilation of similar advantages, the choice by elimination, the list of comparison of advantages and disadvantages, the choice based on compatibility of the options, the choice based on argumentation, the choice base on description, and the choice by visualization of the anticipated result. The students’ will of being surrounded by an environment that is visually pleasant and corresponds to their personal preferences are the main motivations behind their choices

Type I interferons induced by endogenous or exogenous viral infections promote metastasis and relapse of leishmaniasis.

The presence of the endogenous <i>Leishmania</i> RNA virus 1 (LRV1) replicating stably within some parasite species has been associated with the development of more severe forms of leishmaniasis and relapses after drug treatment in humans. Here, we show that the disease-exacerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and signaling in vivo. Moreover, infecting mice with the LRV1-cured <i>Leishmania guyanensis</i> ( <i>LgyLRV1</i> <sup> <i>-</i> </sup> ) strain of parasites followed by type I IFN treatment increased lesion size and parasite burden, quantitatively reproducing the LRV1-bearing ( <i>LgyLRV1</i> <sup> <i>+</i> </sup> ) infection phenotype. This finding suggested the possibility that exogenous viral infections could likewise increase pathogenicity, which was tested by coinfecting mice with <i>L. guyanensis</i> and lymphocytic choriomeningitis virus (LCMV), or the sand fly-transmitted arbovirus Toscana virus (TOSV). The type I IFN antiviral response increased the pathology of <i>L. guyanensis</i> infection, accompanied by down-regulation of the IFN-γ receptor normally required for antileishmanial control. Further, LCMV coinfection of IFN-γ-deficient mice promoted parasite dissemination to secondary sites, reproducing the <i>LgyLRV1</i> <sup> <i>+</i> </sup> metastatic phenotype. Remarkably, LCMV coinfection of mice that had healed from <i>L. guyanensis</i> infection induced reactivation of disease pathology, overriding the protective adaptive immune response. Our findings establish that type I IFN-dependent responses, arising from endogenous viral elements (dsRNA/LRV1), or exogenous coinfection with IFN-inducing viruses, are able to synergize with New World <i>Leishmania</i> parasites in both primary and relapse infections. Thus, viral infections likely represent a significant risk factor along with parasite and host factors, thereby contributing to the pathological spectrum of human leishmaniasis

Impacts of studying in a regional medical campus on practice location

Background: New Brunswick, a bilingual Canadian province without a medical school, negotiated an agreement in 1967 in which places were reserved for francophone medical students in the province of Quebec. In 2006, the Centre de Formation Médicale du Nouveau-Brunswick (CFMNB), a regional medical campus (RMC) of Université de Sherbrooke for its provincial francophone medical students, was established to increase the likelihood of graduates setting up practice in the region. Practice locations of the initial 5 cohorts of CFMNB were analysed to compare data with francophone students trained in Quebec.Methods: Practice locations were determined through Scott’s Medical Database and provincial public registries.  Chi-square and relative risk probability were used to examine the relationship between training location and practice location.Results: Doctors trained at CFMNB were 1.4 times more likely to be practicing in Atlantic Canada compared to those trained at Université de Sherbrooke (main campus) before 2006. Those trained at CFMNB were 1.3 times more likely to go on to practice in the region compared to those trained at Université Laval or Université de Montréal. Conclusion: This study supports the hypothesis that individuals completing a medical program in a Francophone RMC in New Brunswick increases the likelihood of them later practicing in the province or in the wider Atlantic Canada region._______Contexte: Le Nouveau-Brunswick, une province canadienne bilingue ne possédant pas de Faculté de médecine, a négocié en 1967 une entente avec le Québec afin de réserver des places pour ses étudiants francophones souhaitant étudier la médecine.  En 2006, le Centre de formation médicale du Nouveau-Brunswick (CFMNB), un campus médical régional (CMR) de l’Université de Sherbrooke, a été créé afin de permettre aux Néo-Brunswickois d’étudier la médecine en français dans leur province.  L’un des objectifs principaux du CFMNB était d’augmenter les probabilités que les diplômés en médecine s’établissent dans la région.  Les lieux de pratique des médecins issus des 5 premières cohortes du CFMNB ont été analysés afin de les comparer avec ceux des médecins francophones d’origine néo-brunswickoise formés au Québec.Méthodes: Les lieux de pratique ont été déterminés via le répertoire des médecins Scott’s et les registres publics provinciaux.  Des tests de Chi carré et des analyses de risque ont été conduits afin d’étudier la relation entre le lieu de formation et le lieu de pratique.Résultats: Les médecins formés au CFMNB étaient 1.4 fois plus enclins à travailler au Canada atlantique comparativement à ceux formés au campus principal de l’Université de Sherbrooke avant 2006.  Les médecins formés au CFMNB étaient également 1.3 fois plus enclins à travailler dans la région que ceux formés à l’Université Laval ou à l’Université de Montréal.Conclusion: Cette étude supporte l’hypothèse selon laquelle le fait de compléter un programme de médecine francophone dans un CMR francophone au Nouveau-Brunswick augmente les chances de pratiquer au Nouveau-Brunswick ou dans la grande région du Canada atlantique.

NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions.

NLRC5 is a transcriptional regulator of MHC class I (MHCI), which maintains high MHCI expression particularly in T cells. Recent evidence highlights an important NK-T-cell crosstalk, raising the question on whether NLRC5 specifically modulates this interaction. Here we show that NK cells from Nlrc5-deficient mice exhibit moderate alterations in inhibitory receptor expression and responsiveness. Interestingly, NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation. Using T-cell-specific Nlrc5-deficient mice, we show that NK cells surprisingly break tolerance even towards 'self' Nlrc5-deficient T cells under inflammatory conditions. Furthermore, during chronic LCMV infection, the total CD8(+) T-cell population is severely decreased in these mice, a phenotype reverted by NK-cell depletion. These findings strongly suggest that endogenous T cells with low MHCI expression become NK-cell targets, having thus important implications for T-cell responses in naturally or therapeutically induced inflammatory conditions

Anabolism-Associated Mitochondrial Stasis Driving Lymphocyte Differentiation over Self-Renewal

Regeneration requires related cells to diverge in fate. We show that activated lymphocytes yield sibling cells with unequal elimination of aged mitochondria. Disparate mitochondrial clearance impacts cell fate and reflects larger constellations of opposing metabolic states. Differentiation driven by an anabolic constellation of PI3K/mTOR activation, aerobic glycolysis, inhibited autophagy, mitochondrial stasis, and ROS production is balanced with self-renewal maintained by a catabolic constellation of AMPK activation, mitochondrial elimination, oxidative metabolism, and maintenance of FoxO1 activity. Perturbations up and down the metabolic pathways shift the balance of nutritive constellations and cell fate owing to self-reinforcement and reciprocal inhibition between anabolism and catabolism. Cell fate and metabolic state are linked by transcriptional regulators, such as IRF4 and FoxO1, with dual roles in lineage and metabolic choice. Instructing some cells to utilize nutrients for anabolism and differentiation while other cells catabolically self-digest and self-renew may enable growth and repair in metazoa

Exacerbated Leishmaniasis Caused by a Viral Endosymbiont can be Prevented by Immunization with Its Viral Capsid.

Recent studies have shown that a cytoplasmic virus called Leishmaniavirus (LRV) is present in some Leishmania species and acts as a potent innate immunogen, aggravating lesional inflammation and development in mice. In humans, the presence of LRV in Leishmania guyanensis and in L. braziliensis was significantly correlated with poor treatment response and symptomatic relapse. So far, no clinical effort has used LRV for prophylactic purposes. In this context, we designed an original vaccine strategy that targeted LRV nested in Leishmania parasites to prevent virus-related complications. To this end, C57BL/6 mice were immunized with a recombinant LRV1 Leishmania guyanensis viral capsid polypeptide formulated with a T helper 1-polarizing adjuvant. LRV1-vaccinated mice had significant reduction in lesion size and parasite load when subsequently challenged with LRV1+ Leishmania guyanensis parasites. The protection conferred by this immunization could be reproduced in naïve mice via T-cell transfer from vaccinated mice but not by serum transfer. The induction of LRV1 specific T cells secreting IFN-γ was confirmed in vaccinated mice and provided strong evidence that LRV1-specific protection arose via a cell mediated immune response against the LRV1 capsid. Our studies suggest that immunization with LRV1 capsid could be of a preventive benefit in mitigating the elevated pathology associated with LRV1 bearing Leishmania infections and possibly avoiding symptomatic relapses after an initial treatment. This novel anti-endosymbiotic vaccine strategy could be exploited to control other infectious diseases, as similar viral infections are largely prevalent across pathogenic pathogens and could consequently open new vaccine opportunities

Cocaine Intoxication and Thyroid Storm: Similarity in Presentation and Implications for Treatment

Introduction: Cocaine, a widely used sympathomimetic drug, causes thermoregulatory and cardiac manifestations that can mimic a life-threatening thyroid storm. Case: A man presented to the emergency department requesting only cocaine detoxification. He reported symptoms over the last few years including weight loss and diarrhea, which he attributed to ongoing cocaine use. On presentation he had an elevated temperature of 39.4°C and a HR up to 130 beats per minute. Examination revealed the presence of an enlarged, non-tender goiter with bilateral continuous bruits. He was found to have thyrotoxicosis by labs and was treated for a thyroid storm and cocaine intoxication concurrently. The patient was ultimately diagnosed with Graves disease and treated with Iodine-131 therapy. Conclusion: Cocaine use should be considered a possible trigger for thyroid storm. Recognition of thyroid storm is critical because of the necessity for targeted therapy and the significant mortality associated with the condition when untreated.\u2

Review of methods for measuring β-cell function: Design considerations from the Restoring Insulin Secretion (RISE) Consortium

The Restoring Insulin Secretion (RISE) study was initiated to evaluate interventions to slow or reverse the progression of β-cell failure in type 2 diabetes (T2D). To design the RISE study, we undertook an evaluation of methods for measurement of β-cell function and changes in β-cell function in response to interventions. In the present paper, we review approaches for measurement of β-cell function, focusing on methodologic and feasibility considerations. Methodologic considerations included: (1) the utility of each technique for evaluating key aspects of β-cell function (first- and second-phase insulin secretion, maximum insulin secretion, glucose sensitivity, incretin effects) and (2) tactics for incorporating a measurement of insulin sensitivity in order to adjust insulin secretion measures for insulin sensitivity appropriately. Of particular concern were the capacity to measure β-cell function accurately in those with poor function, as is seen in established T2D, and the capacity of each method for demonstrating treatment-induced changes in β-cell function. Feasibility considerations included: staff burden, including time and required methodological expertise; participant burden, including time and number of study visits; and ease of standardizing methods across a multicentre consortium. After this evaluation, we selected a 2-day measurement procedure, combining a 3-hour 75-g oral glucose tolerance test and a 2-stage hyperglycaemic clamp procedure, augmented with arginine

The Transcription Factor Tcf1 Contributes to Normal NK Cell Development and Function by Limiting the Expression of Granzymes.

The transcription factor Tcf1 is essential for the development of natural killer (NK) cells. However, its precise role has not been clarified. Our combined analysis of Tcf1-deficient and transgenic mice indicated that Tcf1 guides NK cells through three stages of development. Tcf1 expression directed bone marrow progenitors toward the NK cell lineage and ensured the survival of NK-committed cells, and its downregulation was needed for terminal maturation. Impaired survival of NK-committed cells was due to excessive expression of granzyme B (GzmB) and other granzyme family members, which induced NK cell self-destruction during maturation and following activation with cytokines or target cells. Mechanistically, Tcf1 binding reduced the activity of a Gzmb-associated regulatory element, and this accounted for the reduced Gzmb expression in Tcf1-expressing NK cells. These data identify an unexpected requirement to limit the expression of cytotoxic effector molecules for the normal expansion and function of NK cells