Les représentations de la pluriethnicité québécoise dans le Mouvement Desjardins: analyse du contenu de la Revue Desjardins de 1998 à 2005

Le Mouvement Desjardins, institution phare du Québec moderne caractérisé par un nationalisme civique et une intégration accrue des immigrants à la majorité francophone, demeure encore aujourd'hui, fortement identifié à ce même groupe. Ce mémoire a pour objet les représentations sociales de la pluriethnicité québécoise chez Desjardins. Une analyse du contenu de la Revue Desjardins de 1998 à 2005 permet de saisir le discours ainsi qu'un point de rupture spatio-temporel établi à l'année 2003, année où l'espace du discours s'élargit pour y inclure l'ouest de l'île de Montréal majoritairement anglophone. D'abord axée sur l'intégration au Mouvement et à la société québécoise dans le souci d'une plus grande représentativité de la population, l'institution passe à une orientation davantage pluraliste favorisant son adaptation à des marchés potentiellement lucratifs. Les catégories linguistiques «anglophone» et «allophone» sont alors davantage utilisées pour aborder l'enjeu pluriethnique banalisant ainsi la spécificité des groupes ethniques qui les composent. Alors que la première période est surtout caractérisée par des perceptions et des orientations générales, l'ouverture en 2003 d'un centre de service destiné à la clientèle allophone et anglophone de l'ouest de l'île constitue l'aboutissement d'un processus de représentation sociale ayant pour fonction l'orientation des pratiques. L'ensemble du discours est nuancé par des obstacles à l'adaptation à la pluriethnicité ainsi que des lacunes internes à l'institution. La concept d'ethnicité est peu utilisé et souvent abordé sous le terme «communauté culturelle» qui peut englober des communautés de nature autre qu'ethnique et qui réduit l'ethnicité à sa seule dimension culturelle. Il omet également de considérer les membres d'un groupe ethnique qui ne s'identifient pas à la communauté. En conclusion, l'étude permet de confirmer l'existence d'un discours sur la pluriethnicité québécoise maintenant bien ancré chez Desjardins et davantage orienté vers l'adaptation de l'institution en offrant des services en anglais et dans d'autres langues.The Desjardins Group is an influential institution in modern Québec characterized by civic nationalism and sustained integration of immigrants into the French-speaking majority. Even today, Desjardins continues to identify strongly with this French-speaking majority. The purpose of this thesis is to explore the social precepts of multi-ethnicity in Québec at Desjardins. An analysis of the contents of the “Revue Desjardins” magazine from 1998 to 2005 allowed the author to understand the Desjardins position and determine a spatiotemporal rupture point in 2003, the year in which Desjardins’ position expanded to include the mostly English-speaking population of western Montreal Island. At the outset, Desjardins focused on integration into the Group and Quebec society, with an underling concern for greater institutional representation among the population. Thereafter, Desjardins adopted a more all-inclusive approach favouring adaptation to potentially lucrative markets. The linguistic categories of “Anglophone” and “allophone” were first used to tone down the specificity of ethnic groups involved. While the initial period was characterized primarily by perceptions and general policy, the inauguration in 2003 of a service centre for the allophone and Anglophone clientele of western Montreal Island was the culmination of a process of social sensitivity to establish policy guidelines. The entire approach was nuanced with obstacles to adaptation to multi-ethnicity, as well as internal institutional shortcomings. The concept of ethnicity was used sparingly, often blanketed by the term “cultural community.” This term embraces communities other than ethnic groups and reduces ethnicity to the simple expression of cultural dimension. The term also avoids pinpointing members of an ethnic group who do not identify with the community. In conclusion, the study confirmed the existence of a position on multi-ethnicity in Québec now solidly anchored within Desjardins and more clearly directed at the institution’s adjustment to offering services in English and other languages

Évaluation des impacts énergétiques et environnementaux de différents modes d'agriculture urbaine en environnement contrôlé

La densification des villes, l’augmentation de la demande de production agricole, l’accessibilité alimentaire, la participation citoyenne, la promotion de l’économie locale, la réduction du transport ou la réduction de l’empreinte environnementale sont d’autant de raisons qui expliquent l’intérêt grimpant pour l’agriculture urbaine. Dans un climat québécois, les productions soutenues sur toute l’année doivent se faire dans des espaces contrôlés. Plusieurs types d’espaces d’agriculture contrôlée peuvent s’intégrer en ville : serres traditionnelles, serres sur toit ou encore des espaces d’agriculture intégrée au bâtiment (eAIB) comme des cultures hydroponiques empilées verticalement. Toutefois, les impacts potentiels de ces types de production peuvent être très différents et sont actuellement peu connus. Également, peu de données sont disponibles pour l’analyse de ces types de production. Dans une optique de réduction de l’empreinte environnementale de la production agricole, il importe de quantifier les impacts potentiels de ces nouveaux types de production. L’objectif principal de ce mémoire est de quantifier les impacts environnementaux potentiels de différents types de production agricole en environnement contrôlé pouvant s’intégrer en ville dans un contexte énergétique québécois. Pour ce faire, quatre scénarios sont comparés en utilisant la méthode d’analyse environnementale du cycle de vie (ACV) : (1) une serre traditionnelle sur sol, (2) une serre sur toit, (3) un eAIB avec éclairage naturel et artificiel, (4) un eAIB avec éclairage artificiel uniquement, qui sont soit chauffées au gaz dans le cas des serres ou climatisés avec des systèmes électriques pour les eAIB. Comme il existe très peu de données disponibles sur les consommations énergétiques de tels scénarios, des modèles énergétiques sont montés pour chaque scénario à l’aide d’outils de simulation de la performance de bâtiment (SPB). Une calibration d’un premier modèle (serre sur sol) est également effectuée afin de renforcer la confiance dans les estimations des gains thermiques des plantes et des consommations énergétiques associées au maintien des conditions de culture (température et humidité). Le modèle calibré a permis d’évaluer certaines mesures de conservation de l’énergie. Parmi les mesures analysées, les économies d’énergie varient entre 5% et 30% et la mesure avec la période de retour sur investissement la plus rapide est l’isolation du mur nord (entre 9 et 16 ans à 3,36 $/GJ). En ce qui a trait aux résultats de l’ACV, ils tendent à démontrer qu’aucun scénario ne performe mieux dans toutes les catégories d’impacts environnementaux. Les scénarios de la serre sur toit et de l’eAIB avec éclairage naturel obtiennent de meilleurs scores de façon générale pour l’ensemble des catégories. Le score du réchauffement climatique potentiel varie entre 0.62 et 2.79 kg CO2 eq. L’analyse de sensibilité effectuée tend à démontrer que les types d’éclairage et le transport n’affectent pas les tendances générales des résultats, mais que les sources d’énergie de chauffage peuvent grandement influencer les résultats. Au Québec, la priorité devrait être donnée à l’utilisation d’énergies renouvelables (maximisation de l’éclairage naturel, utilisation d’électricité pour le chauffage, etc.) pour réduire l’empreinte environnementale de la production agricole

Suppression of the intrinsic apoptosis pathway by sinaptic activity

Synaptic activity promotes resistance to diverse apoptotic insults, the mechanism behind which is incompletely understood. We show here that a coordinated downregulation of core components of the intrinsic apoptosis pathway by neuronal activity forms a key part of the underlying mechanism. Activity-dependent protection against apoptotic insults is associated with inhibition of cytochrome c release in most but not all neurons, indicative of anti-apoptotic signaling both upstream and downstream of this step. We find that enhanced firing activity suppresses expression of the proapoptotic BH3-only member gene Puma in a NMDA receptor-dependent, p53-independent manner. Puma expression is sufficient to induce cytochrome c loss and neuronal apoptosis. Puma deficiency protects neurons against apoptosis and also occludes the protective effect of synaptic activity, while blockade of physiological NMDA receptor activity in the developing mouse brain induces neuronal apoptosis that is preceded by upregulation of Puma. However, enhanced activity can also confer resistance to Puma-induced apoptosis, acting downstream of cytochrome c release. This mechanism is mediated by transcriptional suppression of apoptosome components Apaf-1 and procaspase-9, and limiting caspase-9 activity, since overexpression of procaspase-9 accelerates the rate of apoptosis in active neurons back to control levels. Synaptic activity does not exert further significant anti-apoptotic effects downstream of caspase-9 activation, since an inducible form of caspase-9 overrides the protective effect of synaptic activity, despite activity-induced transcriptional suppression of caspase-3. Thus, suppression of apoptotic gene expression may synergize with other activity-dependent events such as enhancement of antioxidant defenses to promote neuronal survival

Synaptic NMDA receptor activity boosts intrinsic antioxidant defenses

Intrinsic antioxidant defenses are important for neuronal longevity. We found that in rat neurons, synaptic activity, acting via NMDA receptor (NMDAR) signaling, boosted antioxidant defenses by making changes to the thioredoxin-peroxiredoxin (Prx) system. Synaptic activity enhanced thioredoxin activity, facilitated the reduction of overoxidized Prxs and promoted resistance to oxidative stress. Resistance was mediated by coordinated transcriptional changes; synaptic NMDAR activity inactivated a previously unknown Forkhead box O target gene, the thioredoxin inhibitor Txnip. Conversely, NMDAR blockade upregulated Txnip in vivo and in vitro, where it bound thioredoxin and promoted vulnerability to oxidative damage. Synaptic activity also upregulated the Prx reactivating genes Sesn2 (sestrin 2) and Srxn1 (sulfiredoxin), via C/EBPβ and AP-1, respectively. Mimicking these expression changes was sufficient to strengthen antioxidant defenses. Trans-synaptic stimulation of synaptic NMDARs was crucial for boosting antioxidant defenses; chronic bath activation of all (synaptic and extrasynaptic) NMDARs induced no antioxidative effects. Thus, synaptic NMDAR activity may influence the progression of pathological processes associated with oxidative damage

Neuronal Activity Controls the Antagonistic Balance Between Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α and Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptors in Regulating Antioxidant Defenses

Transcriptional coactivators and corepressors often have multiple targets and can have opposing actions on transcription and downstream physiological events. The coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is under-expressed in Huntington's disease and is a regulator of antioxidant defenses and mitochondrial biogenesis. We show that in primary cortical neurons, expression of PGC-1α strongly promotes resistance to excitotoxic and oxidative stress in a cell autonomous manner, whereas knockdown increases sensitivity. In contrast, the transcriptional corepressor silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) specifically antagonizes PGC-1α-mediated antioxidant effects. The antagonistic balance between PGC-1α and SMRT is upset in favor of PGC-1α by synaptic activity. Synaptic activity triggers nuclear export of SMRT reliant on multiple regions of the protein. Concommitantly, synaptic activity post-translationally enhances the transactivating potential of PGC-1α in a p38-dependent manner, as well as upregulating cyclic-AMP response element binding protein-dependent PGC-1α transcription. Activity-dependent targeting of PGC-1α results in enhanced gene expression mediated by the thyroid hormone receptor, a prototypical transcription factor coactivated by PGC-1α and repressed by SMRT. As a consequence of these events, SMRT is unable to antagonize PGC-1α-mediated resistance to oxidative stress in synaptically active neurons. Thus, PGC-1α and SMRT are antagonistic regulators of neuronal vulnerability to oxidative stress. Further, this coactivator–corepressor antagonism is regulated by the activity status of the cell, with implications for neuronal viability. Antioxid. Redox Signal. 14, 1425–1436

Neuronal activity controls the antagonistic between PGC-1α and SMRT in regulating antioxidant defences

Transcriptional coactivators and corepressors often have multiple targets and can have opposing actions on transcription and downstream physiological events. The coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is under-expressed in Huntington's disease and is a regulator of antioxidant defenses and mitochondrial biogenesis. We show that in primary cortical neurons, expression of PGC-1α strongly promotes resistance to excitotoxic and oxidative stress in a cell autonomous manner, whereas knockdown increases sensitivity. In contrast, the transcriptional corepressor silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) specifically antagonizes PGC-1α-mediated antioxidant effects. The antagonistic balance between PGC-1α and SMRT is upset in favor of PGC-1α by synaptic activity. Synaptic activity triggers nuclear export of SMRT reliant on multiple regions of the protein. Concommitantly, synaptic activity post-translationally enhances the transactivating potential of PGC-1α in a p38-dependent manner, as well as upregulating cyclic-AMP response element binding protein-dependent PGC-1α transcription. Activity-dependent targeting of PGC-1α results in enhanced gene expression mediated by the thyroid hormone receptor, a prototypical transcription factor coactivated by PGC-1α and repressed by SMRT. As a consequence of these events, SMRT is unable to antagonize PGC-1α-mediated resistance to oxidative stress in synaptically active neurons. Thus, PGC-1α and SMRT are antagonistic regulators of neuronal vulnerability to oxidative stress. Further, this coactivatorcorepressor antagonism is regulated by the activity status of the cell, with implications for neuronal viability

Suppression of the intrinsic apoptosis pathway by sinaptic activity

Synaptic activity promotes resistance to diverse apoptotic insults, the mechanism behind which is incompletely understood. We show here that a coordinated downregulation of core components of the intrinsic apoptosis pathway by neuronal activity forms a key part of the underlying mechanism. Activity-dependent protection against apoptotic insults is associated with inhibition of cytochrome c release in most but not all neurons, indicative of anti-apoptotic signaling both upstream and downstream of this step. We find that enhanced firing activity suppresses expression of the proapoptotic BH3-only member gene Puma in a NMDA receptor-dependent, p53-independent manner. Puma expression is sufficient to induce cytochrome c loss and neuronal apoptosis. Puma deficiency protects neurons against apoptosis and also occludes the protective effect of synaptic activity, while blockade of physiological NMDA receptor activity in the developing mouse brain induces neuronal apoptosis that is preceded by upregulation of Puma. However, enhanced activity can also confer resistance to Puma-induced apoptosis, acting downstream of cytochrome c release. This mechanism is mediated by transcriptional suppression of apoptosome components Apaf-1 and procaspase-9, and limiting caspase-9 activity, since overexpression of procaspase-9 accelerates the rate of apoptosis in active neurons back to control levels. Synaptic activity does not exert further significant anti-apoptotic effects downstream of caspase-9 activation, since an inducible form of caspase-9 overrides the protective effect of synaptic activity, despite activity-induced transcriptional suppression of caspase-3. Thus, suppression of apoptotic gene expression may synergize with other activity-dependent events such as enhancement of antioxidant defenses to promote neuronal survival

Multiple dating approach (14C, 230Th/U and 36Cl) of tsunami-transported reef-top boulders on Bonaire (Leeward Antilles) – Current achievements and challenges

Dating the transport/deposition time of supratidal coarse-clast deposits is difficult, limiting their value for inferring frequency-magnitude patterns of high-energy wave events. On Bonaire (Leeward Antilles, Caribbean), these deposits form prominent landforms, and transport by one or several Holocene tsunamis is assumed at least for the largest clasts. Although a large dataset of 14C and electron spin resonance (ESR) ages is available for major coral rubble ridges and ramparts, it is still debated whether these data reflect the timing of major events, and how these datasets are biased by the reworking of coral fragments. As an attempt to overcome the current challenges for dating the dislocation of singular boulders, three distinct dating methods are implemented and compared: (i) 14C dating of boring bivalves attached to the boulders; (ii) 230Th/U dating of post-depositional, secondary calcite flowstone and subaerial microbialites at the underside of the boulders; and (iii) surface exposure dating of overturned boulders via 36Cl concentration measurements in corals. Approaches (ii) and (iii) have never been applied to coastal boulder deposits so far. The three 14C age estimates are older than 40 ka, i.e. most probably beyond the applicability of the method, which is attributed to post-depositional diagenetic processes, shedding doubt on the usefulness of this method in the local context. The remarkably convergent 230Th/U ages, all pointing to the Late Holocene period (1.0–1.6 ka), are minimum ages for the transport event(s). The microbialite sample yields an age of 1.23 ± 0.23 ka and both flowstone samples are in stratigraphic order: the older (onset of carbonate precipitation) and younger flowstone layers yield ages of 1.59 ± 0.03 and 1.23 ± 0.03 ka, respectively. Four coral samples collected from the topside of overturned boulders yielded similar 36Cl concentration measurements. However, the computed ages are affected by large uncertainties, mostly due to the high natural chlorine concentration. After correction for the inherited component and chemical denudation since platform emergence (inducing additional uncertainty), the calculated 36Cl ages cluster between 2.5 ± 1.3 and 3.0 ± 1.4 ka for three of four boulders whilst the fourth one yields an age of 6.1 ± 1.8 ka, probably related to a higher inheritance. These 230Th/U and 36Cl age estimates are coherent with a suggested tsunami age of < 3.3 ka obtained from the investigation of allochthonous shell horizons in sediment cores of northwestern Bonaire. Whilst 230Th/U dating of post-depositional calcite flowstone appears to be the most robust and/or accurate approach, these results illustrate the potential and current limitations of the applied methods for dating the dislocation of supralittoral boulders in carbonate-reef settings