179 research outputs found

    Adrift: Attribution & Responsibility in a Changing Climate

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    What if we could witness our own contribution to the warming climate? And how do we know if we’re seeing the "fingerprints" of anthropogenic global warming on an event? Climate change event attribution is a relatively new field of enquiry. Borrowing a formula from climate scientists Notz & Stroeve, visual artist and PhD student Adam SĂ©bire describes how he was able to calculate and saw off exactly the amount of Greenlandic sea-ice that would be destroyed by his carbon emissions flying economy return from Sydney to document it. The multiscreen video artwork created, AnthropoScene IV: Adrift (∆Asea-ice) (2019) touches upon the disconnects that underly our psychological response to climate change

    La gestion des espĂšces vĂ©gĂ©tales exotiques envahissantes prioritaires dans les municipalitĂ©s de l’Estrie

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    L’objectif de cet essai est de dĂ©terminer quelles mĂ©thodes de lutte devraient ĂȘtre privilĂ©giĂ©es par les municipalitĂ©s de l’Estrie pour contrer les espĂšces vĂ©gĂ©tales exotiques envahissantes prioritaires. L’accroissement du commerce international a permis l’introduction de ces plantes au Canada, tandis que leur propagation locale est assurĂ©e par le rĂ©seau routier et les activitĂ©s rĂ©crĂ©otouristiques. Les espĂšces vĂ©gĂ©tales exotiques envahissantes sont dĂ©sormais trĂšs prĂ©sentes en Estrie et engendrent d’importants dommages tels que les pertes de biodiversitĂ©, de rendements agricoles, de valeurs des propriĂ©tĂ©s et d’attraits rĂ©crĂ©otouristiques. Le manque de ressources et de prise de conscience de la gravitĂ© de cette problĂ©matique par les municipalitĂ©s de l’Estrie est Ă  l’origine de l’élaboration de ce document. L’analyse de l’abondance et des impacts des espĂšces vĂ©gĂ©tales exotiques envahissantes de l’Estrie dĂ©montre que le roseau commun (Phragmites australis), la renouĂ©e du Japon (Fallopia japonica), le nerprun bourdaine (Frangula alnus) et le myriophylle Ă  Ă©pis (Myriopyllum spicatum) constituent les quatre espĂšces prioritaires. Par ailleurs, les rĂ©sultats indiquent que les mĂ©thodes prĂ©ventives de lutte Ă  privilĂ©gier sont l’ensemencement des sols mis Ă  nu, l’inspection visuelle des embarcations, la sensibilisation et une gestion appropriĂ©e de l’entretien des emprises routiĂšres. Concernant les mĂ©thodes de contrĂŽle et d’éradication, la couverture vĂ©gĂ©tale et l’ombrage obtiennent la meilleure note, suivies par l’application d’herbicide par contact et enfin, Ă  Ă©galitĂ©, le fauchage, l’arrachage et la toile de jute immergĂ©e. La mise en place de toutes les mĂ©thodes prĂ©ventives mentionnĂ©es ci-dessus est fortement recommandĂ©e aux municipalitĂ©s, contrairement aux postes de lavage. Le contrĂŽle des jeunes colonies d’espĂšces vĂ©gĂ©tales exotiques envahissantes doit privilĂ©gier la couverture vĂ©gĂ©tale et l’ombrage, ainsi que l’arrachage en milieu terrestre et la toile de jute en milieu aquatique. Le fauchage permet de contrĂŽler de vastes colonies terrestres bien Ă©tablies, alors que l’herbicide doit ĂȘtre utilisĂ© en dernier recours pour une Ă©radication rapide en milieu terrestre. Enfin, un suivi des mĂ©thodes mises en place est nĂ©cessaire

    Developmental regulation of the neuroinflammatory responses to LPS and/or hypoxia-ischemia between preterm and term neonates: An experimental study

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    <p>Abstract</p> <p>Background</p> <p>Preterm and term newborns are at high risk of brain damage as well as subsequent cerebral palsy and learning disabilities. Indeed, hypoxia-ischemia (HI), pathogen exposures, and associated intracerebral increase of pro-inflammatory cytokines have all been linked to perinatal brain damage. However, the developmental effects of potential variations of pro- and anti-inflammatory cytokine ratios remain unknown.</p> <p>Methods</p> <p>Using rat models of perinatal brain damage induced by exposures to lipopolysaccharide (LPS) and/or HI at distinct levels of maturity, we compared cytokine expression at stages of cerebral development equivalent to either preterm (postnatal day 1, P1) or term (P12) newborns.</p> <p>Results</p> <p>At P1, expression of anti-inflammatory cytokine within the brain was either not modulated (IL-6, IL-10) or down-regulated (IL-1ra, TGF-ÎČ1) by HI, LPS or LPS+HI. In contrast, there was at P12 an up-regulation of all anti-inflammatory cytokines studied in HI or LPS+HI condition, but not after LPS exposure. Interestingly, IL-1ÎČ was the main pro-inflammatory cytokine up-regulated moderately at P1, and strongly at P12, with a weak co-expression of TNF-α observed mainly at P12. These age-dependant inflammatory reactions were also accompanied, under HI and LPS+HI conditions, at P12 only, by combined: (i) expression of chemokines CINC-1 and MCP-1, (ii) blood-brain barrier (BBB) leakage, and (iii) intracerebral recruitment of systemic immune cells such as neutrophils. In contrast, sole LPS induced IL-1ÎČ responses mainly within white matter at P1 and mainly within gray matter at P12, that were only associated with early MCP-1 (but no CINC-1) induction at both ages, without any recruitment of neutrophils and CD68+ cells.</p> <p>Conclusion</p> <p>HI and LPS+HI induce pro-inflammatory oriented immune responses in both preterm and term like brains, with a maximal inflammatory response triggered by the combination of LPS+HI. The profile of these neuroinflammatory responses presented striking variations according to age: no or down-regulated anti-inflammatory responses associated with mainly IL-1ÎČ release in preterm-like brains (P1), in sharp contrast to term-like brains (P12) presenting stronger anti-and pro-inflammatory responses, including both IL-1ÎČ and TNF-α releases, and BBB leakage. These developmental-dependant variations of neuroinflammatory response could contribute to the differential pattern of brain lesions observed across gestational ages in humans. This also highlights the necessity to take into consideration the maturation stage, of both brain and immune systems, in order to develop new anti-inflammatory neuroprotective strategies.</p

    Impact of ACK/NACK Signalling Errors on High Speed Uplink Packet Access (HSUPA)

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    Abstract -In this paper, the impact of signalling errors on the performance of High Speed Uplink Packet Access (HSUPA) in soft handover (SHO) is investigated. The signalling discussed here is the one related to HARQ operation: acknowledgements (ACK) and negative acknowledgements (NACK) in the downlink. Through simulations, it is shown how ACK/NACK signalling errors affect the throughput in both soft handover and non-soft handover cases

    HANDLING MULTILINGUAL CONTENT IN DIGITAL MEDIA: A CRITICAL ANALYSIS

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    This document expresses and analyzes the need to define a generic method for representing multilingual information in multimedia data. It describes the basic requirements that would bear upon such representations and establishes the potential link with ISO committee TC 37/SC 4 (Language Resource Management) and with XMT (eXtended MPEG-4 Textual format)

    Trazodone regulates neurotrophic/growth factors, mitogen-activated protein kinases and lactate release in human primary astrocytes

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    Background: In the central nervous system, glial cells provide metabolic and trophic support to neurons and respond to protracted stress and insults by up-regulating inflammatory processes. Reactive astrocytes and microglia are associated with the pathophysiology of neuronal injury, neurodegenerative diseases and major depression, in both animal models and human brains. Several studies have reported clear anti-inflammatory effects of anti-depressant treatment on astrocytes, especially in models of neurological disorders. Trazodone (TDZ) is a triazolopyridine derivative that is structurally unrelated to other major classes of antidepressants. Although the molecular mechanisms of TDZ in neurons have been investigated, it is unclear whether astrocytes are also a TDZ target. Methods: The effects of TDZ on human astrocytes were investigated in physiological conditions and following inflammatory insult with lipopolysaccharide (LPS) and tumour necrosis factor-aα (TNF-aα). Astrocytes were assessed for their responses to pro-inflammatory mediators and cytokines, and the receptors and signalling pathways involved in TDZ-mediated effects were evaluated. Results: TDZ had no effect on cell proliferation, but it decreased pro-inflammatory mediator release and modulated trophic and transcription factor mRNA expression. Following TDZ treatment, the AKT pathway was activated, whereas extracellular signal-regulated kinase and c-Jun NH2-terminal kinase were inhibited. Most importantly, a 72-h TDZ pre-treatment before inflammatory insult completely reversed the anti-proliferative effects induced by LPS-TNF-aα. The expression or the activity of inflammatory mediators, including interleukin-6, c-Jun NH2-terminal kinase and nuclear factor ΚB, were also reduced. Furthermore, TDZ affected astrocyte metabolic support to neurons by counteracting the inflammation-mediated lactate decrease. Finally, TDZ protected neuronal-like cells against neurotoxicity mediated by activated astrocytes. These effects mainly involved an activation of 5-HT1A and an antagonism at 5-HT2A/C serotonin receptors. Fluoxetine, used in parallel, showed similar final effects nevertheless it activates different receptors/intracellular pathways. Conclusions: Altogether, our results demonstrated that TDZ directly acts on astrocytes by regulating intracellular signalling pathways and increasing specific astrocyte-derived neurotrophic factor expression and lactate release. TDZ may contribute to neuronal support by normalizing trophic and metabolic support during neuroinflammation, which is associated with neurological diseases, including major depression
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