192 research outputs found
Modélisation de la durabilité des PRFB et PRFV en béton humide basée sur la dégradation fibre/matrice
LâĂ©tude de la durabilitĂ© des polymĂšres renforcĂ©s de fibres (PRF) dans le bĂ©ton est un enjeu majeur de leur dĂ©veloppement en tant quâalternative aux armatures dâacier soumises Ă la corrosion. La simulation Ă long terme de la solution interstitielle est le plus souvent assurĂ©e par lâimmersion des barres de composite dans des solution acides ou basiques, dans lesquelles la tempĂ©rature agit comme accĂ©lĂ©rateur. La littĂ©rature propose principalement des analyses physiques et mĂ©caniques des PRF dans leur globalitĂ©, sans forcĂ©ment concentrer lâĂ©tude sur chaque composant. Câest donc lâobjectif de cette Ă©tude de vouloir suivre lâimpact des solutions corrosives sur un large panel de matĂ©riaux, Ă la fois sur les rĂ©sines pures, les fibres, et les composites qui en dĂ©coulent.
Pour cela, des matĂ©riaux couramment utilisĂ©s en gĂ©nie civil ont Ă©tĂ© choisis : deux types de fibres synthĂ©tiques (verre et basalte) avec diffĂ©rents agents dâensimage, trois types de rĂ©sines thermodurcissables (polyurĂ©thane, Ă©poxy et vinylester), et donc six types de composites (3 PRFV et 3 PRFB) fabriquĂ©s par pultrusion. Les Ă©chantillons ont Ă©tĂ© conditionnĂ©s de façon accĂ©lĂ©rĂ©e Ă 24°C, 40°C et 65°C dans lâeau et en solution alcaline jusquâĂ 10 jours pour les fibres, et entre 2 et 3 mois pour les rĂ©sines et composites. Des tests physiques et mĂ©caniques ont Ă©tĂ© menĂ©s, tels quâun suivi de lâabsorption dâeau, des mesures de la tempĂ©rature de transition vitreuse par DSC, des analyses thermiques et infrarouges et des observations microscopiques.
Contrairement Ă la solution acide, la solution alcaline attaque la fibre de basalte par piquration de façon hĂ©tĂ©rogĂšne, et aucune espĂšce chimique nâest dissoute. La durabilitĂ© des fibres dans lâalkali dĂ©pend de lâagent dâensimage, une mĂȘme fibre nâayant pas le mĂȘme comportement en traction ni en microscopie selon son traitement de surface.
Lâeau provoque dans la rĂ©sine un rĂ©arrangement molĂ©culaire visible par DSC, qui ressemble Ă une plastification irrĂ©versible mais qui ne peut pas ĂȘtre une hydrolyse selon lâanalyse FTIR. Cela sâexplique par la crĂ©ation de deux phases de rĂ©sine, confirmĂ© dans la littĂ©rature par lâobservation de deux pics de Tg par DMA, et par la thĂ©orie des volumes libres par ATM. La relation de Kelley-Bueche simplifiĂ©e permet de conclure que lâabsorption de solvant, eau ou alkali, est le facteur critique initiant la dĂ©gradation de la rĂ©sine.
Une loi fickienne permet dâapproximer la diffusion dâeau dans le polymĂšre et le composite, ce dernier diffusant plus fortement que la rĂ©sine pure, mĂȘme lorsquâaucun vide ou descellement Ă lâinterface nâest constatĂ©. Une interphase aux propriĂ©tĂ©s modifiĂ©es est en fait crĂ©Ă©e autour de la fibre par lâinteraction de la rĂ©sine avec lâensimage et lâeau. Une analyse par Ă©lĂ©ments finis, ainsi que des rĂ©sultats par AFM et micro-TA de la littĂ©rature permettent dâestimer que cette zone diffuse cinq fois plus que la rĂ©sine pure et mesure entre 1 et 6 micromĂštres selon les matĂ©riaux
Oxytocin-induced antinociception in the spinal cord is mediated by a subpopulation of glutamatergic neurons in lamina I-II which amplify GABAergic inhibition
Fast non-genomic effects of progesterone-derived neurosteroids on nociceptive thresholds and pain symptoms
Abstract Fast Inhibitory controls mediated by glycine (GlyRs) and GABAA receptors (GABAARs) play an important role to prevent the apparition of pathological pain symptoms of allodynia and hyperalgesia. The use of positive allosteric modulators of these receptors, specifically expressed in the spinal cord, may represent an interesting strategy to limit or block pain expression. In this study, we have used stereoisomers of progesterone metabolites, acting only via non-genomic effects, in order to evaluate the contribution of GlyRs and GABAARs for the reduction of mechanical and thermal heat hypernociception. We show that 3a neurosteroids were particularly efficient to elevate nociceptive thresholds in naive animal. It also reduced mechanical allodynia and thermal heat hyperalgesia in the carrageenan model of inflammatory pain. This effect is likely to be mediated by GABAA receptors since 3b isomer was inefficient. More interestingly, 3a5b neurosteroid was only efficient on mechanical allodynia while having no effect on thermal heat hyperalgesia. We characterized these paradoxical effects of 3a5b neurosteroid using the strychnine and bicuculline models of allodynia. We clearly show that 3a5b neurosteroid exerts an antinociceptive effect via a positive allosteric modulation of GABAARs but, at the same time, is pronociceptive by reducing GlyR function. This illustrates the importance of the inhibitory amino acid receptor channels and their allosteric modulators in spinal pain processing. Moreover, our results indicate that neurosteroids, which are synthesized in the dorsal horn of the spinal cord and have limited side effects, may be of significant interest in order to treat pathological pain symptoms.
Antinociceptive action of oxytocin involves inhibition of potassium channel currents in lamina II neurons of the rat spinal cord
<p>Abstract</p> <p>Background</p> <p>Growing evidence in the literature shows that oxytocin (OT) has a strong spinal anti-nociceptive action. Oxytocinergic axons originating from a subpopulation of paraventricular hypothalamic neurons establish synaptic contacts with lamina II interneurons but little is known about the functional role of OT with respect to neuronal firing and excitability.</p> <p>Results</p> <p>Using the patch-clamp technique, we have recorded lamina II interneurons in acute transverse lumbar spinal cord slices of rats (15 to 30 days old) and analyzed the OT effects on action potential firing ability. In the current clamp mode, we found that bath application of a selective OT-receptor agonist (TGOT) reduced firing in the majority of lamina II interneurons exhibiting a bursting firing profile, but never in those exhibiting a single spike discharge upon depolarization. Interestingly, OT-induced reduction in spike frequency and increase of firing threshold were often observed, leading to a conversion of the firing profile from repetitive and delayed profiles into phasic ones and sometimes further into single spike profile. The observed effects following OT-receptor activation were completely abolished when the OT-receptor agonist was co-applied with a selective OT-receptor antagonist. In current and voltage clamp modes, we show that these changes in firing are strongly controlled by voltage-gated potassium currents. More precisely, transient I<sub>A </sub>currents and delayed-rectifier currents were reduced in amplitude and transient I<sub>A </sub>current was predominantly inactivated after OT bath application.</p> <p>Conclusion</p> <p>This effect of OT on the firing profile of lamina II neurons is in good agreement with the antinociceptive and analgesic properties of OT described <it>in vivo</it>.</p
Abnormal nociception and opiate sensitivity of STOP null mice exhibiting elevated levels of the endogenous alkaloid morphine
<p>Abstract</p> <p>Background-</p> <p>Mice deficient for the stable tubule only peptide (STOP) display altered dopaminergic neurotransmission associated with severe behavioural defects including disorganized locomotor activity. Endogenous morphine, which is present in nervous tissues and synthesized from dopamine, may contribute to these behavioral alterations since it is thought to play a role in normal and pathological neurotransmission.</p> <p>Results-</p> <p>In this study, we showed that STOP null brain structures, including cortex, hippocampus, cerebellum and spinal cord, contain high endogenous morphine amounts. The presence of elevated levels of morphine was associated with the presence of a higher density of mu opioid receptor with a higher affinity for morphine in STOP null brains. Interestingly, STOP null mice exhibited significantly lower nociceptive thresholds to thermal and mechanical stimulations. They also had abnormal behavioural responses to the administration of exogenous morphine and naloxone. Low dose of morphine (1 mg/kg, i.p.) produced a significant mechanical antinociception in STOP null mice whereas it has no effect on wild-type mice. High concentration of naloxone (1 mg/kg) was pronociceptive for both mice strain, a lower concentration (0.1 mg/kg) was found to increase the mean mechanical nociceptive threshold only in the case of STOP null mice.</p> <p>Conclusions-</p> <p>Together, our data show that STOP null mice displayed elevated levels of endogenous morphine, as well as an increase of morphine receptor affinity and density in brain. This was correlated with hypernociception and impaired pharmacological sensitivity to mu opioid receptor ligands.</p
Long-lasting spinal oxytocin analgesia is ensured by the stimulation of allopregnanolone synthesis which potentiates GABA(A) receptor-mediated synaptic inhibition.
Hypothalamospinal control of spinal pain processing by oxytocin (OT) has received a lot of attention in recent years because of its potency to reduce pain symptoms in inflammatory and neuropathic conditions. However, cellular and molecular mechanisms underlying OT spinal antinociception are still poorly understood. In this study, we used biochemical, electrophysiological, and behavioral approaches to demonstrate that OT levels are elevated in the spinal cord of rats exhibiting pain symptoms, 24 h after the induction of inflammation with an intraplantar injection of λ-carrageenan. Using a selective OT receptor antagonist, we demonstrate that this elevated OT content is responsible for a tonic analgesia exerted on both mechanical and thermal modalities. This phenomenon appeared to be mediated by an OT receptor-mediated stimulation of neurosteroidogenesis, which leads to an increase in GABA(A) receptor-mediated synaptic inhibition in lamina II spinal cord neurons. We also provide evidence that this novel mechanism of OT-mediated spinal antinociception may be controlled by extracellular signal-related protein kinases, ERK1/2, after OT receptor activation. The oxytocinergic inhibitory control of spinal pain processing is emerging as an interesting target for future therapies since it recruits several molecular mechanisms, which are likely to exert a long-lasting analgesia through nongenomic and possibly genomic effects.journal articleresearch support, non-u.s. gov't2013 Oct 16importe
Pain, Parental Involvement, and Oxytocin in the Neonatal Intensive Care Unit
Preterm infants (PTI) typically experience many painful and stressful procedures or events during their first weeks of life in a neonatal intensive care unit, and these can profoundly impact subsequent brain development and function. Several protective interventions during this sensitive period stimulate the oxytocin system, reduce pain and stress, and improve brain development. This review provides an overview of the environmental risk factors experienced by PTI during hospitalization, with a focus on the effects of pain, and early maternal separation. We also describe the long-term adverse effects of the simultaneous experiences of pain and maternal separation, and the potential beneficial effects of maternal vocalizations, parental contact, and several related processes, which appear to be mediated by the oxytocin system
Pain, Parental Involvement, and Oxytocin in the Neonatal Intensive Care Unit
Preterm infants (PTI) typically experience many painful and stressful procedures or events during their first weeks of life in a neonatal intensive care unit, and these can profoundly impact subsequent brain development and function. Several protective interventions during this sensitive period stimulate the oxytocin system, reduce pain and stress, and improve brain development. This review provides an overview of the environmental risk factors experienced by PTI during hospitalization, with a focus on the effects of pain, and early maternal separation. We also describe the long-term adverse effects of the simultaneous experiences of pain and maternal separation, and the potential beneficial effects of maternal vocalizations, parental contact, and several related processes, which appear to be mediated by the oxytocin system
Generalised Anxiety Disorder â A Twin Study of Genetic Architecture, Genome-Wide Association and Differential Gene Expression
Generalised Anxiety Disorder (GAD) is a common anxiety-related diagnosis, affecting approximately 5% of the adult population. One characteristic of GAD is a high degree of anxiety sensitivity (AS), a personality trait which describes the fear of arousal-related sensations. Here we present a genome-wide association study of AS using a cohort of 730 MZ and DZ female twins. The GWAS showed a significant association for a variant within the RBFOX1 gene. A heritability analysis of the same cohort also confirmed a significant genetic component with h2 of 0.42. Additionally, a subset of the cohort (25 MZ twins discordant for AS) was studied for evidence of differential expression using RNA-seq data. Significant differential expression of two exons with the ITM2B gene within the discordant MZ subset was observed, a finding that was replicated in an independent cohort. While previous research has shown that anxiety has a high comorbidity with a variety of psychiatric and neurodegenerative disorders, our analysis suggests a novel etiology specific to AS
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