Mesure du paramètre acoustique non linéaire dans les solvants et dans les polymères

Dans cette étude, une technique d'amplitude finie visant la mesure du paramètre non linéaire B/A fut mise au point puis appliquée à trois familles de solvants à savoir les 1-alkanols, les cétones et les esters, ainsi qu'à deux polymères. Par l'intermédiaire d'une lentille acoustique, un signal fut focalisé dans le milieu à caractériser et l'amplitude du second harmonique généré, mesurée. Le paramètre non linéaire put alors être calculé pour chacun des liquides et solides testés. Les résultats obtenus concernant les liquides permirent de démontrer la variation de B/A avec la longueur de chaîne et la dépendance de ce paramètre avec la vitesse du son. Un modèle fut par la suite établi puis appliqué aux 1-alkanols, obtenant une description de la variation de B/A à la vitesse du son conforme à nos résultats expérimentaux. Le même principe de mesure fut appliqué à deux polymères, montrant le potentiel de cette technique pour déterminer la valeur du paramètre non linéaire dans les solides

Neuroendocrine and neurophysiological effects of interleukin 6 in rheumatoid arthritis

RA is a chronic, systemic, autoimmune disease characterized by inflammation and degradation of the joints, causing significant negative impact on quality of life. In addition to joint disease, symptoms and co-morbidities associated with RA—namely pain, fatigue and mood disorders—are often as debilitating as the disease itself. The pro-inflammatory cytokine IL-6 plays a critical role in RA-associated pathology. However, a greater understanding of the translational effects of IL-6 outside of the immune system is needed. This review discusses our current understanding of emerging aspects of IL-6 in RA-associated pain, fatigue and mood disorders such as depression and anxiety. This review also describes the clinical effects of IL-6 inhibition on these symptoms and co-morbidities in patients with RA

VEGFR2 promotes central endothelial activation and the spread of pain in inflammatory arthritis

Chronic pain can develop in response to conditions such as inflammatory arthritis. The central mechanisms underlying the development and maintenance of chronic pain in humans are not well elucidated although there is evidence for a role of microglia and astrocytes. However in pre-clinical models of pain, including models of inflammatory arthritis, there is a wealth of evidence indicating roles for pathological glial reactivity within the CNS. In the spinal dorsal horn of rats with painful inflammatory arthritis we found both a significant increase in CD11b+ microglia-like cells and GFAP+ astrocytes associated with blood vessels, and the number of activated blood vessels expressing the adhesion molecule ICAM-1, indicating potential glio-vascular activation. Using pharmacological interventions targeting VEGFR2 in arthritic rats, to inhibit endothelial cell activation, the number of dorsal horn ICAM-1+ blood vessels, CD11b+ microglia and the development of secondary mechanical allodynia, an indicator of central sensitization, were all prevented. Targeting endothelial VEGFR2 by inducible Tie2-specific VEGFR2 knock-out also prevented secondary allodynia in mice and glio-vascular activation in the dorsal horn in response to inflammatory arthritis. Inhibition of VEGFR2 in vitro significantly blocked ICAM-1-dependent monocyte adhesion to brain microvascular endothelial cells, when stimulated with inflammatory mediators TNFa and VEGF-A165a. Taken together our findings suggest that a novel VEGFR2-mediated spinal cord gliovascular mechanism may promote peripheral CD11b+ circulating cell transmigration into the CNS parenchyma and contribute to the development of chronic pain in inflammatory arthritis. We hypothesise that preventing this glio-vascular activation and circulating cell translocation into the spinal cord could be a new therapeutic strategy for pain caused by rheumatoid arthritis