CHRONIC PAIN SELF-EFFICACY AS A MEDIATOR OF THE LINK BETWEEN ROMANTIC ATTACHMENT INSECURITY, INDIVIDUAL FUNCTIONING, AND COUPLE SATISFACTION: A PRELIMINARY STUDYS

This preliminary study was inspired by the Attachment-Diathesis Model of Chronic Pain (ADMoCP) and examined pain self-efficacy as a mediator of the relation between people’s insecure romantic attachment and individual functioning, as well couple satisfaction. This study used a sample of 45 adults with chronic pain from the community who have been in couple relationships for at least 6 months. Participants completed self-report measures. Direct links were obtained between 1) insecure romantic attachment (anxiety over abandonment) and pain self-efficacy, 2) pain self-efficacy and individual functioning, 3) insecure romantic attachment and low individual functioning, and 4) insecure romantic attachment and lower couple satisfaction. Results also showed that pain self-efficacy significantly mediates the relation between anxiety over abandonment and individual functioning, thus adding to existing literature as well as providing more support for the ADMoCP. Future research directions are discussed along with clinical implications.Keywords: Chronic Pain. Romantic Attachment. Pain Self-Efficacy. Individual Functioning. RESUMOEste estudo preliminar foi inspirado no Attachment-Diathesis Model of Chronic Pain – ADMoCP e investigou a autoeficácia no manejo da dor como um mediador da ligação entre estilo de apego inseguro nas relações afetivas, funcionamento individual e satisfação conjugal. Este estudo utilizou uma amostra de 45 adultos da comunidade com dor crônica e que estavam em um relacionamento há pelo menos 6 meses. Participantes responderam a questionários de autorrelato. Foram obtidas relações diretas entre 1) estilo de apego inseguro nas relações afetivas (ansiedade de abandono) e autoeficácia no manejo da dor, 2) autoeficácia no manejo da dor e funcionamento individual, 3) estilo de apego inseguro nas relações afetivas e limitações no funcionamento individual e 4) estilo de apego inseguro nas relações afetivas e menor satisfação conjugal. Os resultados também mostraram que a autoeficácia no manejo da dor interfere significativamente na relação entre ansiedade de abandono e funcionamento individual, corroborando a literatura existente bem como fornecendo mais suporte para a ADMoCP. São discutidas futuras direções de pesquisa bem como implicações clínicas.Palavras-chave: Dor Crônica. Apego nas relações afetivas. Autoeficácia no manejo da dor. Funcionamento Individual

CHRONIC PAIN SELF-EFFICACY AS A MEDIATOR OF THE LINK BETWEEN ROMANTIC ATTACHMENT INSECURITY, INDIVIDUAL FUNCTIONING, AND COUPLE SATISFACTION: A PRELIMINARY STUDYS

This preliminary study was inspired by the Attachment-Diathesis Model of Chronic Pain (ADMoCP) and examined pain self-efficacy as a mediator of the relation between people’s insecure romantic attachment and individual functioning, as well couple satisfaction. This study used a sample of 45 adults with chronic pain from the community who have been in couple relationships for at least 6 months. Participants completed self-report measures. Direct links were obtained between 1) insecure romantic attachment (anxiety over abandonment) and pain self-efficacy, 2) pain self-efficacy and individual functioning, 3) insecure romantic attachment and low individual functioning, and 4) insecure romantic attachment and lower couple satisfaction. Results also showed that pain self-efficacy significantly mediates the relation between anxiety over abandonment and individual functioning, thus adding to existing literature as well as providing more support for the ADMoCP. Future research directions are discussed along with clinical implications. Keywords: Chronic Pain. Romantic Attachment. Pain Self-Efficacy. Individual Functioning.   RESUMO Este estudo preliminar foi inspirado no Attachment-Diathesis Model of Chronic Pain – ADMoCP e investigou a autoeficácia no manejo da dor como um mediador da ligação entre estilo de apego inseguro nas relações afetivas, funcionamento individual e satisfação conjugal. Este estudo utilizou uma amostra de 45 adultos da comunidade com dor crônica e que estavam em um relacionamento há pelo menos 6 meses. Participantes responderam a questionários de autorrelato. Foram obtidas relações diretas entre 1) estilo de apego inseguro nas relações afetivas (ansiedade de abandono) e autoeficácia no manejo da dor, 2) autoeficácia no manejo da dor e funcionamento individual, 3) estilo de apego inseguro nas relações afetivas e limitações no funcionamento individual e 4) estilo de apego inseguro nas relações afetivas e menor satisfação conjugal. Os resultados também mostraram que a autoeficácia no manejo da dor interfere significativamente na relação entre ansiedade de abandono e funcionamento individual, corroborando a literatura existente bem como fornecendo mais suporte para a ADMoCP. São discutidas futuras direções de pesquisa bem como implicações clínicas. Palavras-chave: Dor Crônica. Apego nas relações afetivas. Autoeficácia no manejo da dor. Funcionamento Individual

Effect of pressure on the pseudogap and charge density wave phases of the cuprate Nd-LSCO probed by thermopower measurements

We report thermopower measurements under hydrostatic pressure on the cuprate superconductor La1.6−xNd0.4SrxCuO4 (Nd-LSCO), at low temperature in the normal state accessed by suppressing superconduc- tivity with a magnetic field up to H = 31 T. Using an ac thermopower measurement technique suitable for high pressure and high field, we track the pressure evolution of the Seebeck coefficient S. At ambient pressure and low temperature, S/T in Nd-LSCO was recently found to suddenly increase below the pseudogap critical doping p ⋆ = 0.23, consistent with a drop in carrier density n from n = 1 + p above p⋆ to n = p below. Under a pressure of 2.0 GPa, we observe that the large S/T value just below p ⋆ is suppressed. This confirms a previous pressure study based on electrical resistivity and Hall effect, which found that pressure lowers p ⋆, thereby reinforcing the interpretation that this effect is driven by the pressure-induced shift of the van Hove point. It implies that the pseudogap only exists when the Fermi surface is hole-like, which puts strong constraints on theories of the pseudogap phase. We also report thermopower measurements on Nd-LSCO and La1.8−xEu0.2SrxCuO4 in the charge density wave phase near p ∼ 1/8, which reveals a weakening of this phase under pressure.L.T. acknowledges support from the Canadian Institute for Ad- vanced Research (CIFAR) as a CIFAR Fellow and funding from the Institut Quantique, the Natural Sciences and Engi- neering Research Council of Canada (PIN:123817), the Fonds de Recherche du Québec–Nature et Technologies (FRQNT), the Canada Foundation for Innovation (CFI), and a Canada Research Chair. This research was undertaken thanks in part to funding from the Canada First Research Excellence Fund and the Gordon and Betty Moore Foundation’s EPiQS Ini- tiative (Grant No. GBMF5306 to L.T.). The National High Magnetic Field Laboratory is supported by the National Sci- ence Foundation through Grant No. NSF/DMR-1644779 and the State of Florida. J.-S.Z. was supported by NSF MRSEC under Cooperative Agreement No. DMR-1720595.Center for Dynamics and Control of Material

Phonons become chiral in the pseudogap phase of cuprates

The nature of the pseudogap phase of cuprates remains a major puzzle. One of its new signatures is a large negative thermal Hall conductivity κxy, which appears for dopings p below the pseudogap critical doping p∗, but whose origin is as yet unknown. Because this large κxy is observed even in the undoped Mott insulator La2CuO4, it cannot come from charge carriers, these being localized at p=0. Here we show that the thermal Hall conductivity of La2CuO4 is roughly isotropic, being nearly the same for heat transport parallel and normal to the CuO2 planes, i.e. κzy(T)≈κxy(T). This shows that the Hall response must come from phonons, these being the only heat carriers able to move as easily normal and parallel to the planes . At p>p∗, in both La1.6−xNd0.4SrxCuO4 and La1.8−xEu0.2SrxCuO4 with p=0.24, we observe no c-axis Hall signal, i.e. κzy(T)=0, showing that phonons have zero Hall response outside the pseudogap phase. The phonon Hall response appears immediately below p∗=0.23, as confirmed by the large κzy(T) signal we find in La1.6−xNd0.4SrxCuO4 with p=0.21. The microscopic mechanism by which phonons become chiral in cuprates remains to be identified. This mechanism must be intrinsic - from a coupling of phonons to their electronic environment - rather than extrinsic, from structural defects or impurities, as these are the same on both sides of p∗. This intrinsic phonon Hall effect provides a new window on quantum materials and it may explain the thermal Hall signal observed in other topologically nontrivial insulators.Center for Dynamics and Control of Material

Satellite Cells Senescence in Limb Muscle of Severe Patients with COPD

Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec, Québec, Canada Rationale: The maintenance of peripheral muscle mass may be compromised in chronic obstructive pulmonary disease (COPD) due to premature cellular senescence and exhaustion of the regenerative potential of the muscles. Methods: Vastus lateralis biopsies were obtained from patients with COPD (n = 16) and healthy subjects (n = 7). Satellite cell number and the proportion of central nuclei, as a marker of muscle regenerative events, were assessed on cryosections. Telomere lengths, used as a marker of cellular senescence, were determined using Southern blot analyses. Results: Central nuclei proportion was significantly higher in patients with COPD with a preserved muscle mass compared to controls and patients with COPD with muscle atrophy (p,0.001). In COPD, maximal telomere length was significantly decreased compared to controls (p,0.05). Similarly, minimal telomere length was significantly reduced in GOLD III–IV patients with muscle atrophy compared to controls (p,0.005). Minimal, mean and maximum telomere lengths correlated with mid-thigh muscle cross-sectional area (MTCSA) (R = 0.523, p = 0.005; R = 0.435, p = 0.019 and R = 0.491, p = 0.009, respectively). Conclusions: Evidence of increased regenerative events was seen in GOLD III–IV patients with preserved muscle mass. Shortening of telomeres in GOLD III–IV patients with muscle atrophy is consistent with an increased number of senescen

Caractérisation des cellules satellites chez des personnes ayant une maladie pulmonaire obstructive chronique

La maladie pulmonaire obstructive chronique (MPOC) est caractérisée par une obstruction bronchique irréversible et progressive. L'atrophie musculaire périphérique est fréquente dans la MPOC et a un impact négatif sur la qualité de vie, la capacité fonctionnelle et la survie des sujets atteints. Un déficit dans la régénération du tissu musculaire pourrait contribuer au développement de l'atrophie musculaire, mais n'a jamais été directement évalué chez les sujets ayant une MPOC. La maintenance et la réparation du tissu musculaire sont du ressort des cellules satellites. Un nombre insuffisant de cellules satellites combinés ou non à un processus déficient de multiplication et de différenciation pourrait altérer la capacité du tissu musculaire à récupérer adéquatement à la suite d'un exercice physique ou d'un dommage musculaire. Nous proposons l'hypothèse que le potentiel de régénération musculaire est déficient chez les patients ayant une MPOC comparativement à des sujets sains d'âge similaire, contribuant ainsi au développement de l'atrophie musculaire observée chez ceux-ci. Pour vérifier cette hypothèse, un modèle de culture cellulaire primaire obtenu à partir d'échantillons musculaires a dû être développé. Ce projet permettra pour la première fois de mettre en culture et de caractériser les cellules satellites musculaires provenant de biopsies de patients ayant une MPOC. et d'évaluer leur potentiel de régénération. De plus, ce modèle pourra être utilisé pour répondre à différentes questions associées à la signalisation musculaire propre à la MPOC

Altération de la régénération musculaire dans la maladie pulmonaire obstructive chronique

Altération de la régénération musculaire dans la maladie pulmonaire obstructive chronique. La maladie pulmonaire obstructive chronique (MPOC) est caractérisée par une obstruction bronchique irréversible et progressive. L’atrophie musculaire périphérique y est fréquente et a un impact négatif sur la capacité fonctionnelle et la survie des sujets atteints. Toutefois, on ignore si une altération du processus de régénération musculaire est un processus ayant cours dans l’atrophie musculaire périphérique. Le but de la présente thèse était donc d’étudier les cellules satellites, principales cellules responsables de la régénération musculaire dans les muscles périphériques de patients ayant une MPOC. Dans un premier temps, nous avons évalué l’historique de réplication du tissu musculaire et la sénescence des cellules satellites. Les changements morphologiques ayant lieu dans le muscle au cours de la progression de la maladie rendent le muscle plus susceptible aux dommages, induisant un raccourcissement prématuré des télomères. Un raccourcissement des télomères chez les sujets ayant une MPOC avec atrophie est concomitant avec une augmentation du nombre de cellules satellites sénescentes et de l’épuisement du potentiel de régénération compromettant le maintien de la masse musculaire chez ces sujets. Dans un deuxième et troisième temps, nous avons étudié les étapes amenant une cellule satellite vers une cellule musculaire dans les muscles périphériques et respiratoires de patients ayant une MPOC comparativement à des sujets contrôles. Les cellules satellites sont impliquées dans la réparation du tissu musculaire. Dans les cellules satellites provenant des sujets ayant une MPOC, une altération de la prolifération et de la différentiation a été observée. Ces résultats sont compatibles avec une altération de la régénération musculaire pouvant conduire à l’atrophie musculaire dans la MPOC. Le quatrième volet de ce projet s’intéressait à l’impact d’un entraînement en résistance sur l’activité des cellules satellites et le rôle joué par la myostatine dans ce contexte. La littérature montre que l’exercice en résistance est bien toléré et aide les patients ayant une MPOC à retrouver une meilleure qualité de vie. Cependant, il semble qu’ils n’y répondent pas tous aussi bien que les sujets contrôles. La capacité de réponse des cellules satellites à un entraînement en résistance semble inadéquate, suggérant ainsi un défaut de leur activation. Dans la dernière étude de cette thèse, nous avons voulu évaluer l’impact de l’inflammation systémique en étudiant SAA1, une protéine de phase aiguë et p21, une protéine du cycle cellulaire dans la dégradation des protéines des cellules musculaires. Les liens de causalité entre l’affection primaire et les différentes comorbidités demeurent nébuleux dans la MPOC. SAA1 et p21 sont augmentés dans les muscles squelettiques des patients ayant une MPOC et par ailleurs, SAA1 est capable d’induire la dégradation des protéines musculaires. Cette thèse expose les premiers éléments impliquant l’altération de la régénération musculaire avec la dysfonction musculaire observée chez les patients ayant une MPOC. Ces résultats vont certainement contribuer au développement de nouvelles thérapies et stratégies d’intervention dans le but d’améliorer la qualité de vie des personnes atteintes d’une MPOC. En somme, les travaux effectués dans le cadre de la présente thèse montrent que plusieurs mécanismes agissent de concert avec l’inactivité physique afin d’induire le phénotype dysfonctionnel dans les muscles des patients ayant une MPOC.Skeletal muscle regeneration is altered in skeletal muscles of patients with Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Disease is associated with an irreversible and a progressive airflow obstruction. In COPD, the loss of muscle mass has a significant impact on quality of life and is associated with premature death. Many biochemical factors have been proposed to trigger and perpetuate the skeletal muscle atrophy in COPD. The maintenance of peripheral muscle mass may be compromised in patients with COPD due to premature cellular senescence and exhaustion of the regenerative potential of the muscles. Shortening of telomeres in patients with COPD is consistent with an increased number of senescent satellite cells and an exhausted muscle regenerative capacity, compromising the maintenance of muscle mass in these individuals. Muscle mass maintenance relies on the delicate regulation between protein degradation, synthesis and the addition of new myonuclei from satellite cells. Comparing the signalisation involved in the skeletal muscle regeneration between two muscles with different levels of activation within the same subjects is an interesting strategy to evaluate the impact of local versus systemic factors in the regulation of skeletal muscle regeneration. Impaired satellite cell activation, proliferation and differentiation affecting skeletal muscle regeneration could contribute to the progression of muscle dysfunction in patients with COPD. Resistance training, as provided in pulmonary rehabilitation, is an essential tool to promote muscle hypertrophy and increase muscle strength. However, hypertrophic response to resistance training is heterogeneous in patients with COPD. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease. Although the inflammatory response has been linked to the initiation and development of muscle atrophy, discrepancies exist in the literature concerning the presence and the nature of systemic and/or local inflammatory response in patients with COPD. This inflammation could be linked to the skeletal muscle protein imbalance and ultimately atrophy. The quest to identify a key inflammatory factor that could orchestrate the signaling cascade involved in contractile protein synthesis/degradation or even tissue renewal in peripheral muscles of patients with COPD is of major importance for future direction in this research field. This thesis demonstrates for the first time the role played by satellite cells in muscle atrophy associated with COPD. Better knowledge of the regenerative capacity in the context of COPD will enhance the understanding of the atrophying process and deepen the reasoning on training interventions in this population

Satellite cells quantification.

<p><b>A</b>) <i>Vastus lateralis</i> muscle cryosections were labeled for co-expression and localization of nuclear Paired box transcription factor 7 (green), DAPI (blue) and laminin (red). Cells positive for pax7 or NCAM (not shown) and DAPI located between the plasmalemma and the basal lamina were counted as satellite cells (white arrow). The number of satellite cells is expressed over 100 fibres and reported as a ratio. Ratio are calculated from 9 COPD and MTCSA >70 cm², 7 COPD and MTCSA <70 cm² and 7 healthy subjects. <b>B</b>) The numbers of nuclei having a positive label for Pax7 (white) and NCAM (black) were counted as satellite cells. Cells positive for pax7 or NCAM and DAPI located between the plasmalemma and the basal lamina were counted as satellite cells. The number of satellite cells is expressed over 100 fibres and reported as a ratio; ANOVA; p>0.05.</p