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Background: Advances in pediatric oncology have significantly increased survival rates, yet have introduced challenges in managing long-term treatment side effects. This study process introduces an interdisciplinary clinical intervention program rooted in the family resilience framework, aimed at improving well-being across the cancer trajectory for children and their families, especially those in Canadian communities far from specialized oncology centers with limited access to resources. Methods: Employing an intervention mapping approach, this program collaboratively involves patients, families, professionals, and researchers. It aims to identify vulnerability factors, establish a logic model of change, and devise comprehensive strategies that include professional interventions alongside self-management tools. These strategies, tailored to address biopsychosocial and spiritual challenges, are adapted to the unique contexts of communities distant from specialized cancer treatment centers. A mixed-methods approach will evaluate program effectiveness. Expected results: Anticipated outcomes include the empowerment of families with self-management tools and professional support, designed to mitigate biopsychosocial and spiritual complications. By addressing the specific needs and limitations of these communities, the program strives to improve the overall health and well-being of both undergoing treatment and survivorship phases. Discussion: By focusing on comprehensive care that includes both professional interventions and self-management, this initiative marks a significant shift toward a holistic, family-centered approach in pediatric oncology care for remote communities. It underlines the necessity of accessible interventions that confront immediate and long-term challenges, aiming to elevate the standard of care by emphasizing resilience, professional support, and family empowerment in underserved areas

Background and aims Statin-associated muscle symptoms (SAMS) are frequently reported. Nevertheless, few data on objective measures of muscle function are available. Recent data suggesting an important nocebo effect with statin use could confound such effects. The objective was to assess if subjective and objective measures of muscle function improve after drug withdrawal in SAMS reporters. Methods Patients (59 men, 33 women, 50.3±9.6 yrs.) in primary cardiovascular prevention composed three cohorts: statin users with (SAMS, n = 61) or without symptoms (No SAMS, n = 15), and controls (n = 16) (registered at clinicaltrials.gov, NCT01493648). Force (F), endurance (E) and power (P) of the leg extensors (ext) and flexors (fle) and handgrip strength (Fhg) were measured using isokinetic and handheld dynamometers, respectively. A 10-point visual analogue scale (VAS) was used to self-assess SAMS intensity. Measures were taken before and after two months of withdrawal. Results Following withdrawal, repeated-measures analyses show improvements for the entire cohort in Eext, Efle, Ffle, Pext and Pfle (range +7.2 to +13.3%, all p≤0.02). Post-hoc analyses show these changes to occur notably in SAMS (+8.8 to +16.6%), concurrent with a decrease in subjective perception of effects in SAMS (VAS, from 5.09 to 1.85). Fhg was also improved in SAMS (+4.0 to +6.2%) when compared to No SAMS (-1.7 to -4.2%) (all p = 0.02). Conclusions Whether suffering from "true" SAMS or nocebo, those who reported SAMS had modest but relevant improvements in muscle function concurrent with a decrease in subjective symptoms intensity after drug withdrawal. Greater attention by clinicians to muscle function in frail statin users appears warranted.

Background Physical impairments cause an important functional decline in patient with cancer and survivor. Despite a profound need for physical therapy, many people are unable to access the required services due, in part, to the limited availability of cancer physical therapy programs. The model of community-based rehabilitation presents an opportunity to increase access to outpatient physiotherapy services in Saguenay-Lac-St-Jean. Aim The aim of this study was to assess the feasibility of a 10-weeks physical therapy program for cancer patients and survivor in the local community. Method A pre-post study was conducted using Bowen’s framework to measure the feasibility of a 10-weeks personalized physical therapy program. Feasibility outcomes focused on demand, acceptability, implementation, practicality and limited-efficacity. Limited efficacity testing was done intra-group from paired comparisons of pre- and postintervention by calculating mean differences and 95% confidence intervals for normally distributed data or mean and sum of ranks for non-normally distributed data. Results Over 19 months, thirty-one people were contacted and eighteen people completed the program [Mean age 54.54 (SD 12.16)]. The most frequent reasons to explain demand for our program were low muscle endurance, weak muscles, range of motion restrictions, reduced functional capacity, poor sleep quality and pain. Participant attended 94.3% of scheduled appointments. Existing equipment of the not-forprofit physiotherapy clinic of University of Quebec in Chicoutimi were used to run the program in the community setting. Participants reported high satisfaction and there were no major adverse events. Main barriers to project included COVID-19 restrictions and participants motivation. Participants made gains in pain, functionalca pacity, muscle strength and walk distance. Conclusions A 10-weeks personalized physical therapy program in Saguenay-Lac-St-Jean community is feasible and safe to improve the

J’aimerais souhaiter la bienvenue à tout le monde ; je me nomme Kevin Stein et je suis co-rédacteur en chef du Journal of Cancer Rehabilitation. Bienvenue à notre tout premier webinaire en direct sur le rôle de l’exercice dans la réadaptation après un cancer. Nous avons des participants de plus de 40 pays à travers le monde, couvrant 6 des 7 continents. Au nom de mon co-rédacteur en chef Vittorio Mattioli et de l’ensemble du de rédaction de JCR, je tiens à vous souhaiter la bienvenue à cet événement en direct. Je veux vous présenter le Journal of Cancer Rehabilitation, un nouveau journal qui a été lancé il y a deux ans. Il s’agit d’une revue trimestrielle internationale à comité de lecture. Jusqu’à présent, nous avons 13 articles cautionnés par comité de lecture. C’est un journal en libre accès ; les articles sont soumis à un examen rigoureux par les pairs et sont publiés en ligne dès leur acceptation. Je tiens à remercier les membres ainsi que le comité de rédaction du JCR pour sa contribution. Merci à tous. Je veux également mentionner une initiative spéciale du JCR pour les jeunes chercheurs en début de carrière. J’aimerais présenter nos panélistes: • Nicole L. Stout, DPT, CLT-LANA, FAPTA • Martijn Stuiver, PhD • Morten Quist, PhD, PT • Kathryn Schmitz, PhD, MPH

Introduction: Low back pain (LBP) is the most common musculoskeletal complaint in pregnancy, being responsible for many negative impacts. Objective: To evaluate the effect of LBP on static and dynamic balance in pregnant women and whether pregnancy mediates the results compared to non-pregnant women. Methods: 44 women (mean age 30 yrs) participated voluntarily in this study: 16 pregnant women with LBP starting in pregnancy, 14 pregnant women without LBP and 14 non-pregnant women as a group control. Participants were assessed for static postural balance using a force platform and dynamic mobility balance using the Timed Up and Go (TUG) test. Results: The pregnant women with LBP showed significant (P < 0.04, for mean, d= 1,2) poor postural balance in static tests (force platform), in the area of COP eyes open. In dynamic balance (TUG test), statistical difference was found between the groups (P 0.038) and the effect size were moderate to strong in the comparison between the three groups. The most sensitive differences were reported mainly between pregnant women with LBP versus non-pregnant control group in balance measures from force platform. Conclusion: The findings indicate that LBP associated to pregnant clinical status can decrease the balance capacity in women. These results have implication for balance evaluation and retraining in pregnant women with and without LBP from rehabilitation or prevention programs.

The muscle membrane, sarcolemma, must be firmly attached to the basal lamina. The failure of proper attachment results in muscle injury, which is the underlying cause of Duchenne muscular dystrophy (DMD), where mutations in the dystrophin gene disrupts the firm adhesion. In DMD patients, even moderate contraction causes damage, leading to progressive muscle degeneration. The damaged muscles are repaired through myogenesis. Consequently, myogenesis is highly active in DMD patients, and the repeated activation of myogenesis leads to the exhaustion of the myogenic stem cells. Therefore, approaches to reducing the risk of the exhaustion are to develop a treatment that strengthens the interaction between the sarcolemma and the basal lamina, and increases the efficiency of myogenesis. Galectin-3 is an oligosaccharide-binding protein and known to be involved in cell–cell interactions and cell–matrix interactions. Galectin-3 is expressed in myoblasts and skeletal muscle while its function in muscle remains elusive. In this study, we found evidence that galectin-3 and the monosaccharide N-acetylglucosamine, which increases the ligands (oligosaccharides) of galectin-3, promotes myogenesis in vitro. Moreover, in the mdx mouse model of DMD, treatment with N-acetylglucosamine increased the muscle force production. Our results demonstrate that treatment with N-acetylglucosamine can mitigate the burden of DMD.

Anti-inflammatory modalities are commonly used for the treatment of various musculoskeletal injuries. Although inflammation was originally believed to interfere with skeletal muscle regeneration, several recent studies have highlighted the beneficial effects of inflammatory cells on muscle healing. This discrepancy is attributable to an evolving understanding of the complex inflammatory process. To better appreciate the paradoxical roles of inflammation, clinicians must have a better comprehension of the fundamental mechanisms regulating the inflammatory response. In this perspective article, cellular, animal, and human studies were analyzed to summarize recent knowledge regarding the impact of inflammation on muscle regeneration in acute or chronic conditions. The effect of anti-inflammatory drugs on the treatment of various muscle injuries was also considered. Overall, this work aims to summarize the current state of the literature on the inflammatory process associated with muscle healing in order to give clinicians the necessary tools to have a more efficient and evidence-based approach to the treatment of muscle injuries and disorders.

Background The Ste20-like kinase, SLK, plays an important role in cell proliferation and cytoskeletal remodeling. In fibroblasts, SLK has been shown to respond to FAK/Src signaling and regulate focal adhesion turnover through Paxillin phosphorylation. Full-length SLK has also been shown to be essential for embryonic development. In myoblasts, the overexpression of a dominant negative SLK is sufficient to block myoblast fusion. Methods In this study, we crossed the Myf5-Cre mouse model with our conditional SLK knockout model to delete SLK in skeletal muscle. A thorough analysis of skeletal muscle tissue was undertaken in order to identify defects in muscle development caused by the lack of SLK. Isometric force analysis was performed on adult knockout mice and compared to age-matched wild-type mice. Furthermore, cardiotoxin injections were performed followed by immunohistochemistry for myogenic markers to assess the efficiency muscle regeneration following SLK deletion. Results We show here that early deletion of SLK from the myogenic lineage does not markedly impair skeletal muscle development but delays the regenerative process. Interestingly, adult mice (~6 months) display an increase in the proportion of central nuclei and increased p38 activation. Furthermore, mice as young as 3 months old present with decreased force generation, suggesting that the loss of SLK impairs myofiber stability and function. Assessment of structural components revealed aberrant localization of focal adhesion proteins, such as FAK and paxillin. Our data show that the loss of SLK results in unstable myofibers resulting in a progressive myopathy. Additionally, the loss of SLK resulted in a delay in muscle regeneration following cardiotoxin injections. Conclusions Our results show that SLK is dispensable for muscle development and regeneration but is required for myofiber stability and optimal force generation.

The discovery of receptor-activator of nuclear factor kB (RANK), its ligand RANKL, and the soluble decoy receptor osteoprotegerin (OPG) pathway led to a clearer understanding of bone remodeling and homeostasis. While there is a strong association between osteoporosis and skeletal muscle dysfunction, the functional relevance of a particular biological pathway that synchronously regulates bone and skeletal muscle physiopathology remains elusive. Our recent article published in the American Journal of Physiology (Cell Physiology) showed that RANK is also expressed in fully differentiated C2C12 myotubes and skeletal muscles. We used the Cre-Lox approach to inactivate muscle RANK (RANKmko) and showed that RANK deletion preserves the force of denervated fast-twitch EDL muscles. However, RANK deletion had no positive impact on slow-twitch Sol muscles. In addition, denervating RANKmko EDL muscles induced an increase in the total calcium concentration ([CaT]), which was associated with a surprising decrease in SERCA activity. Interestingly, the levels of STIM-1, which mediates Ca2+ influx following the depletion of SR Ca2+ stores, were markedly higher in denervated RANKmko EDL muscles. We speculated that extracellular Ca2+ influx mediated by STIM-1 may be important for the increase in [CaT] and the gain of force in denervated RANKmkoEDL muscles. Overall, these findings showed for the first time that the RANKL/RANK interaction plays a role in denervation-induced muscle atrophy and dysfunction.

The discovery of receptor-activator of nuclear factor kB (RANK), its ligand RANKL, and the soluble decoy receptor osteoprotegerin (OPG) pathway led to a clearer understanding of bone remodeling and homeostasis. While there is a strong association between osteoporosis and skeletal muscle dysfunction, the functional relevance of a particular biological pathway that synchronously regulates bone and skeletal muscle physiopathology remains elusive. Our recent article published in the American Journal of Physiology (Cell Physiology) showed that RANK is also expressed in fully differentiated C2C12 myotubes and skeletal muscles. We used the Cre-Lox approach to inactivate muscle RANK (RANKmko) and showed that RANK deletion preserves the force of denervated fast-twitch EDL muscles. However, RANK deletion had no positive impact on slow-twitch Sol muscles. In addition, denervating RANKmko EDL muscles induced an increase in the total calcium concentration ([CaT]), which was associated with a surprising decrease in SERCA activity. Interestingly, the levels of STIM-1, which mediates Ca2+ influx following the depletion of SR Ca2+ stores, were markedly higher in denervated RANKmko EDL muscles. We speculated that extracellular Ca2+ influx mediated by STIM-1 may be important for the increase in [CaT] and the gain of force in denervated RANKmkoEDL muscles. Overall, these findings showed for the first time that the RANKL/RANK interaction plays a role in denervation-induced muscle atrophy and dysfunction.

Background : Cumulative evidence indicates that statins induce myotoxicity. However, the lack of understanding of how statins affect skeletal muscles at the structural, functional, and physiological levels hampers proper healthcare management. The purpose of the present study was to investigate the early after-effects of lovastatin on the slow-twitch soleus (Sol) and fast-twitch extensor digitorum longus (EDL) muscles. Methods : Adult C57BL/6 mice were orally administrated with placebo or lovastatin [50 mg/kg/d] for 28 days. At the end of the treatment, the isometric ex vivo contractile properties of the Sol and EDL muscles were measured. Subtetanic and tetanic contractions were assessed and contraction kinetics were recorded. The muscles were then frozen for immunohistochemical analyses. Data were analyzed by two-way ANOVA followed by an a posteriori Tukey’s test. Results : The short-term lovastatin treatment did not induce muscle mass loss, muscle fiber atrophy, or creatine kinase (CK) release. It had no functional impact on slow-twitch Sol muscles. However, subtetanic stimulations at 10 Hz provoked greater force production in fast-twitch EDL muscles. The treatment also decreased the maximal rate of force development (dP/dT) of twitch contractions and prolonged the half relaxation time (1/2RT) of tetanic contractions of EDL muscles. Conclusions : An early short-term statin treatment induced subtle but significant changes in some parameters of the contractile profile of EDL muscles, providing new insights into the selective initiation of statin-induced myopathy in fast-twitch muscles.

Receptor-activator of nuclear factor kB (RANK), its ligand RANKL and the soluble decoy receptor osteoprotegerin (OPG)are the key regulators of osteoclast differentiation and bone remodeling. Here we show that RANK is also expressed in fully differentiated myotubes and skeletal muscle. Muscle RANK deletion (RANKmko) has inotropic effects in denervated, but not in sham, extensor digitorum longus (EDL) muscle preventing the loss of maximum specific force while promoting muscle atrophy, fatigability and increased proportion of fast-twitch fibers. In denervated EDL muscles, RANK deletion markedly increased stromal interaction molecule 1 (Stim1) content, a calcium sensor, and altered activity of the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA) modulating Ca2+ storage. Muscle RANK deletion had no significant effects on the sham or denervated slow-twitch soleus (Sol) muscles. These data identify a novel role for RANK as a key regulator of calcium storage and SERCA activity, ultimately affecting denervated skeletal muscle function.

Les lésions musculaires sont des blessures fréquentes et d’origines diverses. Une réaction inflammatoire d’intensité variée est généralement associée à la plupart des atteintes musculaires. Cette réaction inflammatoire était traditionnellement considérée néfaste pour la guérison musculaire et les anti-inflammatoires ont longtemps été le traitement de choix pour ce type de blessures. Bien que certaines études scientifiques aient démontré que l’inflammation pouvait induire des dommages collatéraux, de nouvelles évidences s’accumulent en faveur d’un rôle essentiel de certaines cellules inflammatoires pour une régénération musculaire optimale. En particulier, l’aptitude des macrophages à changer d’un profil pro-inflammatoire à anti-inflammatoire fait de ces derniers des acteurs centraux de la régénération musculaire. Cet article vise à synthétiser les connaissances actuelles quant aux effets des différentes cellules inflammatoires (résidentes et infiltrantes) sur la fonction des cellules myogéniques et sur la régénération musculaire.

Objective: To evaluate whether a 12-week supervised exercise program promotes an active lifestyle throughout pregnancy in pregnant women with obesity. Methods: In this preliminary randomised trial, pregnant women (body mass index ≥ 30 kg/m2) were allocated to either standard care or supervised training, from 15 to 27 weeks of gestation. Physical activity was measured by accelerometry at 14, 28 and 36 weeks, while fitness (oxygen consumption (VO2) at the anaerobic threshold), nutrition (caloric intake and macronutrients percentage) and anthropometry were assessed at 14 and 28 weeks of gestation. Analyses were performed using repeated measures ANOVA. Results: A total of fifty (50) women were randomised, 25 in each group. There was no time-group interaction for time spent at moderate and vigorous activity (pinteraction = 0.064), but the exercise group’s levels were higher than controls’ at all times (pgroup effect = 0.014). A significant time-group interaction was found for daily physical activity (p = 0.023); similar at baseline ((22.0 ± 6.7 vs 21.8 ± 7.3) x 104 counts/day) the exercise group had higher levels than the control group following the intervention ((22.8 ± 8.3 vs 19.2 ± 4.5) x 104 counts/day, p = 0.020) and at 36 weeks of gestation ((19.2 ± 1.5 vs 14.9 ± 1.5) x 104 counts/day, p = 0.034). Exercisers also gained less weight than controls during the intervention period despite similar nutritional intakes (difference in weight change = -0.1 kg/week, 95% CI -0.2; -0.02, p = 0.016) and improved cardiorespiratory fitness (difference in fitness change = 8.1%, 95% CI 0.7; 9.5, p = 0.041). Conclusions: Compared with standard care, a supervised exercise program allows pregnant women with obesity to maintain fitness, limit weight gain and attenuate the decrease in physical activity levels observed in late pregnancy