Mètodes mixtos en la investigació de les ciències de l’activitat física i l’esport

La investigació en les ciències de l’activitat física i l’esport ha estat influenciada prioritàriament per procediments quantitatius adaptats d’altres àrees del coneixement. L’aparició de nous paradigmes, mètodes i procediments d’investigació ens ofereix un nombre més gran de possibilitats de combinació d’instruments per a l’anàlisi de l’activitat física i l’esport que pot enriquir tot el procés investigador. En aquest article presentem, mitjançant exemples d’investigacions, els mètodes mixtos (Mixed Method Approach), que proposen conjugar dades de naturalesa quantitativa i qualitativa en el mateix estudi. Aquesta nova perspectiva metodològica s’està refermant amb força en l’última dècada d’acord amb la necessitat actual de plantejaments més integrats en la investigació de la motricitat humana

Métodos mixtos en la investigación de las ciencias de la actividad física y el deporte

La investigación en las ciencias de la actividad física y el deporte ha estado influenciada prioritariamente por procedimientos cuantitativos adaptados de otras áreas del conocimiento. La aparición de nuevos paradigmas, métodos y procedimientos de investigación nos ofrecen mayor número de posibilidades de combinación de instrumentos para el análisis de la actividad física y el deporte que puede enriquecer todo el proceso investigador. En este artículo presentamos, mediante ejemplos de investigaciones, los métodos mixtos (Mixed Method Approach) que proponen conjugar datos de naturaleza cuantitativa y cualitativa en el mismo estudio. Esta nueva perspectiva metodológica se está afianzando con fuerza en la última década acorde con la necesidad actual de planteamientos más integrados en la investigación de la motricidad humana

Therapeutic Targets in Amyotrophic Lateral Sclerosis: Focus on Ion Channels and Skeletal Muscle

Amyotrophic Lateral Sclerosis is a neurodegenerative disease caused by progressive loss of motor neurons, which severely compromises skeletal muscle function. Evidence shows that muscle may act as a molecular powerhouse, whose final signals generate in patients a progressive loss of voluntary muscle function and weakness leading to paralysis. This pathology is the result of a complex cascade of events that involves a crosstalk among motor neurons, glia, and muscles, and evolves through the action of converging toxic mechanisms. In fact, mitochondrial dysfunction, which leads to oxidative stress, is one of the mechanisms causing cell death. It is a common denominator for the two existing forms of the disease: sporadic and familial. Other factors include excitotoxicity, inflammation, and protein aggregation. Currently, there are limited cures. The only approved drug for therapy is riluzole, that modestly prolongs survival, with edaravone now waiting for new clinical trial aimed to clarify its efficacy. Thus, there is a need of effective treatments to reverse the damage in this devastating pathology. Many drugs have been already tested in clinical trials and are currently under investigation. This review summarizes the already tested drugs aimed at restoring muscle-nerve cross-talk and on new treatment options targeting this tissue

Statin‐induced myopathy: Translational studies from preclinical to clinical evidence

Statins are the most prescribed and effective drugs to treat cardiovascular diseases (CVD). Nevertheless, these drugs can be responsible for skeletal muscle toxicity which leads to reduced compliance. The discontinuation of therapy increases the incidence of CVD. Thus, it is essential to assess the risk. In fact, many studies have been performed at preclinical and clinical level to investigate pathophysiological mechanisms and clinical implications of statin myotoxicity. Consequently, new toxicological aspects and new biomarkers have arisen. Indeed, these drugs may affect gene transcription and ion transport and contribute to muscle function impairment. Identifying a marker of toxicity is important to prevent or to cure statin induced myopathy while assuring the right therapy for hypercholesterolemia and counteracting CVD. In this review we focused on the mechanisms of muscle damage discovered in preclinical and clinical studies and high-lighted the pathological situations in which statin therapy should be avoided. In this context, preventive or substitutive therapies should also be evaluated

Working time satisfaction in aging nurses

Satisfaction with working time could represent an index of good balance between work and life and predict satisfactory work ability and endurance of aged workers. This study is aimed at checking whether elderly nurses who were satisfied with working hours had a better work ability index than those unsatisfied, and finding which factors were related to satisfaction of working time with reference to general \u201cwell being\u201d and/or \u201cprivate life\u201d. The study sample consisted of 3,174 female nurses recruited in six European countries within the Nurses\u2019 Early Exit Study. All were rotating shiftworkers (nights included) and 12.95 % were over 45 years of age. A composite questionnaire, including demands at work and in private life, working conditions, individual resources and alternatives to nursing profession, was administered to the participants at baseline and 1 yr later (Time 1). Work ability index (WAI) at time 1 was used as outcome, whereas age groups and satisfaction of working time at baseline were used as predictors, after adjusting for family status and number of children < 7yrs of age. Also \u201csatisfaction with working time\u201d at Time 1 was used as outcome, whereas working hours, job demand, leisure time, influence on planning rotas, family status, number of children, work/family conflicts, sleep at Time 0 were included as potential determinants. Conditional Random Forest analysis was used to evaluate high, moderate or weak importance of these determinants. Nurses satisfied with working time at time 0 showed a higher WAI (time1) than those unsatisfied in all age groups, also over 50. Less work/family conflicts and better quality and quantity sleep turned out to be the best predictors of satisfaction with working time. Consistently, the importance of the other predictors differs when the outcome is \u201csatisfaction with working time\u201d related to general well-being rather than to private life

Canine Melanoma Immunology and Immunotherapy: Relevance of Translational Research

In veterinary oncology, canine melanoma is still a fatal disease for which innovative and long-lasting curative treatments are urgently required. Considering the similarities between canine and human melanoma and the clinical revolution that immunotherapy has instigated in the treatment of human melanoma patients, special attention must be paid to advancements in tumor immunology research in the veterinary field. Herein, we aim to discuss the most relevant knowledge on the immune landscape of canine melanoma and the most promising immunotherapeutic approaches under investigation. Particular attention will be dedicated to anti-cancer vaccination, and, especially, to the encouraging clinical results that we have obtained with DNA vaccines directed against chondroitin sulfate proteoglycan 4 (CSPG4), which is an appealing tumor-associated antigen with a key oncogenic role in both canine and human melanoma. In parallel with advances in therapeutic options, progress in the identification of easily accessible biomarkers to improve the diagnosis and the prognosis of melanoma should be sought, with circulating small extracellular vesicles emerging as strategically relevant players. Translational advances in melanoma management, whether achieved in the human or veterinary fields, may drive improvements with mutual clinical benefits for both human and canine patients; this is where the strength of comparative oncology lies

Alteration of stim1/orai1-mediated soce in skeletal muscle: Impact in genetic muscle diseases and beyond

Intracellular Ca2+ ions represent a signaling mediator that plays a critical role in regulating different muscular cellular processes. Ca2+ homeostasis preservation is essential for maintaining skeletal muscle structure and function. Store-operated Ca2+ entry (SOCE), a Ca2+-entry process activated by depletion of intracellular stores contributing to the regulation of various function in many cell types, is pivotal to ensure a proper Ca2+ homeostasis in muscle fibers. It is coordinated by STIM1, the main Ca2+ sensor located in the sarcoplasmic reticulum, and ORAI1 protein, a Ca2+-permeable channel located on transverse tubules. It is commonly accepted that Ca2+ entry via SOCE has the crucial role in short-and long-term muscle function, regulating and adapting many cellular processes including muscle contractility, postnatal development, myofiber phenotype and plasticity. Lack or mutations of STIM1 and/or Orai1 and the consequent SOCE alteration have been associated with serious consequences for muscle function. Importantly, evidence suggests that SOCE alteration can trigger a change of intracellular Ca2+ signaling in skeletal muscle, participating in the pathogenesis of different progressive muscle diseases such as tubular aggregate myopathy, muscular dystrophy, cachexia, and sarcopenia. This review provides a brief overview of the molecular mechanisms underlying STIM1/Orai1-dependent SOCE in skeletal muscle, focusing on how SOCE alteration could contribute to skeletal muscle wasting disorders and on how SOCE components could represent pharmacological targets with high therapeutic potential