European Journal of Translational Myology最新文献

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a condition characterized by altered liver function due to fatty accumulation, which can lead to liver inflammation and, in advanced stages, liver carcinoma. MASLD is closely linked to several metabolic alterations, such as obesity and insulin resistance, which directly affect skeletal muscles and contribute to the development of sarcopenia. Sarcopenia is the loss of muscle mass and strength, leading to decreased physical performance in severe stages. Skeletal muscles secrete molecules known as myokines under various conditions, such as exercise or diseases like MASLD. These myokines modulate communication between the skeletal muscle and other tissues. These myokines regulate muscle mass and, in pathological conditions, contribute to the development of sarcopenia. Emerging evidence highlights the crucial role of myokines in regulating skeletal muscle metabolism and function in MASLD. Myokines influence muscle metabolism, inflammation, and insulin sensitivity, offering potential therapeutic targets for managing muscle atrophy and sarcopenia in the context of MASLD. Understanding the interaction between myokines and skeletal muscle may lead to novel interventions to mitigate MASLD progression and sarcopenia. This review examines the mechanisms by which myokines regulate skeletal muscle metabolism and function in the context of MASLD.

Lung cancer, a severe malignancy with poor prognosis, poses a formidable public health challenge. Beyond conventional risk factors such as smoking, evidence suggests that chronic respiratory diseases also contribute to its development. Among these, asthma, the second most prevalent chronic respiratory condition, is recognized as a risk factor for lung cancer. Nevertheless, the underlying molecular link between these two diseases remains elusive. Our study, leveraging multi-cohort data integration and employing Weighted Gene Co-expression Network Analysis (WGCNA), identified conserved shared genes between lung cancer and asthma. By constructing the functional landscape of these shared genes, we underscored the pivotal roles of pathways related to lung development and cellular metabolic homeostasis in the pathogenesis of both lung cancer and asthma. Utilizing machine learning-based screening, we identified three hub biomarkers: P2RY14, ANXA3, and SLIT2, which could serve as diagnostic tools for these diseases. In summary, our research provides invaluable insights into the shared mechanisms underlying asthma and lung cancer, and potential diagnostic biomarkers.

Advanced intraoperative anesthesia techniques have improved patient cooperation, stabilized hemodynamic status, and reduced postoperative pain and disability, especially in reconstructive limb surgeries. The Wide-Awake Local Anesthetic No Tourniquet (WALANT) technique has recently been adopted due to its peculiar advantages, but comparative studies of its benefits and limitations against general anesthesia are not well explored in FCR tendon transfer surgery. This study investigates outcomes of Flexor Carpi Radialis (FCR) tendon transfer surgery in patients with radial nerve injuries using either the Wide-Awake approach or general anesthesia. In this cross-sectional study, we included patients with confirmed radial nerve injuries who underwent FCR tendon transfer from 2019 to 2024. Participants were then divided into two groups; one received the WALANT anesthesia (200 ml epinephrine 1:400000 and 0.25% lidocaine buffered with sodium bicarbonate), while the other received general anesthesia. Data was collected from the medical records and the Hospital Information System (HIS). The intensity of pain, postoperative opioid consumption, wrist and finger function, and levels of patient satisfaction were measured both before and one month after surgery. There was no statistical difference between the groups regarding pain intensity, postoperative opioid dosage, and symptom severity. However, the WALANT group exhibited significantly less motor dysfunction in the postoperative period, which resulted in a much higher level of patient satisfaction compared to general anesthesia. WALANT provides quicker recovery of motor function and results in higher patient satisfaction when compared to general anesthesia for FCR tendon transfer surgeries. This approach thus leads to an earlier return to daily activities and occupational duties, which in turn helps improve overall patient satisfaction post-surgery.

Irisin's response to Resistance Exercise (RE) remains unclear. We investigated plasma and salivary irisin levels following acute moderate load/high volume (ML/HV) RE and explored correlations with muscle damage markers. Eight healthy, resistance-trained young males (23.3±2.5 yrs) completed one ML/HV RE session (full-body, 30 sets to failure, 70% 1RM). Plasma/saliva irisin, plasma Creatine Kinase (CK), and Visual Analogue Scale (VAS) for muscle soreness were assessed at baseline, 15 min, 24h, and 48h post-exercise. Plasma irisin increased significantly by ~9% (p=0.01) and salivary irisin by ~4% (p=0.02) at 15 min post-exercise, returning towards baseline by 24h. A strong correlation (rho=0.8, p=0.03) existed between percentage changes in plasma and salivary irisin at 15 min. CK and VAS peaked at 24h (p<0.001; p=0.02 vs 48h, respectively), but showed no significant correlation with irisin changes. Acute ML/HV RE elicits a transient increase in plasma and salivary irisin. Saliva may be a useful non-invasive proxy for irisin changes post-RE. This acute irisin response appears independent of EIMD markers in this population. Findings require confirmation in larger studies.

The European Society for Clinical Evaluation of Balance Disorders (ESCEBD), based in Nancy, France, has been meeting yearly since 2005 to discuss equilibrium-related themes that are not yet clearly defined or standardized. One of our latest discussions was with regard to outlining strategies of internal and external compensation that may be used to cope with balance disorders. A Committee was elected to discuss the mechanisms of compensation that may be involved in coping with balance system disorders. Compensation, referring to the immediate or short-term adaptive mechanisms that are used to counterbalance the effects of deficiencies that disrupt balance maintenance, can include alternative strategies, resources, or environmental supports to overcome deficits or challenges associated with a deficiency. The strategies can be internal (i.e. utilizing the individual's own multi-sensory neural integration, motor, and cognitive resources) or external (i.e. modifying the environment, or using assistive or adaptive devices) to reduce fall hazard and enhance safety. This report focuses principally on internal compensation, generated by sensorimotor processes of the central nervous system (CNS) in response to impairment of either sensory information (e.g. vestibular pathologies), the musculoskeletal system (e.g. lower limb amputation and myopathies) or the CNS itself (e.g. upper motor neuron syndrome). The multifactorial process of compensation may explain the limitations encountered by the CNS in compensating for complex bodily impairments and may also limit our understanding of how the CNS adapts to balance disorders. Newly developed devices, such as wearable sensory substitution devices, are on the horizon as possible tools.

The complexity of schizophrenia, particularly in cases resistant to traditional pharmacological treatments, poses significant challenges for clinicians and researchers. This systematic review synthesizes existing evidence on the effectiveness of deep brain stimulation in treating treatment-resistant schizophrenia. Utilizing the PRISMA 2020 guidelines, a comprehensive literature search was conducted in March 2025 using the "Connected Papers" tool and other sources such as Web of Science, PubMed, PsycINFO, Embase, and Scopus, focusing on studies related to "deep brain stimulation," "treatment-resistant schizophrenia," and "refractory schizophrenia." Four studies met the eligibility criteria, revealing that deep brain stimulation targeting specific brain regions, particularly the nucleus accumbens, can lead to significant symptomatic improvements in approximately 30% of patients unresponsive to conventional antipsychotics. Despite ten adverse events recorded across thirteen procedures, deep brain stimulation offers potential benefits for select individuals. While not universally superior to existing treatments, deep brain stimulation could inform clinical practice and decision-making, highlighting its role in multidisciplinary treatment frameworks. The findings underscore the importance of innovative therapeutic approaches in psychiatry and suggest broader implications for neuromodulation techniques across various psychiatric and neurological disorders, promoting personalized and effective treatment paradigms in mental healthcare.

Tessitore, Costelli et al. were among the first to report a previously unnoticed loss of heart mass in cachectic mice suffering from a severe tumor burden. At the time both the general consensus definition of cachexia and the cancer cachexia classification did not exist. In particular, cancer cachexia is a syndrome characterized by muscle wasting leading to body weight loss in the presence of cancer. More recently, Zhou et al. highlighted once more the existence of a tumor-induced loss of heart mass in a murine model of cancer cachexia. This study generated a new line of research aimed at exploring the mechanisms underlying cardiac wasting in the presence of cancer. Cardiac wasting in the presence of cancer-induced cachexia is distinct from and other than cardiac cachexia, i.e. the atrophy of skeletal muscle induced by cardiac pathologies. However, over the years we have noticed that expressions such as "cardiac cachexia", "cardiac atrophy", and "muscle cachexia"  - that sound alike but are very different - are often mistakenly used. In particular, we are afraid that these misunderstandings may suggest to inexperienced readers that cardiac cachexia is a form of cardiac muscle atrophy, which is not. To add insult to injury, some authors use the expression "muscle cachexia" meaning muscle atrophy, which, as a consequence, may suggest to naive readers that cardiac cachexia is a form of cardiac muscle atrophy. We aim here to clarify the terminology describing these conditions, so as to avoid the misleading use of related expressions: cardiac atrophy and cardiac cachexia may sound alike but are very different. In particular, it is the expression "cardiac cachexia" that raises a problem of ambiguity and should be handled with care. [...].

Cognitive impairment significantly affects physical function in dementia patients, but variations across dementia types and levels of cognitive decline remain unclear. This retrospective cross-sectional study included 874 patients (80.75 ± 8.00 years; 60.4% female) with different dementia types and cognitive impairment levels. Six physical function tests were administered: the De Morton Mobility Index (DEMMI), 6-minute walking test (6MTW), 10-meter walking test (10MWT), hand grip strength (HGS), 30-second chair stand (30sSTS), and the timed "Up & Go" test (TUG). Cognitive function was assessed using the Mini-Mental State Examination (MMSE). The Mild Cognitive Impairment (MCI) group outperformed Alzheimer's Dementia (AD) and Vascular Dementia (VaD) on DEMMI, 30sSTS and HGS (p < 0.001, η² = 0.012 to 0.052). Differences in the 6MWT were significant in ANOVA but disappeared after adjusting for sex and age (p = 0.066). Severe cognitive impairment was linked to significantly lower physical performance across all measures (p < 0.001, η² = 0.037 to 0.064). Physical function profiles vary by dementia type and cognitive decline level, highlighting the need for targeted interventions to address specific physical challenges.

The discovery that skeletal muscle can respond adaptively to use, even to the extent of re-expressing its genome, overturned two paradigms and led to new insights into gene regulation and a variety of clinical applications.

We describe the case of a 54-year-old patient, who was admitted to our Rehabilitation Unit with diagnosis of Guillain-Barré Syndrome (GBS). Neurophysiological investigation revealed an axonal polyneuropathy, with impairment of the motor component and preserved sensory function. Despite rapid diagnosis, therapeutic treatment and customized progressive rehabilitation program, nine months after the onset of the disease he presented severe motor sequelae and functional impairment. Patient's hospitalization lasted about two months, while he performed a conventional rehabilitation training. Besides, he underwent a 4-week comprehensive rehabilitation treatment, including both conventional and robotic multidimensional trainings, for 5 1-h sessions per week. Despite the residual global impairment, this treatment, specifically tailored on patient's skills and progress, promoted improvements in functional abilities such as motricity, trunk control, and activities of daily living. Therefore, this case report evidenced the feasibility and efficacy of a multidimensional robotic therapeutic approach along with conventional treatment in the post-acute phase of GBS.