Skeletal Muscle Of Patients Research Articles

Deep learning using preoperative magnetic resonance imaging information to predict early recovery of urinary continence after robot-assisted radical prostatectomy.

To investigate whether a deep learning model from magnetic resonance imaging information is an accurate method to predict the risk of urinary incontinence after robot-assisted radical prostatectomy. This study included 400 patients with prostate cancer who underwent robot-assisted radical prostatectomy. Patients using 0 or 1 pad/day within 3months after robot-assisted radical prostatectomy were categorized into the "good" group, whereas the other patients were categorized into the "bad" group. Magnetic resonance imaging DICOM data, and preoperative and intraoperative covariates were assessed. To evaluate the deep learning models from the testing dataset, their sensitivity, specificity and area under the receiver operating characteristic curve were analyzed. Gradient-weighted class activation mapping was used to visualize the regions of deep learning interest. The combination of deep learning and naive Bayes algorithm using axial magnetic resonance imaging in addition to clinicopathological parameters had the highest performance, with an area under the receiver operating characteristic curve of 77.5% for predicting early recovery from post-prostatectomy urinary incontinence, whereas machine learning using clinicopathological parameters only achieved low performance, with an area under the receiver operating characteristic curve of 62.2%. The gradient-weighted class activation mapping methods showed that deep learning focused on pelvic skeletal muscles in patients in the good group, and on the perirectal and hip joint regions in patients in the bad group. Our results suggest that deep learning using magnetic resonance imaging is useful for predicting the severity of urinary incontinence after robot-assisted radical prostatectomy. Deep learning algorithms might help in the choice of treatment strategy, especially for prostate cancer patients who wish to avoid prolonged urinary incontinence after robot-assisted radical prostatectomy.

Role of Myokines in Myositis Pathogenesis and Their Potential to be New Therapeutic Targets in Idiopathic Inflammatory Myopathies.

Idiopathic inflammatory myopathies (IIM) represent a heterogeneous group of autoimmune diseases whose treatment is often a challenge. Many patients, even after immunosuppressive therapy, do not respond to treatment, so new alternatives have been sought for this. Therefore, other signaling pathways that could contribute to the pathogenesis of myositis have been investigated, such as the expression of myokines in skeletal muscle in response to the inflammatory process. In this review, we will refer to these muscle cytokines that are overexpressed or downregulated in skeletal muscle in patients with various forms of IIM, thus being able to contribute to the maintenance of the autoimmune process. Some muscle cytokines, through their antagonistic action, may be a helpful contributor to the disease modulation, and thus, they could represent personalized treatment targets. Here, we consider the main myokines involved in the pathogenesis of myositis, expressing our view on the possibility of using them as potential therapeutic targets: interleukins IL-6, IL-15, and IL-18; chemokines CXCL10, CCL2, CCL3, CCL4, CCL5, and CCL20; myostatin; follistatin; decorin; osteonectin; and insulin-like 6. An interesting topic regarding the complex connection between myokines and noninflammatory pathways implied in IIM has also been briefly described, because it is an important scientific approach to the pathogenesis of IIM and can be a therapeutic alternative to be considered, especially for the patients who do not respond to immunosuppressive treatment.

Aerobic Exercise Training in Patients With mtDNA-Related Mitochondrial Myopathy.

In patients with mitochondrial DNA (mtDNA) mutation, a pathogenic mtDNA mutation is heteroplasmically distributed among tissues. The ratio between wild-type and mutated mtDNA copies determines the mtDNA mutation load of the tissue, which correlates inversively with oxidative capacity of the tissue. In patients with mtDNA mutation, the mutation load is often very high in skeletal muscle compared to other tissues. Additionally, skeletal muscle can increase its oxygen demand up to 100-fold from rest to exercise, which is unmatched by any other tissue. Thus, exercise intolerance is the most common symptom in patients with mtDNA mutation. The impaired oxidative capacity in skeletal muscle in patients with mtDNA mutation results in limitation in physical capacity that interferes with daily activities and impairs quality of life. Additionally, patients with mitochondrial disease due to mtDNA mutation often live a sedentary lifestyle, which further impair oxidative capacity and exercise tolerance. Since aerobic exercise training increase mitochondrial function and volume density in healthy individuals, studies have investigated if aerobic training could be used to counteract the progressive exercise intolerance in patients with mtDNA mutation. Overall studies investigating the effect of aerobic training in patients with mtDNA mutation have shown that aerobic training is an efficient way to improve oxidative capacity in this condition, and aerobic training seems to be safe even for patients with high mtDNA mutation in skeletal muscle.

MEF2c-Dependent Downregulation of Myocilin Mediates Cancer-Induced Muscle Wasting and Associates with Cachexia in Patients with Cancer.

Skeletal muscle wasting is a devastating consequence of cancer that contributes to increased complications and poor survival, but is not well understood at the molecular level. Herein, we investigated the role of Myocilin (Myoc), a skeletal muscle hypertrophy-promoting protein that we showed is downregulated in multiple mouse models of cancer cachexia. Loss of Myoc alone was sufficient to induce phenotypes identified in mouse models of cancer cachexia, including muscle fiber atrophy, sarcolemmal fragility, and impaired muscle regeneration. By 18 months of age, mice deficient in Myoc showed significant skeletal muscle remodeling, characterized by increased fat and collagen deposition compared with wild-type mice, thus also supporting Myoc as a regulator of muscle quality. In cancer cachexia models, maintaining skeletal muscle expression of Myoc significantly attenuated muscle loss, while mice lacking Myoc showed enhanced muscle wasting. Furthermore, we identified the myocyte enhancer factor 2 C (MEF2C) transcription factor as a key upstream activator of Myoc whose gain of function significantly deterred cancer-induced muscle wasting and dysfunction in a preclinical model of pancreatic ductal adenocarcinoma (PDAC). Finally, compared with noncancer control patients, MYOC was significantly reduced in skeletal muscle of patients with PDAC defined as cachectic and correlated with MEF2c. These data therefore identify disruptions in MEF2c-dependent transcription of Myoc as a novel mechanism of cancer-associated muscle wasting that is similarly disrupted in muscle of patients with cachectic cancer. SIGNIFICANCE: This work identifies a novel transcriptional mechanism that mediates skeletal muscle wasting in murine models of cancer cachexia that is disrupted in skeletal muscle of patients with cancer exhibiting cachexia.

Ação da L-glutamina via oral por 7 dias na estrutura e função muscular de pacientes com HIV/AIDS em uso de terapia antirretroviral

Introduction: Patients infected with the human immunodeficiency virus (HIV) have prolonged survival with the use of antiretroviral therapy (ART). The chronic evolution of the disease allows the appearance of changes in several systems, including nutritional impairment and muscular function. The objective of this study is to observe the action of orally administered L-glutamine on the skeletal muscles of patients with HIV/AIDS in chronic use of ART. Methods: Seropositive patients adhered to ART were divided into two groups: a) GG - glutamine group (n=10) and b) GM - maltodextrin group (n=9). The groups were supplemented orally and for 7 days, GG with 0.5 mg/kg/day of L-glutamine and GM with 0.5 mg/kg/day of maltodextrin. The analyzed variables were: parameters of muscle strength and muscle mass, evaluated by collection instruments, respectively, dynamometry and bioimpedance. Results: There was a reduction in body weight (p=0.043) and an increase in biceps strength (p=0.006) in GG. In GM, there was an increase in body weight, accompanied by gain of muscle mass and loss of fat amount, without causing significant changes in body mass index. Conclusion: L-glutamine, orally supplemented, for 7 days, increased the muscle strength of the biceps of seropositive patients taking ART.

The psoas muscle index distribution and influence of outcomes in an Asian adult trauma population: an alternative indicator for sarcopenia of acute diseases.

Sarcopenia has been shown to be an independent negative predictor in various diseases. The measurement of pre-defined criteria of skeletal muscle in patients with acute disease is usually unavailable. Therefore, we evaluate the psoas muscle area based on computed tomography (CT) imaging as an alternative for sarcopenia in an Asian trauma population. 939 trauma patients were enrolled and had CT imaging performed primarily for trauma indications. The cross-sectional area of psoas muscle at the base of the fourth lumbar vertebral was measured on these CTs. Psoas muscle index (PMI) was calculated and analyzed to determine sex-specific cut-off values to define the "extremely low psoas muscle index" (ELPMI) group. Psoas muscle index was significantly higher in males (1065.09 ± 230.51mm2/m2in males vs 719.57 ± 147.39 mm2/m2in females, p < 0.001) and decreased gradually with aging (p < 0.001). PMI of the subset of patients aged 18-40 (n = 462) weas analyzed to determine sex-specific cut-off values for ELPMI. PMI cut-off values for ELPMI (2 SD below mean) were 675mm2/m2 for males and 490mm2/m2 for females. The entire trauma cohort was further analyzed, and ELPMI was identified as an independent risk factor for a longer length of intensive unit stay (β coefficient = 3.881, p = 0.011). Data from young trauma adults were used to establish cut-off values for ELPMI, which is a longer ICU stay predictor. These cut-off values for ELPMI may apply to other acute disease entities.

Cardiometabolic risk factor clustering in patients with deficient branched‐chain amino acid catabolism: A case‐control study

Classical organic acidemias (OAs) result from defective mitochondrial catabolism of branched-chain amino acids (BCAAs). Abnormal mitochondrial function relates to oxidative stress, ectopic lipids and insulin resistance (IR). We investigated whether genetically impaired function of mitochondrial BCAA catabolism associates with cardiometabolic risk factors, altered liver and muscle energy metabolism, and IR. In this case-control study, 31 children and young adults with propionic acidemia (PA), methylmalonic acidemia (MMA) or isovaleric acidemia (IVA) were compared with 30 healthy young humans using comprehensive metabolic phenotyping including in vivo 31 P/1 H magnetic resonance spectroscopy of liver and skeletal muscle. Among all OAs, patients with PA exhibited abdominal adiposity, IR, fasting hyperglycaemia and hypertriglyceridemia as well as increased liver fat accumulation, despite dietary energy intake within recommendations for age and sex. In contrast, patients with MMA more frequently featured higher energy intake than recommended and had a different phenotype including hepatomegaly and mildly lower skeletal muscle ATP content. In skeletal muscle of patients with PA, slightly lower inorganic phosphate levels were found. However, hepatic ATP and inorganic phosphate concentrations were not different between all OA patients and controls. In patients with IVA, no abnormalities were detected. Impaired BCAA catabolism in PA, but not in MMA or IVA, was associated with a previously unrecognised, metabolic syndrome-like phenotype with abdominal adiposity potentially resulting from ectopic lipid storage. These findings suggest the need for early cardiometabolic risk factor screening in PA.

TDP-43 promotes the formation of neuromuscular synapses through the regulation of Disc-large expression in Drosophila skeletal muscles

BackgroundThe ribonuclear protein TDP-43 has been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS), with genetic mutations being linked to the neurological symptoms of the disease. Though alterations in the intracellular distribution of TDP-43 have been observed in skeletal muscles of patients suffering from ALS, it is not clear whether such modifications play an active role in the disease or merely represent an expression of muscle homeostatic mechanisms. Also, the molecular and metabolic pathways regulated by TDP-43 in the skeletal muscle remain largely unknown. Here, we analyze the function of TBPH, the Drosophila melanogaster ortholog of TDP-43, in skeletal muscles.ResultsWe modulated the activity of TDP-43 in Drosophila muscles by means of RNA interference and observed that it is required to promote the formation and growth of neuromuscular synapses. TDP-43 regulated the expression levels of Disc-large (Dlg), and restoring Dlg expression either in skeletal muscles or in motoneurons was sufficient to suppress the locomotive and synaptic defects of TDP-43-null flies. These results were validated by the observation of a decrease in Dlg levels in human neuroblastoma cells and iPSC-differentiated motoneurons derived from ALS patients, suggesting similar mechanisms may potentially be involved in the pathophysiology of the disease.ConclusionsOur results help to unveil the physiological role of TDP-43 in skeletal muscles as well as the mechanisms responsible for the autonomous and non-autonomous behavior of this protein concerning the organization of neuromuscular synapses.

Assessment of skeletal muscle in patients with stable coronary artery disease: clinical significance and associations

Aim. To assess skeletal muscle in patients with stable coronary artery disease (CAD) before coronary artery bypass grafting (CABG), the factors associated with its deterioration, and possible clinical significance. Material and methods. The study included 77 patients (68 men and 9 women, aged 51-69 years) who were admitted to the cardiology department for pre-CABG testing. All patients underwent routine laboratory and instrumental examination. In addition, the subjects underwent a six-minute walk test and lower limb muscle strength testing. Participants were divided into two groups: group 1 (n=45; 58,44%) — patients with mean strength score of lower limb extensor muscles less than the median (mean 20 kg/s), group 2 (n=32; 41,56%) — more than the median (mean 32,5 kg/s). The groups were comparable in main demographic and anthropometric parameters, risk factors for atherosclerosis, concomitant pathology, history of atherothrombotic events, laboratory and instrumental data, as well as CABG outcomes. Results. When assessing the skeletal muscle in CAD patients before surgery, the median lower limb extensor strength score was 25 kg/s. Patients from group 1 had a higher incidence of myocardial infarction (MI) in history (p=0,021), decreased left ventricle ejection fraction (p=0,025), increased heart rate (p=0,025) and leukocyte count (p=0,036). In such patients, there was a significant increase of postoperative complications of CABG surgery (p=0,003). According to multivariate regression analysis, MI history (p = 0.011) and a higher leukocyte count (p=0,042) were independent predictors of decrease in lower limb muscle strength. Conclusion. The obtained results can be used in the preparation of rehabilitation programs for patients before CABG surgery.

Assessment of skeletal muscle in patients with stable coronary artery disease: clinical significance and associations

Assessment of skeletal muscle in patients with stable coronary artery disease: clinical significance and associations

Alterations in activin A–myostatin–follistatin system associate with disease activity in inflammatory myopathies

The aim of this study was to investigate the systemic and skeletal muscle levels of atrophy-associated myokines in patients with idiopathic inflammatory myopathies (IIM) and their association with clinical characteristics of myositis. A total of 94 IIM patients and 162 healthy controls were recruited. Of those, 20 IIM patients and 28 healthy controls underwent a muscle biopsy. Circulating concentrations of myostatin, follistatin, activin A and TGF-β1 were assessed by ELISA. The expression of myokines and associated genes involved in the myostatin signalling pathway in muscle tissue was determined by real-time PCR. We report decreased levels of circulating myostatin (median 1817 vs 2659 pg/ml; P = 0.003) and increased follistatin (1319 vs 1055 pg/ml; P = 0.028) in IIM compared with healthy controls. Activin A levels were also higher in IIM (414 vs 309 pg/ml; P = 0.0005) compared with controls. Myostatin was negatively correlated to muscle disease activity assessed by physician on visual analogue scale (MDA) (r = -0.289, P = 0.015) and positively to manual muscle testing of eight muscles (r = 0.366, P = 0.002). On the other hand, follistatin correlated positively with MDA (r = 0.235, P = 0.047). Gene expression analysis showed higher follistatin (P = 0.003) and myostatin inhibitor follistatin-like 3 protein (FSTL3) (P = 0.008) and lower expression of activin receptor type 1B (ALK4) (P = 0.034), signal transducer SMAD3 (P = 0.023) and atrophy marker atrogin-1 (P = 0.0009) in IIM muscle tissue compared with controls. This study shows lower myostatin and higher follistatin levels in circulation and attenuated expression of myostatin pathway signalling components in skeletal muscle of patients with myositis, a newly emerging pattern of the activin A-myostatin-follistatin system in muscle wasting diseases.

Search for Mechanisms of Pathogenesis of Atrophy and Regeneration of Skeletal Muscles in Patients in Long-Term Unconsciousness

Search for Mechanisms of Pathogenesis of Atrophy and Regeneration of Skeletal Muscles in Patients in Long-Term Unconsciousness

Ras associated with diabetes may play a role in fracture nonunion development in rats

BackgroundRad is the prototypic member of a subfamily of Ras-related small G-proteins and is highly expressed in the skeletal muscle of patients with type II diabetes. Our previous microarray analysis suggested that Rad may mediate fracture nonunion development. Thus, the present study used rat experimental models to investigate and compare the gene and protein expression patterns of both Rad and Rem1, another RGK subfamily member, in nonunions and standard healing fractures.MethodsStandard healing fractures and nonunions (produced via periosteal cauterization at the fracture site) were created in the femurs of 3-month-old male Sprague-Dawley rats. At post-fracture days 7, 14, 21, and 28, the fracture callus and fibrous tissue from the standard healing fractures and nonunions, respectively, were harvested and screened (via real-time PCR) for Rad and Rem1 expression. The immunolocalization of both encoded proteins was analyzed at post-fracture days 14 and 21. At the same time points, hematoxylin and eosin staining was performed to identify the detailed tissue structures.ResultsResults of real-time PCR analysis showed that Rad expression increased significantly in the nonunions, compared to that in the standard healing fractures, at post-fracture days 14, 21, and 28. Conversely, immunohistochemical analysis revealed the immunolocalization of Rad to be similar to that of Rem1 in both fracture types at post-fracture days 14 and 21.ConclusionsRad may mediate nonunion development, and thus, may be a promising therapeutic target to treat these injuries.

The role of muscle tissue in the pathogenesis of chronic heart failure — the potential of exposure (FORMA study)

Aim. To determine whether the skeletal muscle of patients with chronic heart failure (CHF) retains the ability to regenerate and grow; to compare the effectiveness of long aerobic trainings, calculated by an individualized method, and conventionally calculated trainings (VO 2 peak values), in relation to the severity of heart failure, exercise tolerance (ET), and ergoreflex activity (ERGO). Material and methods . The study included 297 patients with stable III functional class (FC) CHF, receiving optimal therapy. The presence of heart failure was found in all patients at least 6 months before the start of the study (age — 18-65 years, body mass index (BMI) — 19-28 kg/height, m 2 . Initially, the study performed a cardiorespiratory test (CRT) with an assessment of gas composition, acid-base balance of the blood and ERGO activity. Patients were randomized into 2 groups: experimental (EG) and control (CG). For EG, based on the determination of the lactate threshold (LT), after 1 and 3 months the CRT was repeated and the training walking mode was dynamically recounted according to the new LT level. For CG, the training walking mode was calculated based on the VO2peak values. All patients trained for 6 months. At the end of the training, diagnostic CRT was performed, and the activity of EGO was evaluated. Eleven patients with CHF and 3 healthy donors before the start of the training underwent a biopsy of the gastrocnemius muscle. Results. It was shown that the potential for muscle differentiation of satellite skeletal muscle precursor cells obtained from patients with CHF with a reduced ejection fraction (HFrEF) does not differ in vitro from the potential of satellite cells of healthy donors. After 6 months of training, the severity of CHF decreased to FC II in 75% of EG patients, and among CG patients — in 44%; the main indicators of the stages of compensatory mechanisms activation during physical exertion (VO 2 LT and VO 2 peak) in EG increased more than in the CG (10,8±0,4, 18,7±0,7 ml/min/kg and 9,5±0,8, 15,3±0,9 ml/min/kg, with p 1 <0,01, p 2 <0,05, p 3 <0,01, respectively). Conclusion. In vitro, the potential for muscle differentiation, regeneration and growth of satellite skeletal muscle precursor cells obtained from patients with HFrEF does not differ from the potential of satellite cells of healthy donors. Aerobic training in patients with III FC chronic heart failure calculated by definition of LT, relating to safety is not worse than the results calculated by the level of VO 2 peak. Aerobic training in patients with III FC chronic heart failure calculated by definition of LT, compared with the usual mode of training walking, significantly reduce the activity of ergoreflex, increase ET, reduce the severity of CHF. In patients with III FC CHF, training walking for more than 1,5 hours/day determined by the level of LT, contributes to the development of physiological reverse myocardial remodeling to a greater extent than aerobic training calculated by the conventional method.

Correction of Glycogen Synthase Kinase 3β in Myotonic Dystrophy 1 Reduces the Mutant RNA and Improves Postnatal Survival of DMSXL Mice.

Myotonic dystrophy type 1 (DM1) is a multisystem neuromuscular disease without cure. One of the possible therapeutic approaches for DM1 is correction of the RNA-binding proteins CUGBP1 and MBNL1, misregulated in DM1. CUGBP1 activity is controlled by glycogen synthase kinase 3β (GSK3β), which is elevated in skeletal muscle of patients with DM1, and inhibitors of GSK3 were suggested as therapeutic molecules to correct CUGBP1 activity in DM1. Here, we describe that correction of GSK3β with a small-molecule inhibitor of GSK3, tideglusib (TG), not only normalizes the GSK3β-CUGBP1 pathway but also reduces the mutant DMPK mRNA in myoblasts from patients with adult DM1 and congenital DM1 (CDM1). Correction of GSK3β in a mouse model of DM1 (HSALR mice) with TG also reduces the levels of CUG-containing RNA, normalizing a number of CUGBP1- and MBNL1-regulated mRNA targets. We also found that the GSK3β-CUGBP1 pathway is abnormal in skeletal muscle and brain of DMSXL mice, expressing more than 1,000 CUG repeats, and that the correction of this pathway with TG increases postnatal survival and improves growth and neuromotor activity of DMSXL mice. These findings show that the inhibitors of GSK3, such as TG, may correct pathology in DM1 and CDM1 via several pathways.

Diabetic Muscle Infarction: A Rare End-Organ Vascular Complication of Diabetes

Diabetic muscle infarction (DMI) is a rare microvascular complication of spontaneous ischemic necrosis of skeletal muscle in patients with poorly controlled diabetes. We herein describe the case of a 26-year-old woman with a history of type I diabetes and accompanying diabetic microvascular complications of neuropathy, nephropathy and retinopathy, who presented with sudden onset of swelling and sharp pain in her bilateral thighs. T2-weighted MRI imaging revealed subcutaneous edema and sub-fascial, hyper-intense enhancement of proximal thigh musculature. DMI has a relatively non-specific clinical presentation; therefore, physician awareness is key for early diagnosis, as aggressive management has been associated with poor patient outcomes. With poor long-term prognosis and high reoccurrence, DMI acts as an indicator of vascular end-organ damage.

Skeletal muscle DNA methylation modifications and psychopharmacologic treatment in bipolar disorder

Both severe mental illness and atypical antipsychotics have been independently associated with insulin resistance and weight gain. Altered regulation of skeletal muscle DNA methylation may play a role. We aimed to evaluate DNA methylation modifications in human skeletal muscle samples to further understand its potential role in the metabolic burden observed in psychiatric patients and psychopharmacologic treatment. Subjects were included in our study if they had a bipolar diagnosis and were currently treated with a mood stabilizer or atypical antipsychotic. A healthy control group free of psychiatric or physical disease was also included for comparisons. Anthropometric, BMI and hemoglobin A1C (HbA1C%) were measured. Fasting skeletal muscle biopsies were obtained and methylation levels of 5-methycytosine (5-mC), 5-hydroxymethylcytosine (5-hmC) and 5-formylcytosine (5-fC) were measured. Skeletal muscle global methylation of 5-mC and 5-fC were significantly higher in bipolar subjects compared to healthy controls. 5-mC was significantly higher in the AAP group compared to the mood stabilizer group. Significant correlations were observed between 5-fC methylation and HbA1C%. Our findings suggest that psychiatric disease and treatment may influence some methylation measures in the skeletal muscle of patients with bipolar disorder, which may be further influenced by medication treatment.

Upregulation of programmed cell death ligand 1 expression in the skeletal muscle of patients with myasthenia gravis

Upregulation of programmed cell death ligand 1 expression in the skeletal muscle of patients with myasthenia gravis

P.387A novel in situ hybridisation (ISH) assay mapping the in-frame pseudoexon 11 (pE11) expression in cultured dermal fibroblasts (CDF) and skeletal muscle in patients with severe collagen VI disease due to a deep intronic mutation in COL6A1

P.387A novel in situ hybridisation (ISH) assay mapping the in-frame pseudoexon 11 (pE11) expression in cultured dermal fibroblasts (CDF) and skeletal muscle in patients with severe collagen VI disease due to a deep intronic mutation in COL6A1

P.303Ultrashort-TE magnetic resonance imaging does not reveal alterations of short-T2-signal fraction in patients with congenital myopathies

To look for alterations of the short-T2 NMR-signal fraction in the skeletal muscle of patients with congenital myopathies (CM). Non-invasive quantification of endomysial fibrosis would constitute an important biomarker of disease progression and response to treatments, but it still remains an open problem. It has been previously stated that the short-T2 signal observed in UTE MRI could reflect extra cellular matrix content, suggesting UTE as a good candidate to fulfil this objective. Fat-fraction (FF), T2*, and short-T2-fraction (sT2f) maps were extracted in the calf of 16 controls and 10 patients with CM. Regions of interest (ROIs) were traced in the Soleus, Gastrocnemius Lat. and Med. muscles, which presented no visible aponeurosis. The average and standard deviation, of FF, T2* and sT2f were calculated for each ROI. Both quantities were compared between the two groups (Ctrl and CM) using one-way ANOVA. FF, FF heterogeneity and T2* heterogeneity were increased in CM patients (p<0.001). T2* correlated with FF (r=-0.24, p<0.001) and FF heterogeneity (r=-0.33, p<0.001). T2* heterogeneity correlated with FF (r=0.70, p<0.001) and FF heterogeneity (r=0.58, p<0.001). No differences were observed for sT2f and T2*. sT2f correlated with FF (r=-0.50, p<0.001) and FF heterogeneity (r=-0.33, p<0.001). Increased T2* heterogeneity probably reflects the differences of T2* characterizing muscle and adipose tissue, as evidenced by the positive correlation between T2* heterogeneity and FF. Also, an increase of the local magnetic susceptibility gradients induced by fatty infiltration might lead to a reduction of T2*. Although fibrosis is one of the pathologic features of CM, no alteration of sT2f was observed in patients. One possible explanation is that the short-T2 signal observed in UTE MRI arises from a large ensemble of macromolecules, including the contractile apparatus, and/or their hydration layers. So the replacement of myofibers by connective tissue might not significantly impact on the observed sT2f.