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Background Motor symptoms of spinal cord injury (SCI) considerably impair quality of life and are associated with a high risk of secondary diseases. So far, no pharmacological treatment is available for these symptoms. Therefore, we conducted a randomized, double‐blinded, placebo‐controlled study in dogs with spontaneous SCI due to disc herniation to test whether a reduction of spinal inhibitory activity by intramuscular injections of tetanus neurotoxin (TeNT) alleviates motor symptoms such as muscle atrophy or gait function. Methods To this end, 25 dogs were treated with injections of either TeNT or placebo into their paretic hindlimb muscles. Effects of TeNT on muscle thickness were assessed by ultrasound, while effects on gait function were measured using the modified functional scoring system in dogs. Results Four weeks after the TeNT injections, muscle thickness of the gluteus medius muscle (before median 1.56 cm [inter‐quartile range IQR 1.34–1.71 cm] and after median 1.56 cm [IQR 1.37–1.85 cm], P‐value 0.0133) as well as of the rectus femoris muscle (before median 0.76 cm [IQR 0.60–0.98 cm] and after median 0.93 cm [IQR 0.65–1.05 cm], P‐value 0.0033) significantly increased in the TeNT group. However, there was no difference in gait function between the TeNT and placebo groups. The treatment was well tolerated by all dogs without any signs of generalized tetanus symptoms or any spreading of effects beyond the lumbar level of the injected hindlimbs. Conclusions With regard to the beneficial effects on muscle thickness, intramuscular injections of TeNT represent the first pharmacological approach that focally reverses muscle atrophy in SCI. Moreover, the study data support the safety of this treatment when TeNT is used at low dose.

In this study, 10 fish species, Jayan flounder ( Pseudorhombus javanicus ); Oriental sole ( Eurgglossa arientalis ); Oange-spotted grouper ( Epinephelus coioides ); Blacktip trevally ( Caranx heberi ); Towbar seabream ( Acanthopagrus bifascia ); Smalltooth emperor ( Lethrinus microdon ); Spangled emperio ( Lethrinus nebulous ); Sharptooth hammer croaker ( Johnius vogleri ); Bigeye croaker ( Pennahia anea ) and Redspine thread bream ( Nemipterus nemurus ), were examined in El-Jubail province, Saudi Arabia, Arabian Gulf region over three years from 2017 to 2020. The examined fish species showed muscular atrophy in a total percent of 1.1%, but with variable percentages of affections in each species. The highest incidence (2.06%) was oberved in Spangled emperior ( Lethrinus nebulous ) while the lowest incidence (0.40%) was in Orange spotted grouper ( Epinephelus coioides ) and Smalltooth emperor ( Lethrinus microdon ). The affected fishes appeared with sunken eyes, severe emaciation, and prominent loss of skeletal muscle mass. During dissection, the muscular tissue in some examined species was rough while in others, it was edematous and gelatinous, and the internal organs of all fishes were atrophied. For routine histopathological examination, the tissue samples were fixed in 10% buffered neutral formalin. The examined tissue sections of the affected muscles showed variable degrees of histopathological changes depending on the species. Vacuolation of muscle fibers, Zenker’s necrosis and myophagia were common in some species, while melanophores aggregation, edema, and hemorrhages were the most commonly observed changes in others. This study focused on the impact of this myodegenerative disease on the marketability of these edible fish species. Further investigation is needed to understand the impact of genetic predisposition, environmental pollution and other etiological agents on the occurrence of this phenomenon in this location.

Background The Leizhou Black Goat (LZBG), a prominent breed in tropical China’s meat goat industry, frequently exhibits inherent muscle atrophy and malnutrition-related traits. Particularly, muscles critical for support, such as the legs, often display severe symptoms. This study aimed to investigate the differential genes and signaling pathways influencing muscle development and atrophy across various muscle locations in LZBG from a muscular atrophy-affected family. Results Differential expression analysis revealed 536 mRNAs with significant differences across three muscle groups. Marked variations in mRNA expression patterns were observed between leg and back muscles versus abdominal muscles, reflecting characteristics similar to those found in limb-girdle muscular dystrophy. The analysis identified several key differentially expressed genes implicated in muscle development and atrophy, including PITX1 , COLQ , ZIC1 , SBK2 , and TBX1 , showed Significant difference expression levels and expression patterns with normal individuals. Functional annotation and protein interaction network analysis indicated enrichment of these genes in muscle-related pathways. Protein interaction network analysis identified five key clusters related to muscle function and development. Conclusion The mRNA expression patterns of the leg and back muscles in LZBG from a muscular atrophy-affected family differed significantly from those of the abdominal muscle, displaying typical characteristics of limb-girdle muscular dystrophy. Genes such as PITX1 , TBX1 , SBK2 , TCAP , and COLQ were identified as key regulators of muscle development and contributors to muscle atrophy. These findings enhance our understanding of the mechanisms underlying muscular atrophy in LZBGs. The identification of key genes and pathways provides valuable insights for developing future breeding strategies aimed at improving meat production efficiency.

Background Muscle atrophy and intramuscular fatty infiltration, as well as their association with prognosis, have not been quantified in dogs with spontaneous hypercortisolism (HC). Objective To quantitatively evaluate muscle atrophy and IM fatty infiltration in dogs with HC and determine their prognostic impact. Animals Fifty‐three dogs with HC and 66 control dogs without HC. Methods Retrospective cohort study. Medical records and computed tomography images obtained between 2014 and 2021 were evaluated. Kaplan‐Meier curves and log‐rank tests were used to analyze the effect of muscle atrophy and IM fatty infiltration on the prognosis of dogs with HC. Results Dogs with HC showed lower visually measured cross‐sectional area (VCSA) and cross‐sectional area based on attenuation (HCSA) than control dogs (median [interquartile range IQR]: 50.3 mm2/mm [36.2‐67.8] vs 66.7 mm2/mm [48.0‐85.9]; P < .001; 30.4 mm2/mm [13.7‐57.2] vs 54.8 mm2/mm [39.7‐71.5]; P < .001, respectively). Dogs with HC had lower epaxial muscle attenuation (L3HU) than control dogs (median [IQR]: 21.2 Hounsfield [HU] [12.4‐28.2] vs 33.2 HU [22.6‐43.6]; P < .001). Dogs with HC with lower HCSA or L3HU had shorter survival (median [IQR]: 670 days [222‐673] vs 949 days [788‐1074], P < .01; 523 days [132‐670] vs 949 days [756‐1074], P < .01, respectively) but not lower VCSA (median [IQR]: 673 days [132‐788] vs 949 days [523 to not applicable]; P = .30). Conclusion and Clinical Importance Hypercortisolism in dogs causes muscle atrophy and IM fatty infiltration and is associated with poor prognosis.

Background An E321G mutation in MYH1 was recently identified in Quarter Horses (QH) with immune‐mediated myositis (IMM) defined by a phenotype of gross muscle atrophy and myofiber lymphocytic infiltrates. Hypothesis/Objectives We hypothesized that the MYH1 mutation also was associated with a phenotype of nonexertional rhabdomyolysis. The objective of this study was to determine the prevalence of the MYH1 mutation in QH with exertional (ER) and nonexertional (nonER) rhabdomyolysis. Animals Quarter Horses: 72 healthy controls, 85 ER‐no atrophy, 56 ER‐atrophy, 167 nonER horses selected regardless of muscle atrophy. Methods Clinical and histopathologic information and DNA was obtained from a database for (1) ER > 2 years of age, with or without atrophy and (2) nonER creatine kinase (CK) ≥ 5000 U/L, <5 years of age. Horses were genotyped for E321G MYH1 by pyrosequencing. Results The MYH1 mutation was present in a similar proportion of ER‐no atrophy (1/56; 2%) and in a higher proportion of ER‐atrophy (25/85; 29%) versus controls (4/72; 5%). The MYH1 mutation was present in a significantly higher proportion of nonER (113/165; 68%) than controls either in the presence (39/42; 93%) or in absence (72/123; 59%) of gross atrophy. Lymphocytes were present in <18% of muscle samples with the MYH1 mutation. Conclusions and Clinical Importance Although not associated with ER, the MYH1 mutation is associated with atrophy after ER. The MYH1 mutation is highly associated with nonER regardless of whether muscle atrophy or lymphocytic infiltrates are present. Genetic testing will enhance the ability to diagnose MYH1 myopathies (MYHM) in QH.

Background Little is known about the spectrum of underlying disorders in dogs with unilateral masticatory muscle (MM) atrophy. Objectives To evaluate the clinical presentation, magnetic resonance imaging (MRI) findings, and outcome of dogs with unilateral MM atrophy. Animals Sixty‐three client‐owned dogs. Methods The medical database was retrospectively reviewed for dogs that underwent MRI for evaluation of unilateral MM atrophy. Imaging studies were reviewed and follow‐up information was obtained from telephone interviews. Results Presumptive trigeminal nerve sheath tumor (pTNST) was diagnosed in 30 dogs (47.6%); survival time varied from 1 day to 21 months (median, 5 months). Other extra‐axial mass lesions were observed in 13 dogs (20.6%); survival time varied from 6 days to 25 months (median, 2.5 months). In 18 dogs (28.6%), no abnormalities were observed on MRI; neurological signs only progressed in 1 dog. Diagnosis had a significant influence on the type of neurological abnormalities, with additional neurological deficits observed in most dogs with pTNST and in all dogs with other extra‐axial mass lesions. Diagnosis had a significant effect on euthanasia at the time of diagnosis and likelihood of neurological deterioration. Dogs with mass lesions were more likely to be euthanized or experience neurological deterioration, whereas these outcomes occurred less often in dogs in which no causative lesion could be identified. Conclusions and Clinical Importance Trigeminal nerve sheath tumors should not be considered the only cause of unilateral MM atrophy. Our results illustrate the importance of performing a neurological examination and MRI when evaluating dogs with unilateral MM atrophy.

The prevalence of clinical signs and factors triggering muscle atrophy and rhabdomyolysis associated with an MYH1 mutation in Quarter Horses and related breeds (QH) remain poorly understood. Determine the prevalence and potential triggers of atrophy and stiffness in horses homozygous reference (N/N), heterozygous (My/N), and homozygous (My/My) for the MYH1 mutation. Two-hundred seventy-five N/N, 100 My/N, and 10 My/My QH. A retrospective case-control study using a closed-ended questionnaire completed by clients of the Veterinary Genetics Laboratory at the University of California, Davis. History of clinical signs, disease, vaccination and performance were analyzed by genotype using contingency testing. Atrophy occurred in proportionately more horses with MYH1 (My) than N/N QH and more frequently in My/My than My/N QH (P < .001; My/My 8/10 [80%], My/N 17/100 [17%], N/N 29/275 [11%]). More My/My horses had rapid atrophy (P < .001), with recurrence in 50%. Fewer My/My horses recovered versus My/N QH (P < .001). Stiffness was common across genotypes (P = .100; My/My 4/10 [40%], My/N 18/100 [18%], N/N 48/275 [17%]). Three months before the observed atrophy and stiffness, 47% of MYH1 QH were vaccinated or had respiratory or gastrointestinal disease. Horses achieving 100% expected performance did not differ across genotypes (50% My/My, 71% My/N, 55% N/N), but, only 4/10 My/My QH were competing. My/N horses achieved national or world championships or both. Approximately 20% of My/N QH develop rapid atrophy. Atrophy is more common (80%) in homozygous My/My QH and less likely to resolve. Inciting causes such as vaccination and infection are inapparent in over half of cases.

Diabetes is characterized by high blood glucose level termed hyperglycemia affecting skeletal muscle structure and function by an unclear molecular mechanism. This study aimed to investigate the effect and underlying mechanism(s) of hyperglycemia on skeletal muscle both in vitro and in vivo. Treatment with hyperglycemic condition (25 mM) for 48 h significantly inhibited C2C12 myoblast proliferation detected by MTT assay whilst flow cytometry revealed an interruption of the cell cycle at subG1 and G2/M phases. An exposure to hyperglycemic condition significantly decreased the myosin heavy chain (MHC) protein expression in the differentiated myotube and tibialis anterior (TA) muscle of Wistar rats. In addition, the muscle cross-section area (MCA) of TA muscle in diabetic rats were significantly decreased compared to the non-diabetic control. Western blotting analysis of C2C12 myoblasts and differentiated myotubes revealed the increased expressions of cleaved-caspase-9 and cleaved-caspase-3, but not cleaved-caspase-8. Of note, these caspases in the TA muscles were not changed under hyperglycemic condition. Quantitative real-time polymerase chain reaction (qRT-PCR) of the hyperglycemic myoblasts and TA muscles revealed modulation of the gene expression of sirtuins (SiRTs). In C2C12 myoblasts, the expressions of SIRT1, SIRT2 and SIRT4 were upregulated whilst SIRT7 was downregulated. Meanwhile, the expressions of SIRT1, SIRT2 in TA muscles were upregulated whilst SIRT4 was downregulated. Taken together, this study showed that hyperglycemia induced cell cycle arrest and apoptosis in myoblasts, and protein degradation and atrophy in skeletal muscle most likely via modulation of SiRTs gene expression.

Cachexia, or muscle wasting, is a serious health threat to victims of radiological accidents or patients receiving radiotherapy. Here, we propose a non-human primate (NHP) radiation-induced cachexia model based on clinical and molecular pathology findings. NHP exposed to potentially lethal partial-body irradiation developed symptoms of cachexia such as body weight loss in a time- and dose-dependent manner. Severe body weight loss as high as 20–25% was observed which was refractory to nutritional intervention. Radiographic imaging indicated that cachectic NHP lost as much as 50% of skeletal muscle. Histological analysis of muscle tissues showed abnormalities such as presence of central nuclei, inflammation, fatty replacement of skeletal muscle and muscle fiber degeneration. Biochemical parameters such as hemoglobin and albumin levels decreased after radiation exposure. Levels of FBXO32 (Atrogin-1), ActRIIB and myostatin were significantly changed in the irradiated cachectic NHP compared to the non-irradiated NHP. Our data suggest NHP that have been exposed to high dose radiation manifest cachexia-like symptoms in a time- and dose-dependent manner. This model provides a unique opportunity to study the mechanism of radiation-induced cachexia and will aid in efficacy studies of mitigators of this disease.

Sleeping disease in rainbow trout is characterized by an abnormal swimming behaviour of the fish which stay on their side at the bottom of the tanks. This sign is due to extensive necrosis and atrophy of red skeletal muscle induced by the sleeping disease virus (SDV), also called salmonid alphavirus 2. Infections of humans with arthritogenic alphaviruses, such as Chikungunya virus (CHIKV), are global causes of debilitating musculoskeletal diseases. The mechanisms by which the virus causes these pathologies are poorly understood due to the restrictive availability of animal models capable of reproducing the full spectrum of the disease. Nevertheless, it has been shown that CHIKV exhibits a particular tropism for muscle stem cells also known as satellite cells. Thus, SDV and its host constitute a relevant model to study in details the virus-induced muscle atrophy, the pathophysiological consequences of the infection of a particular cell-type in the skeletal muscle, and the regeneration of the muscle tissue in survivors together with the possible virus persistence. To study a putative SDV tropism for that particular cell type, we established an in vivo and ex vivo rainbow trout model of SDV-induced atrophy of the skeletal muscle. This experimental model allows reproducing the full panel of clinical signs observed during a natural infection since the transmission of the virus is arthropod-borne independent. The virus tropism in the muscle tissue was studied by immunohistochemistry together with the kinetics of the muscle atrophy, and the muscle regeneration post-infection was observed. In parallel, an ex vivo model of SDV infection of rainbow trout satellite cells was developed and virus replication and persistence in that particular cell type was followed up to 73 days post-infection. These results constitute the first observation of a specific SDV tropism for the muscle satellite cells.