Muscle Creatine Kinase Research Articles

AMPK-mediated energy metabolism disorders are associated with impaired type IIB muscle fiber regeneration in broiler chickens with wooden breast myopathy.

Abstract Introduction Idiopathic inflammatory myopathies (IIMs) are a heterogeneous disease group characterised by a subacute course of muscle weakness and inflammatory muscle changes that are presumed to be caused by autoimmune mechanisms. Immune-mediated necrotising myopathy (IMNM) is a distinct subgroup of inflammatory myopathy characterised by myofibre necrosis with minimal inflammatory infiltrates on muscle biopsy, highly elevated creatine kinase levels, and infrequent extra-muscular involvement. We will discuss a case of a 36-year-old lady presenting with nonspecific joint pains with mildly raised CK and anti-CCP positivity without clinical evidence of inflammatory arthritis eventually re-presenting two years later with significant muscle weakness. Case description A 36-year-old morbidly obese female patient initially presented with an episode of self-limited inflammatory arthralgia. There were no features of inflammatory arthritis despite significantly positive anti-CCP antibodies and rheumatoid factor. CRP was elevated at 14 mg/L. LFTs were noted to be deranged with ALT of 100 u/l and AST of 95 u/l. Creatine kinase (CK) was mildly raised at 279. She re-presented two years later with worsening mobility resulting in a fall and a hip dislocation. On examination, there was significant weakness particularly in the lower limbs with leg hip extensors and flexors having significantly reduced power at 2/5 with diminished reflexes in lower limbs. CRP was raised at 60 mg/l and CK was found to be 14000u/l. EMG showed myopathic changes; however, it was a difficult study due to high BMI. There were no extra muscular manifestations. Inflammatory myopathy was suspected and high dose steroids were commenced with DMARD therapy (methotrexate). Extended myositis panel showed anti-SRP positivity with the muscle biopsy identifying necrotising myopathy. Her immunosuppression was therefore augmented with the addition of rituximab. There was slow clinical and biochemical improvement after two doses of rituximab treatment. After initial response, CK remained elevated at 885u/l with clinical improvement having plateaued and the patient still having difficulty standing from a lying position and performing simple daily tasks. Therefore, through collaboration between the neurology and rheumatology team, treatment was augmented by addition of monthly IVIG which resulted in significant improvement in muscle function and CK levels improving to 265u/l. She was also reviewed and managed by the rehabilitation team of physiotherapists and occupational therapist throughout her treatment. The patient has recently expressed her strong wish to pursue pregnancy in the near future which currently poses a therapeutic dilemma around adjustment of immunosuppression to support her, having only just achieved disease remission on combination of immunomodulatory therapies. Discussion IMNM can be classified based on the proposed European Neuromuscular Centre (ENMC) criteria. It can also be characterised by myositis-associated antibodies which guides treatment. Preserving and maximising functional status is the major aim and desirable outcome of treatment. Corticosteroids are the first line of management for quick response. Steroid sparing agents are recommended; however, there are no specific clinical trials to support a specific agent of choice. For anti-SRP disease, rituximab instead or in addition to methotrexate is recommended. Early rituximab is often favoured in anti-SRP disease, as per the ENMC guidelines. Despite early introduction of combination of rituximab and methotrexate, together with corticosteroid, our patient demonstrated active disease both clinically and biochemically, with further improvement following addition of monthly courses of IVIG therapy. Having recently achieved disease stability, the patient is keen to pursue her first pregnancy, which poses several therapeutic dilemmas. Given the severity of her disorder, which requires combined immunosuppression, we need to carefully consider a suitable switch in her treatment which would be safe in pregnancy without jeopardising her prognosis. Other medications used in IMNM include azathioprine, mycophenolate mofetil, tacrolimus, cyclosporine, and cyclophosphamide, though evidence on individual agent efficacy remains limited. Azathioprine is an attractive replacement for methotrexate and IVIG are considered safe in pregnancy. However, we need to ensure disease stability for several months after changing immunosuppression. There are few data available on outcomes of pregnancy in patients with idiopathic inflammatory myopathies (IIM) and the influence of pregnancy on the activity of inflammatory muscle disease. Key learning points 1. Anti-SRP-associated IMNM is associated with significant muscle weakness and disability. 2. Young age of onset is a poor prognosticating factor. 3. Subtle biochemical changes (mildly raised CK and deranged liver function tests) can be picked up earlier in the disease course prior to clinical presentation of actual muscle weakness as in this case. 4. There are no clinical trials to guide management, and treatment is largely based on ENMC guidelines along with expert opinion and clinical observations. 5. An MDT approach is paramount in long-term management. 6. There are very limited data available on outcomes of pregnancy in patients with IIM and the influence of pregnancy on the activity of inflammatory muscle disease.

Abstract Introduction This case describes a 50-year-old man with clinically amyopathic dermatomyositis (CADM) and anti-MDA5 antibody positivity, who developed rapidly progressive interstitial lung disease (RP-ILD), complicated by pneumomediastinum, pneumothorax, and multi-organ failure. Despite classic skin findings and systemic symptoms, initial absence of muscle involvement and normal muscle enzymes delayed escalation to steroid-sparing immunosuppression. High-resolution CT initially suggested fibrosis without active inflammation. Anti-MDA5 positivity was confirmed following deterioration. This case highlights the importance of early recognition, timely immunosuppression, and multidisciplinary input in high-risk autoimmune ILD, where delays in treatment can lead to devastating outcomes despite maximal supportive care. Case description The patient was referred to his local rheumatologist in September with rash, myalgia, and arthralgia. Classic cutaneous features raised suspicion for dermatomyositis. He had no proximal muscle weakness, and both CK and EMG were normal. He had a markedly raised ferritin of 1700 µg/L, while CRP was normal (4 mg/L). A skin biopsy showed features of lichenoid dermatitis, consistent with connective tissue disease and in keeping with dermatomyositis. He was started on prednisolone 40 mg daily. A few weeks later, he developed worsening fatigue and new breathlessness. Chest X-ray was normal, but HRCT in October showed peripheral interstitial fibrosis. MDT radiology review concluded this represented established fibrosis with no evidence of active inflammation. CK remained normal, ENA including anti-Jo1 was negative, and no disease-modifying, steroid sparing agent was started. By November, he had further respiratory decline with clinical evidence of surgical emphysema. CT confirmed pneumomediastinum and subcutaneous emphysema. He was admitted and received IV methylprednisolone. Immunosuppressive escalation (cyclophosphamide and rituximab) was planned but postponed due to febrile illness. He subsequently tested positive for anti-MDA5 antibody after transfer to the tertiary centre. His condition worsened with bilateral pneumothoraces and respiratory failure. Despite chest drains, IVIg and plasma exchange, he continued to deteriorate. Cyclophosphamide and rituximab were discussed but not initiated due to sepsis risk. He was deemed unsuitable for ECMO or transplant by local and national MDTs. He died in December. Discussion This case illustrates the potentially aggressive course of anti-MDA5-positive clinically amyopathic dermatomyositis (CADM) with rapidly progressive ILD (RP-ILD). Early diagnostic uncertainty was compounded by normal CK, absent muscle weakness and EMG findings, which delayed immunosuppressive escalation. Although CRP was normal, ferritin was elevated (1700 µg/L) at initial presentation, likely indicating early systemic inflammation. Skin biopsy supported the diagnosis, but HRCT was interpreted as stable fibrosis, further contributing to therapeutic hesitation. The subsequent identification of anti-MDA5 positivity clarified the diagnosis and explained the rapidly worsening ILD. MDA5-positive CADM is associated with a high risk of RP-ILD, pneumomediastinum, and poor prognosis. Early and aggressive immunosuppression is recommended, often with combination regimens involving corticosteroids, rituximab, and cyclophosphamide. Unfortunately, in this case, treatment was delayed due to concurrent infection and concerns about immunosuppression risk. Despite the use of IVIg and plasma exchange as bridging therapies, his deterioration continued. The development of pneumomediastinum and pneumothorax were recognised prognostic red flags. Even with multidisciplinary input and ICU support, ECMO and transplantation were not viable options due to disease severity and instability. This case highlights the critical importance of recognising CADM presentations, interpreting HRCT findings in context, and initiating immunosuppression early when clinical suspicion is high. Raised ferritin, even with normal muscle enzymes and CRP, may be a useful adjunct biomarker in identifying patients at risk of severe disease. The availability and turnaround time of the extended myositis antibody panels can influence management decisions and outcomes. Key learning points 1. Recognising MDA5-positive CADM: dermatomyositis can present without muscle involvement. The presence of characteristic rash and systemic symptoms, particularly with respiratory decline, should raise early suspicion for CADM and prompt anti-MDA5 testing. 2. Importance of serology access: anti-MDA5 positivity is strongly associated with rapidly progressive ILD and poor prognosis. Early access to extended myositis panels can guide management and risk stratification. 3. HRCT interpretation in context: radiological reporting of “fibrosis without inflammation” must be weighed against clinical symptoms. A single CT does not exclude active ILD. Early ILD-MDT discussion is essential. 4. Treatment timing in RP-ILD: in high-risk patients, early combination immunosuppression is crucial. Even when infection risk exists, the window to act may be small. This case supports the potential need for upfront dual or triple therapy in anti-MDA5 disease. 5. Prognostic markers: pneumomediastinum and pneumothorax in anti-MDA5 ILD are associated with high mortality. These features should trigger urgent re-evaluation of the treatment plan and escalation. 6. Markedly elevated ferritin levels may indicate systemic immune activation and have been associated with worse outcomes in anti-MDA5-positive ILD. In this case, ferritin was significantly raised (1700 µg/L) despite a normal CRP, highlighting its potential value as an early red flag for disease severity, even in the absence of classical inflammatory markers. Ferritin should be considered alongside clinical features and imaging when risk-stratifying patients and planning early aggressive treatment.

Background. Delayed-Onset Muscle Soreness (DOMS) is a phenomenon that arises from muscle damage following uncommon or intense eccentric exercise, with symptoms persisting for a few days. The condition is characterized by muscle pain, reduced muscle strength, limited range of motion, and general discomfort that affects performance and disrupts the exercise program. Objectives. This study aimed to investigate the effect of Selenium supplementation on DOMS and muscle damage after performing heavy eccentric exercise. Materials and methods. An experimental pre-post control group design was used in this study. A total of 44 male students from the Sports Science Department of the State University of Surabaya (Universitas Negeri Surabaya) were randomly and double-blindly assigned to either a selenium supplementation group (n = 22) or a placebo group (n = 22). The participants in both groups were instructed to consume one selenium or placebo capsule for 28 days. Following the 28-day supplementation period, both groups underwent a 10-set x 10-rep bench stepping-test. Delayed Onset Muscle Soreness (DOMS) and Creatine Kinase (CK) levels were assessed at 24 and 48 hours in the post-exercise phase. Results. The findings of the study demonstrated that during the 24 to 48-hour period following heavy eccentric exercise, both groups experienced a reduction in Delayed Onset Muscle Soreness (DOMS) and CK plasma levels. However, the selenium supplementation group exhibited a significantly greater reduction in DOMS and CK levels compared to the placebo group (p < 0.05). This suggests that selenium supplementation may enhance the natural recovery process, rather than being solely responsible for the observed reduction in these markers. Conclusions. In conclusion, Selenium supplementation may lower the likelihood of muscle injury following heavy eccentric exercise, as it effectively decreases plasma DOMS and CK levels in the bloodstream.

BackgroundFootball matches induce acute and residual fatigue, impairing neuromuscular, metabolic, and perceptual performance. Hydrogen-rich water (HRW) is a novel intervention with antifatigue and antioxidative properties. The intermittent high-intensity nature of football, which includes frequent accelerations, decelerations, sprints, changes of direction, and physical contacts, imposes substantial demands on both central and peripheral physiological systems. This results in acute fatigue, observable during or immediately after a match, and residual fatigue, which can persist for 24-72 hours post match, depending on the intensity, match context, and recovery strategies.ObjectiveThis study will investigate the effects of pre-exercise HRW administration versus a placebo on neuromuscular performance, biochemical markers, and perceptual measures of fatigue during a 72-hour recovery after a simulated football match.MethodsUsing a randomized, double-blinded, placebo-controlled, parallel design, elite junior football players will undergo neuromuscular performance assessments (repeated sprint ability and countermovement jump test). Metabolic fatigue will be measured by creatine kinase level and muscle soreness, rated using a visual analog scale. These assessments will occur at critical time points: immediately post warm-up; directly following the simulated football match to detect acute fatigue; and 24, 48, and 72 hours after training sessions to detect residual fatigue.ResultsData collection has been scheduled with the clubs to coincide with the beginning of the players’ transition period (ie, at the start of August 2025). The expected duration of data collection, including the initial medical examination, is planned to be 1 month. We anticipate publishing the results in late 2025 or during the first half of 2026.ConclusionsThis study will assess the influence of molecular hydrogen on acute fatigue manifestation and recovery quality during a 72-hour period after a simulated football match. The potential positive effects of molecular hydrogen, such as attenuation of oxidative stress, reduction in muscle damage markers, and accelerated neuromuscular recovery, may contribute to faster restoration of functional capacities. If confirmed, these effects could enhance players’ readiness to return to high-intensity training and optimize the structure of microcycles in competitive periods. Additionally, understanding the recovery dynamics facilitated by HRW may inform evidence-based recovery strategies and support individualized player monitoring frameworks. The possible positive effect of molecular hydrogen would speed up the players’ readiness to train after the match and help protect players against illness and noncontact injuries.

Introduction and Objective: We investigated the role of insulin/IGF1 signaling in cardiac function and lifespan of MDKO mice (Irs1L/L•Irs2L/L•CreMck) generated by MCK (muscle creatine kinase) driven Cre expression in striated and cardiac muscle. Methods: MDKO mice died by 30 days of age with severe cardiomyopathy. Deletion of FoxO1 and FoxO3a in MDKO mice (MQKO mice) slowed progression of cardiomyopathy, extending lifespan to 80 days. MDKO mice showed severely reduced Akt→mTOR signaling so we investigated whether genetic activation of mTorc1 in MTKO mice (Irs1L/L•Irs2L/L•Tsc1L/L•CreMck) could attenuate cardiomyopathy and extend lifespan. Results: Lifespan increased to 220 days, but MTKO mice showed cardiac dysfunction (reduced ejection fraction) at 112 days of age. Full activation of mTorc1 appeared to be essential to compensate for insulin/IGF resistance because partial activation of mTorc1 caused severe cardiomyopathy and death of MDKO•Tsc1L/+ mice by 40 days of age. Unexpectedly, HFD (high fat diet) feeding of MDKO•Tsc1+/- mice restored the lifespan from 40 to 220 days. HFD also significantly increased lifespan of MQKO mice from 80 to 178 days; however, HFD did not increase the lifespan of MTKO mice beyond 220 days. Thus, HFD or muscle Tsc1 deletion appears to extend lifespan during chronic insulin/IGF1 resistance. Cardiac glucose uptake was significantly reduced in MTKO mice; however, cardiac fatty acid uptake did not increase. Lactate might nourish the cardiac muscle of MTKO mice as cardiac lactate transporters increased significantly while circulating lactate decreased. Consistently, lactate treatment of MTKO mice corrected cardiac function, including ejection fraction and structural cardiac parameters (left ventricle internal diameter). MTKO mice fed lactate survived until the experiment was terminated at 280 days. Conclusion: Overall, these results suggest that the progression of fatal cardiomyopathy in MDKO mice was rescued by mTorc1 activity through genetic and/or nutritional manipulation. Disclosure O. Stoehr: None. R. Tao: None. K.D. Copps: None. M.F. White: Board Member; HPRL (Housey Pharmaceutical Research Laboratory).

Climate-related hazards are a leading health and safety concern for working populations. Technological advancements have made real-time collection of core body temperature, a measure of heat strain, more feasible in non-clinical settings. Researchers and practitioners are now faced with how to best summarize a plethora of core body temperature data. Core body temperature data were collected over the course of the workday for 128 agricultural workers in Guatemala from December 2021 to April 2023. Concurrently, measures of heat-related health effects (reduced kidney function, muscle breakdown, and dehydration) were collected. Using linear mixed-effect regression models we assessed the performance of 14 summary measures of core body temperature on the heat-related health effects of interest. Model performance was compared using AIC and BIC. There was no consistent summary statistic that provided the best fit based on AIC or BIC for all four heat-related health effects. The difference between the observed CBT and the average of the first 60min of the cleaned workday data (delta) provided the best performance for percent change in creatine kinase (muscle breakdown), serum creatinine (reduced kidney function), and serum osmolality (dehydration). The area under the curve (AUC) performed best for dichotomous indicator of acute kidney injury. Choice of how to operationalize longitudinal measurements of core body temperature generated using ingestible core body temperature pills should be driven by the research question and health effect of interest.

Imaging findings of scleroderma-associated myopathy: A systematic literature review.

A Comparative Estimation of Aldolase - A and Creatine Kinase-Muscle Levels in Arthritis Patients and Snail Consuming Subjects

Resveratrol (trans-3,4',5-trihydroxystilbene, RES) is a stilbenoid naturally present in a variety of plants. Although there are several reports about its anti-fatigue activity, its impact on intensive exercise-induced fatigue and the underlying mechanisms are yet not well understood. In the present study, we established a swimming exercise protocol in mice that is similar to the fatigue condition induced by a long period of intensive exercise and explored the effect of RES on fatigue and the mechanisms from the perspective of intestinal injury and gut microbiota. The results revealed that RES significantly prolonged exhaustive swimming time in fatigued mice and improved the serum indexes associated with fatigue, including serum glucose, lactic acid (LA), urea nitrogen (BUN), lactate dehydrogenase (LDH), creatine kinase (CK), catalase (CAT), glutathione peroxidase (GSH-Px), and glycogen storage in liver and muscle. Meanwhile, RES increased the expressions of ZO-1, Occludin, and Claudin-1, thereby enhancing intestinal barrier integrity and inhibiting mRNA expressions of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in the colon, thereby improving the pathological injury in the colon. Importantly, RES modified gut microbiota dysbiosis by increasing the diversity of gut microbiota, regulating microbiota associated with inflammation and fatty acid metabolism at the phylum (Bacteroidetes and Firmicutes), family (Erysipelotrichaceae, Enterobacteriaceae, and Prevotellaceae), and genus (Brevundimonas diminuta, Coprobacillus, Megasphaera, and Lactobacillus) levels, respectively. The results supplemented the anti-fatigue mechanism for RES from the perspective of intestinal injury and gut microbiota. The detailed mechanisms and associated metabonomics analysis remain for further study.

This study investigated differences in muscle twitch force between slow and fast progressors of amyotrophic lateral sclerosis (ALS) to better understand disease heterogeneity and identify potential biomarkers of disease progression. Forty-four ALS patients were classified as slow or fast progressors based on disease progression rates. Electrophysiological assessments, including compound muscle action potential (CMAP) and muscle force measurements, were conducted. Creatine kinase (CK) levels were also evaluated. Slow progressors demonstrated significantly higher muscle peak force and area under the curve (AUC) compared to fast progressors, reflecting greater muscle strength and endurance. CK levels were also elevated in slow progressors. Despite similar CMAp values, slow progressors retained greater muscle strength, possibly due to a reduced degeneration of fast-twitch fibers and compensatory axonal sprouting. These adaptations may preserve muscle function and elevate CK levels, suggesting better muscle integrity in slow progressors. Muscle function profiles and CK levels are promising indicators of ALS progression. These findings could enhance early detection of disease progression and lead to targeted interventions to preserve muscle function. Further research is needed to validate these results and explore the underlying functional mechanisms of disease heterogeneity.

ABSTRACTBarth syndrome is a mitochondrial disorder with hallmarks of cardiac and skeletal muscle weakness. It is caused by pathogenic variants in the X-linked gene tafazzin (TAZ), required for cardiolipin remodeling. Previously described germline and conditional Taz knockout models are not ideal for therapeutic development because they lack the combination of robust survival to adulthood, cardiomyopathy and skeletal muscle weakness. We characterized a cardiac and skeletal muscle-specific Taz knockout model (TazmKO) in which Cre recombinase is expressed from the muscle creatine kinase promoter (mCK-Cre). TazmKO mice survived normally. Cardiolipin composition was abnormal in both heart and skeletal muscle. TazmKO had reduced heart function by 2 months of age, and function progressively declined thereafter. Reduced treadmill endurance and diminished peak oxygen consumption were evident by 3 months of age, suggesting reduced skeletal muscle function. Electron microscopy showed abnormalities in mitochondrial structure and distribution. Overall, TazmKO mice display diminished cardiac function and exercise capacity while maintaining normal survival. This model will be useful for studying the effects of TAZ deficiency in striated muscles and for testing potential therapies for Barth syndrome.

Background: It has been observed that severe muscle damage induced by drop jumps has a significant effect on cell-free DNA (cfDNA) concentration. We hypothesized that a reduced volume of drop jumps would indicate a dose-dependent release of cfDNA. Methods: Seven participants (aged 21 ± 1.5 years) performed 25, and 4 participants (aged 22 ± 1.8 years) performed 10, intermittent drop jumps (DJs) at 20 s intervals (DJ-25 and DJ-10 groups). We measured cfDNA, creatine kinase (CK), lactate concentrations and delayed-onset muscle soreness (DOMS) before and at several time points up to 96 h after exercise. Results: There was a significant increase in plasma cfDNA levels immediately post-exercise in the DJ-25 group (p = 0.012). CK levels increased at 6, 12, 24 and 48 h post-exercise (p = 0.003, p < 0.001, p < 0.001, p = 003, accordingly) in the DJ-25 group. In the DJ-25 group only, DOMS values were increased at 12, 24 and 48 h post-exercise (p < 0.05). Conclusion: cfDNA is responsive to muscle-damaging exercise in a dose-dependent manner, as only 25 DJs resulted in an immediate increase in cfDNA concentrations after exercise, while 10 DJs were insufficient to elicit any change. Keywords: biomarker; eccentric exercise; muscle damage

Introduction: Apart from its financial burden, Chemotherapy presents a induced Peripheral Neuropathy with motor deficits and muscle cachexia. This has lead to discouragement and stoppage of cancer treatment regimen, and poor quality of life with heavy financial Implications. This study was aimed to determine the effects of β-caryophyllene (BCP) on muscle function of gastrocnemius in oxaliplatin induced peripheral neuropathy of male wistar rat. Method: The rats used in this study were grouped into 5 groups (n=9).Except for normal control , all animals were treated with Oxaliplatin (4 mg kg-1) to induce Peripheral neuropathy. Apart from the Negative control, others were treated daily with Doluxetine at 10 mg kg-1 (control 3), BCPat 25mg kg-1 ( Group 4) and BCP at 50 mg kg-1(group 5). For each week of the 21 days, the rats were assessed for motor coordination deficit and muscle strength while their samples were assessed for muscle injury and muscle weight of the gastrocnemius weekly. Means less than 0.05 (˂0.05) were considered statistically significant. Result: BCP caused an improvement in motor co-ordination with decreases in muscle inflammation, creatine kinase and myoglobin levels with a weekly decrease in muscle inflammation. Muscle endurance also improved in BCP- treatment with increased relative gastrocnemius muscle weight. Discussion: This study emphasized the importance of muscle function as needed diagnostic tool in assessment of recovery of cancer patients while demonstrating the positive impact of BCP on pain sensitivity, motor deficit and muscle function during peripheral neuropathy.

BackgroundDeep hypothermic circulatory arrest (DHCA) can cause systemic inflammatory response (SIR) and ischemia-reperfusion (I/R) injury, potentially exacerbating organ failure. Ulinastatin (UTI) is a frequently employed anti-inflammatory medication in clinical practice, but different timing and dosage may influence its protective efficacy.Methods24 rats were randomly divided into four groups. Three different doses of UTI (3/10/30 × 104 U/kg; low/medium/high dose) were administered in the DHCA rat model, with a control group that underwent DHCA without UTI administration. Inflammatory markers and routine clinical indicators of myocardial, hepatic, and renal tissue injury were evaluated. All rats underwent the standard DHCA procedure.ResultsInterleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and neutrophil elastase (ELA-2) levels in rats exposed to DHCA gradually increased after rewarming. Compared with the DHCA-only group, both the low dose of UTI (UTI-L) and the medium dose of UTI (UTI-M) significantly reduced IL-6 (p = 0.017, p = 0.022 ), TNF-α (p = 0.003, p < 0.001), ELA-2 levels ( p = 0.018, p = 0.001), and elevated IL-10 levels ( p < 0.001, p < 0.001) 4 h post-weaning from cardiopulmonary bypass (CPB). In addition, compared with the DHCA group, both the UTI-L and UTI-M group showed significantly lower levels of cardiac troponin I (p = 0.001, p = 0.001), creatine kinase muscle and brain isoenzyme (CK-MB) (p < 0.001, p < 0.001), creatinine (p < 0.001, p < 0.001), blood urea nitrogen (p = 0.002, p = 0.021), aspartate transaminase (p < 0.001, p < 0.001) and alanine aminotransferase (p < 0.001, p < 0.001) at the end of the experiment. The hematoxylin-eosin staining results of kidney and liver tissue damage were alleviated in the UTI-L and UTI-M groups. The high dose of UTI (UTI-H) group did not exhibit dose-dependent anti-inflammatory effects and was associated with aggravated injury to the heart, liver, and kidney.ConclusionThis study demonstrated that the administration of low to medium doses of UTI during DHCA significantly attenuated the levels of IL-6, TNF-α, and ELA-2, elevated the level of the anti-inflammatory factor IL-10, and provided protective effects on myocardial, hepatic, and renal tissues.

Burn injuries cause severe muscle wasting and weakness. However, the relative contribution of neuromuscular junction (NMJ) degradation remains elusive. We investigated the associations of plasma c-terminal agrin fragment-22 (CAF22), a marker of NMJ degradation, with muscle decline in burn patients. We recruited male patients with burns (n = 32, age = 32.3 ± 4.5 years, percent burn area = 15.2 ± 2.3) and age-matched controls to evaluate handgrip strength (HGS), skeletal muscle mass index (SMI), phase angle, and creatine kinase and plasma levels of CAF22, c-reactive protein, and 8-isoprostanes. We used an unpaired t-test and regression analysis for statistics. The burn patients had lower HGS, SMI, and phase angle than the controls (all p &lt; 0.05). These patients also exhibited higher plasma CAF22, CRP, 8-isoprostanes, and creatine kinase than the controls (all p &lt; 0.05), suggesting NMJ degradation and heightened inflammation and oxidative stress. Correlation analysis revealed significant correlations of plasma CAF22 with HGS and phase angle in the burn patients, suggesting the potential contributions of NMJ degradation to muscle weakness and atrophy (both p &lt; 0.05). We also found correlations of plasma CRP with HGS and phase angle in these patients (both p &lt; 0.05). Altogether, NMJ degradation appears to play a significant role in burn-induced muscle injury and may warrant further investigation for potential therapeutic interventions.

IntroductionInflammatory myopathies (IM) are a group of severe autoimmune diseases, sharing some similarities, whose cause is unknown and treatment is empirical.While C-protein-induced myositis (CIM), the most currently used mouse model...

Pathogenic variants in the RYR1 gene have been associated with a variety of conditions, ranging from congenital myopathy to adult manifestations. Our aim was to characterize the p.Leu2286Val variant in 17 Basque patients, to accurately determine its correlation with clinical features and to explore the possible founder effect of the variant. Families harbouring the p.Leu2286 RYR1 variant underwent a detailed clinical evaluation, including muscle magnetic resonance imaging, electromyography and muscle biopsy. Haplotypes were analysed in available patients and their relatives. Individuals carrying the p.Leu2286Val shared a common haplotype, suggesting a founder event in the Basque Country population. The most prevalent features were exertional myalgia, high creatine kinase (CK) levels, cramps and muscle hypertrophy. None of the patients carrying only the p.Leu2286Val showed progression to severe muscle weakness and muscle magnetic resonance imaging showed a heterogeneous muscle involvement. Muscle biopsy revealed non-specific findings in two patients and features associated with central core disease in one patient carrying only the p.Leu2286Val and two patients harbouring an additional RYR1 variant. Three individuals carrying an in trans RYR1 variant presented with an earlier onset and more severe phenotype. Here, it is shown that the dominantly inherited p.Leu2286Val RYR1 founder variant is associated with a milder phenotype of exercise intolerance, myalgia and hyperCKemia.

A 69-year-old woman with left-sided breast cancer developed elevated creatine kinase levels and muscle weakness in her extremities after treatment with pembrolizumab. The patient was diagnosed with immune checkpoint inhibitor (ICI)-related myositis. Although the patient had no symptoms of dysphagia, we evaluated her swallowing function because esophageal dysfunction is a known complication of idiopathic inflammatory myopathy. A videofluoroscopic swallowing study detected barium residues in the lower esophagus. Furthermore, high-resolution manometry showed impaired upper esophageal sphincter opening and absence of esophageal peristalsis, which improved partially after immunotherapy. These findings suggest that esophageal dysfunction may be an unrecognized complication of ICI-related myositis.

Abstract The measurement of muscle creatine kinase (CKm) activity in the bloodstream has been used as a parameter for prospecting muscle injuries in soccer. This approach is based on the proposition that intense muscular activity is often associated with structural micro-injuries in contractile components of skeletal muscle. Once installed, tissue damage favors inflammatory activity, leading to the process of muscle pain. Strikinly, there is still no correlation between increased CKm in the bloodstream and the occurrence of muscle injuries, further complicating the interpretation of CKm as a reliable biomarker. CKm is a protein with a relatively high molecular weight and is primarily drained by the lymphatic system in a slow kinetic process which is, therefore, drained by the lymphatic system in a slow kinetic process. Once it enters the bloodstream, the enzyme can be rapidly degraded, being difficult to determine the protein's actual values. Therefore, the increase in CKm in the bloodstream of athletes may be a reflection of chronic muscle contraction, the intensity of training/games in the current period, and delayed-onset muscle soreness rather than direct incidence of muscle injury. Finally, there remains a lack of evidence supporting a direct relationship between increased CKm levels and performance indices.