• Korean Journal of Radiology
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• v.25 no.3
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• pp.277-288
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• 2024

Objective: We previously found that the incidence of sarcopenia increased with declining glucose metabolism of muscle in patients with treatment-naïve diffuse large B-cell lymphoma (DLBCL). This study aimed to investigate the relationship between sarcopenia and muscle glucometabolism using ¹⁸F-FDG PET/CT at baseline and end-of-treatment, analyze the changes in these parameters through treatment, and assess their prognostic values. Materials and Methods: The records of 103 patients with DLBCL (median 54 years [range, 21-76]; male:female, 50:53) were retrospectively reviewed. Skeletal muscle area at the third lumbar vertebral (L3) level was measured, and skeletal muscle index (SMI) was calculated to determine sarcopenia, defined as SMI < 44.77 cm²/m² and < 32.50 cm²/m² for male and female, respectively. Glucometabolic parameters of the psoas major muscle, including maximum standardized uptake value (SUVmax) and mean standardized uptake value (SUVmean), were measured at L3 as well. Their changes across treatment were also calculated as ΔSMI, ΔSUVmax, and ΔSUVmean; Δbody mass index was also calculated. Associations between SMI and the metabolic parameters were analyzed, and their associations with progression-free survival (PFS) and overall survival (OS) were identified. Results: The incidence of sarcopenia was 29.1% and 36.9% before and after treatment, respectively. SMI (P = 0.004) was lower, and sarcopenia was more frequent (P = 0.011) at end-of-treatment than at baseline. The SUVmax and SUVmean of muscle were lower (P < 0.001) in sarcopenia than in non-sarcopenia at both baseline and end-of-treatment. ΔSMI was positively correlated with ΔSUVmax of muscle (P = 0.022). Multivariable Cox regression analysis showed that sarcopenia at end-of-treatment was independently negatively associated with PFS (adjusted hazard ratio [95% confidence interval], 2.469 [1.022-5.965]), while sarcopenia at baseline was independently negatively associated with OS (5.051 [1.453-17.562]). Conclusion: Sarcopenic patients had lower muscle glucometabolism, and the muscular and metabolic changes across treatment were positively correlated. Sarcopenia at baseline and end-of-treatment was negatively associated with the prognosis of DLBCL.

• Korean Journal of Veterinary Research
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• v.41 no.1
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• pp.85-87
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• 2001

A case of disseminated lymphoblastic lymphosarcoma is reported in an aborted bovine fetus 7 month in gestation. Grossly, numerous tan firm nodules, 2 to 5 mm in diameter were scattered throughout the myocardium and skeletal muscle. The corticomedullary junction of the kidney was discolored to whitish tinct. Histologically, compact sheet of monomorphic lymphoblastic lymphoid cell infiltration was noted in the myocardium and skeletal muscle. Neoplastic cell infiltration was also noted in the corticomeullary junction and deep cortical regions of the kidney, lung and the liver. This is believed to be the first reported case of lymphosarcoma in an aborted bovine fetus in Korea.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.10
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• pp.1473-1477
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• 2007

Four-and-a-half LIM-only protein 3 (FHL3) is a member of the LIM protein superfamily and can participate in mediating protein-protein interaction by binding one another through their LIM domains. In this study, the 5'- and 3'- cDNA ends were characterized by RACE (Rapid Amplification of the cDNA Ends) methodology in combination with in silico cloning based on the partial cDNA sequence obtained. Bioinformatics analysis showed FHL3 protein contained four LIM domains and four LIM zinc-binding domains. In silico mapping assigned this gene to the gene cluster MTF1-INPP5B-SF3A3-FHL3-CGI-94 on pig chromosome 6 where several QTL affecting intramuscular fat and eye muscle area had previously been identified. Transcription of the FHL3 gene was detected in spleen, liver, kidney, small intestine, skeletal muscle, fat and stomach, with the greatest expression in skeletal muscle. The A/G polymorphism in exon II was significantly associated with birth weight, average daily gain before weaning, drip loss rate, water holding capacity and intramuscular fat in a Landrace-derived pig population. Together, the present study provided the useful information for further studies to determine the roles of FHL3 gene in the regulation of skeletal muscle cell growth and differentiation in pigs.

• Journal of Life Science
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• v.12 no.1
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• pp.55-60
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• 2002

The differentiation of skeletal muscle precursor cells in culture is marked by the transcriptional activation of muscle-specific genes and the morphological differentiation of myoblast into multinucleate myotube. In this study, we examined the effect of TSA (Trichostatin A) on WF-kB DNA binding activity and muscle cell fusion in the process of myogenesis. Under TSA treatment, C2C12 myoblast could not fuse to myotube and its NF-kB DNA binding activity was also blocked. To investigate whether these phenomenons were affected by TSA in direct or not, differentiation media (DM) used to differentiate cells without TSA was concentrated and added to C2C12 myoblast with TSA simultaneously. C2C12 myoblast was fused to myotube and NF-kB DNA binding activity was recovered. These results suggest that TSA affects on the differentiation of myoblast, perhaps through several factors, by inhibiting myoblst fusion and blocking NF-kB DNA binding activity.

• The Journal of Korean Physical Therapy
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• v.15 no.2
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• pp.100-110
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• 2003

The purpose of this article is to understand of the muscle adaptation based on myosin heavy chain. Especially, skeletal muscle dadptation in related to aging, unloading, training will discussed. MHC expression is highly plastic in muscles of adult mammals in accordance with the environmental conditions. These changes is called muscle plasticity. The plasticity is the atility of muscle cell to alter either the quantity of protein or the type of protein. MHC is both an important structural and regulatory protein comprising the contractile apparatus.

• Biomedical Science Letters
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• v.18 no.3
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• pp.276-282
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• 2012

High-intensive endurance exercises induce cell changes in body, changes in structures and functions of the heart, the muscles, the cartilages, and the liver, as well as increase of inflammatory cytokine. The purpose of this study was to estimate the biochemical changes in the liver and muscles during ultra-marathon race (100 km) by sections. The blood of the subjects was collected before the marathon as a control in order to analyze serum creatine kinase (CK), lactic dehydrogenase (LDH), asprtate aminotransferase (AST), alanine aminotransferase (ALT), total(T)-bilirubin, direct(D)-bilirubin, total protein, albumin, uric acid, gamma-glutamyltranspeptidase (${\gamma}$-GTP), alkaline phosphatase (ALP), creatinine, blood urea nitrogen (BUN), and high sensitive C-reactive protein (hs-CRP) concentrations. The CK, LDH, D-bilirubin, AST and ALT concentrations at 50 km and 100 km were significantly increased compared to the control (P<0.05). The markers at 100 km were higher than those at 50 km (P<0.05). The T-bilirubin and hs-CRP concentrations showed no difference among the groups, whereas the markers at 100 km were higher than those of the control and at 50 km (P<0.05). In conclusion, this study shows that the ultra-marathon race (100 km) may induce the damage of the skeletal muscle, liver and kidney, intravascular hemolysis and inflammatory responses.

• Childhood Kidney Diseases
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• v.13 no.2
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• pp.261-266
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• 2009

Rhabdomyolysis, the clinical syndrome caused by the injury to skeletal muscle resulting in the release of muscle cell contents into the systemic circulation, has been described in association with various factors. The causes include crush injury, skeletal muscle overuse, heat, drug, abuse of alcohols and metabolic disorders as well as several types of viral and bacterial infections. We report two cases of rhabdomyolysis, which were complicated by uncommon causes, parainfluenza virus type I infection and hypernatremia.

• Herbal Formula Science
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• v.29 no.1
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• pp.45-55
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• 2021

Objectives : This study was conducted to evaluate the anti-atrophic effect of polycan in dexamethasone-induced skeletal muscle atrophy in vitro model. Methods : C2C12 myoblast were differentiated into myotube by 2% horese serum medium for 6 days, and then treated polycan extract at different concentrations for 24h. The effect of dexamethasone on the induction of muscle atrophy and expression of atrophy-related genes in differentiated C2C12 myotubes using a GSH, ROS, real-time PCR, western blots analysis. Results : The results showed that Treatment with polycan (100 and 200 ㎍/㎖) noncytotoxic levels on both myoblast and myotube. Polycan decreased the ROS level overproduced with dexamethasone and improved the depletion of GSH level. Dexamethasone showed a decrease in myotube diameter, which was associated with up-regulation muscle-specific ubiquitin ligases markers, such as atrogin-1, FoxO3, myostatin and muscle RING finger-1 (MuRF1), and down-regulation of myogenin, MEF2, Myogenic regulatory factor 5, 6 and MyoD. The results showed that polycan treatment significantly dose-dependently inhibited it. Furthermore, decreased expressions of PI3K/Akt signal pathway by dexamethasone were reversed by treatment with polycan. Conclusions : Thus, polycan suppresses dexamethasone induced muscle atrophy in C2C12 myotube in vitro model through activation of PI3K/Akt pathway and protective effect of improve skeletal muscle function.

• BMB Reports
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• v.49 no.6
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• pp.303-304
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• 2016

Myoblast fusion is important for skeletal muscle formation. Even though the knowledge of myoblast fusion mechanism has accumulated over the years, the initial signal of fusion is yet to be elucidated. Our study reveals the novel function of a phosphatidylserine (PS) receptor, stabilin-2 (Stab2), in the modulation of myoblast fusion, through the recognition of PS exposed on myoblasts. During differentiation of myoblasts, Stab2 expression is higher than other PS receptors and is controlled by calcineurin/NFAT signaling on myoblasts. The forced expression of Stab2 results in an increase in myoblast fusion; genetic ablation of Stab2 in mice causes a reduction in muscle size, as a result of impaired myoblast fusion. After muscle injury, muscle regeneration is impaired in Stab2-deficient mice, resulting in small myofibers with fewer nuclei, which is due to reduction of fusion rather than defection of myoblast differentiation. The fusion-promoting role of Stab2 is dependent on its PS-binding motif, and the blocking of PS-Stab2 binding impairs cell-cell fusion on myoblasts. Given our previous finding that Stab2 recognizes PS exposed on apoptotic cells for sensing as an "eat-me" signal, we propose that PS-Stab2 binding is required for sensing of a "fuse-me" signal as the initial signal of myoblast fusion.

• YAKHAK HOEJI
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• v.31 no.5
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• pp.296-301
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• 1987

Polyamines of Korean red ginseng were extracted with 5% trichloroacetic acid and purified by ion exchange chromatography using Dowex-50Wx8 resin. Four spots having R$_f$ values of 0.19, 0.28, 0.35, and 0.45 were detected. It was observed under microscopy that those polyamines stimulated the growth and differentiation of chicken embryonic muscle cell. The development of muscle cells from the stage of myoblast to that of myotube was found to be enhanced by those polyamines. It was also observed that those polyamines most likely lengthened, the life-span of the cultured chicken embryonic skeletal muscle cells.