• Animal Bioscience
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• v.36 no.6
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• pp.953-961
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• 2023

Objective: This study aimed to investigate the effect of dorsal cranial myopathy (DCM) on chicken meat quality. Methods: Sixty-six Ross 308 AP broilers, 47 days old, of both sexes, weighing about 3.51 kg, were slaughtered according to standard industrial practices, and evaluated for meat color, pH, chemical composition, collagen content, fatty acid profile, and histopathological parameters. Comparisons between normal and DCM-affected meat were performed using Student's t-test at the 5% significance level. Results: Histological analysis of muscle tissues affected by DCM showed myofiber degeneration, proliferation of inflammatory cells, fibroplasia, and necrosis with fibrosis. DCM samples had lower protein content and higher moisture, ash, insoluble collagen, total collagen, and pH. DCM-affected meat was redder and more yellowish. There were no differences in lipid or soluble collagen contents between groups. DCM-affected meat had higher percentages of arachidonic acid (C20:4n-6) and eicosapentaenoic acid (C20:5n-3). Conclusion: This study revealed that DCM-affected meat exhibits considerable changes in quality parameters.

• Journal of Life Science
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• v.30 no.8
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• pp.672-679
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• 2020

Distal myopathy is a clinically and genetically heterogeneous group of degenerative diseases of the distal muscle. Glycogen storage disease type IXD (GSD9D) is a metabolic distal myopathy characterized by muscle deficiency of phosphorylase kinase, a key regulatory enzyme in glycogen metabolism. Affected individuals may develop muscle weakness, degeneration, and cramps, as well as abnormal muscle pain and stiffness after exercise. It has been reported that mutations in the PHKA1 gene which encodes the alpha subunit of muscle phosphorylase kinase cause GSD9D. In this study, we examined a Korean GSD9D family with a c.3314T>C (p.I1105T) mutation in the PHKA1 gene. This mutation has not been previously reported in any mutation database nor was it found in 500 healthy controls. The mutation region is well conserved in various other species, and in silico analysis predicts that it is likely to be pathogenic. To date, only seven mutations in the PHKA1 gene have been documented, and this is the first report of Korean GSD9D patients. This study also describes and compares the clinical symptoms and pathological conditions of previously reported cases and these Korean patients. We believe that our findings will be useful for the molecular diagnosis of GSD9D.

• Journal of Life Science
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• v.31 no.5
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• pp.464-474
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• 2021

Inflammation induced by metabolic syndromes, cancers, injuries, and sepsis can alter cellular metabolism by reducing mitochondrial function via oxidative stress, thereby resulting in neuropathy and muscle atrophy. In this study, we investigated whether butyrate, a short chain fatty acid produced by gut microbiota, could prevent mitochondrial dysfunction and muscle atrophy induced by lipopolysaccharide (LPS) in the C2C12 cell line. LPS-activated MAPK signaling pathways increased the levels of the mitochondrial fission signal, p-DRP1 (Ser616), and the muscle atrophy marker, atrogin 1. Interestingly, butyrate significantly inhibited the phosphorylation of JNK and p38 and reduced the atrogin 1 level in LPS-treated C2C12 cells while increasing the phosphorylation of DRP1 (Ser637) and levels of mitofusin2, which are both mitochondrial fusion markers. Next, we investigated the effect of MAPK inhibitors, finding that butyrate had the same effect as JNK inhibition in C2C12 cells. Also, butyrate inhibited the LPS-induced expression of pyruvate dehydrogenase kinase 4 (PDK4), resulting in decreased PDHE1α phosphorylation and lactate production, suggesting that butyrate shifted glucose metabolism from aerobic glycolysis to oxidative phosphorylation. Finally, we found that these effects of butyrate on LPS-induced mitochondrial dysfunction were caused by its antioxidant effects. Thus, our findings demonstrate that butyrate prevents LPS-induced muscle atrophy by improving mitochondrial dynamics and metabolic stress via the inhibition of JNK phosphorylation. Consequently, butyrate could be used to improve LPS-induced mitochondrial dysfunction and myopathy in sepsis.

• Journal of Yeungnam Medical Science
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• v.34 no.1
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• pp.137-139
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• 2017

Dermatomyositis (DM) is characterized by progressive proximal limb weakness and typical skin manifestations. The histological findings that show perifascicular atrophy and deposition of membrane attack complex are pathognomic features of DM. Dermatomyositis is categorized into classical DM and non-classical DM, which includes amyopathic DM and DM sine dermatitis. DM sine dermatitis is seldom described because of its rarity, making the diagnosis more challenging. We report a case of DM sine dermatitis, a rare phenotype of DM.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.45-47
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• 2014

• Annals of Clinical Neurophysiology
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• v.2 no.1
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• pp.31-35
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• 2000

Focal myositis is a benign inflammatory pseudotumor of a skeletal muscle that clinically mimics a tumor of soft tissue, but the cause of which is obscure. I report here a case of multifocal recurrent nonpainful myositis found in a 68-year-old man who showed a subacute multifocal recurrent nonpainful inflammatory myopathy affecting discrete muscle groups with spontaneous remission and/or some medication.

• Journal of Digestive Cancer Research
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• v.10 no.2
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• pp.112-116
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• 2022

Idiopathic inflammatory myopathy (IIM) is known for its association with malignant diseases. Moreover, various solid organ malignancies, such as ovarian, breast, lung, esophageal, stomach, and colorectal cancers, have been reported to occur with IIM. Furthermore, its relationship with hematologic malignancies, including non-Hodgkin lymphoma, myeloma, and leukemia, has been reported. However, to date, IIM related to pancreatic cancer has scarcely been reported, particularly in patients with polymyositis (PM). Therefore, here we report a case of PM developed immediately after the diagnosis of pancreatic ductal adenocarcinoma.

• Journal of fish pathology
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• v.3 no.2
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• pp.81-91
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• 1990

Nutritional ceroidosis accompanied with histopathological changes such as myopathy and visceral ceroidosis, was experimentally induced by feeding the oxidized feed with the peroxide value of 98meq/kg, to common carp resulting in some motalities of carp. To see the effect of treacetment survivors of the above fish were orally administered by feeding diets containing daily doses of 3mg and 6mg of glutathione per kg fish for 10 days or 20 days. While control and 3mg dosage group retained viscerral ceroidosis and showed evidence myopathy histo pathologically, the fish treated with 6mg of glutathione for 20days showed obvious reduction of macrophages of ceroid in the viscera.

• Journal of Haehwa Medicine
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• v.18 no.2
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• pp.1-12
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• 2009

Most of the cholesterol is synthesized by liver in the body while about one of third is taken via dietary. The main functions of cholesterol is to protect membranes in cell surface, avoid the arterial bleeding by hypertension, and prolong the life of erythrocytes, and so on. However, overload of cholesterol leads to arteriosclerosis associated with leading death cause. Lack of physical activity, emotional and environmental stress, and low intake of protein or vitamin E induce the unbalance between HDL- and LDL-cholesterol so become a basis of ischemic disorders in heart, brain and elsewhere in the body. So far, four major classes of medications for hyperlipidemia are HMG-CoA reductase inhibitors (statins), bile acid sequestrants, nicotinic acid, and fibric acids. The statins can lower LDL and levels triglyceride, but may induce myopathy and an elevation of liver enzyme levels. The bile acid sequestrants lower LDL levels and raise HDL levels with no effect on triglyceride levels but side effects of gastrointestinal (GI) distress, constipation, and a decrease in the absorption of other drugs. Nicotinic acid and fibric acids lower LDL and triglyceride levels with showing flushing, hyperglycemia, hyperuricemia, GI distress, and hepatotoxicity dyspepsia, gallstones, myopathy, and unexplained noncardiac death as adverse effects. Above western drugs lower cholesterol by 15 to 30% while all have notable adverse effects. In traditional medicine, hyperlipidemia is regarded as retention of phlegm and fluid disease. Etiology and pathogenesis of hyperlipidemia is basically based on Spleen-Deficiency and Phlegm-Stagnation, accumulation and stasis of -heat, and Qi & blood stagnation induced by Phlegm-damp, water-dampness, and blood stasis. Thereby, strengthening Spleen and dissolving Phlegm, clearing away heat and diuresis, and supplementing Qi and activating blood circulation are commonly used therapeutic methods for hyperlipidemia. The traditional herbal medicine, have been used for patients with CVA, hypertension or hyperlipidemia in Oriental hospital or Oriental clinic. The lock and key theory is used to develop most of western medicine, however many diseases are caused by mixed factors in body-complex system. We expect that Oriental pharmacological theory could be newborn as a novel drug showing high advantage of blood levels of lipidsand QOL of performance without side effects.

• The Korean Journal of Nuclear Medicine
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• v.14 no.2
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• pp.41-44
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• 1980

To evaluate the change of serum myoglobin in the thyroid disease, we measured serum myoglobin by radioimmunoassay in 24 normal subjects, 34 patients with hyperthyroidism (20 untreated, 14 treated) and 5 patients with hypothyroidism. The mean values of serum myoglobin in 24 normal control, 20 untreated hyperthyroidism, and 14 treated hyperthyroidism were $50.9{\pm}17.0ng/ml,\;39.1{\pm}20.3ng/ml\;and\;51.0{\pm}18.3ng/ml$ respectively. The serum myoglobin level of untreated hyperthyroidism seemed to be lower than that of normal control without statistical significance. The serum myoglobin levels in 5 patients with hypothyroidism ranged 28-156 ng/ml, and 3 patients showed increased serum myoglobin level. We observed one case with severe degree of thyrotoxic myopathy whose serum myoglobin level was markedly elevated initially and was decreased to normal range after treatment. This results suggests that the determination of serum myoglobin might be useful in the evaluation of thyrotoxic myopathy.