• Journal of Korean Academy of Nursing
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• v.41 no.6
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• pp.834-842
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• 2011

Purpose: The purpose of this study was to determine the effect of dehydroepiandrosterone (DHEA) on recovery of muscle atrophy induced by Parkinson's disease. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 20 ${\mu}g$) into the left striatum using stereotaxic surgery. Rats were divided into two groups; the Parkinson's disease group with vehicle treatment (Vehicle; n=12) or DHEA treatment group (DHEA; n=22). DHEA or vehicle was administrated intraperitoneally daily at a dose of 0.34 mmol/kg for 21 days. At 22-days after DHEA treatment, soleus, plantaris, and striatum were dissected. Results: The DHEA group showed significant increase (p<.01) in the number of tyrosine hydroxylase (TH) positive neurons in the lesioned side substantia nigra compared to the vehicle group. Weights and Type I fiber cross-sectional areas of the contralateral soleus of the DHEA group were significantly greater than those of the vehicle group (p=.02, p=.00). Moreover, extracellular signal-regulated kinase (ERK) phosphorylation significantly decreased in the lesioned striatum, but was recovered with DHEA and also in the contralateral soleus muscle, Akt and ERK phosphorylation recovered significantly and the expression level of myosin heavy chain also recovered by DHEA treatment. Conclusion: Our results suggest that DHEA treatment recovers Parkinson's disease induced contralateral soleus muscle atrophy through Akt and ERK phosphorylation.

• Journal of Korean Biological Nursing Science
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• v.10 no.1
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• pp.88-95
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• 2008

Purpose: The purpose of this study was to examine the effect of neuropathic pain by peripheral nerve injury on mass and Type I and II fiber cross-sectional areas on hindlimb muscles of the neuropathic pain model rat. Method: Adult male Sprague-Dawley rats (body weight 200-220 g) were assigned to one of two groups: a neuropathic pain group (n=7) that had a ligation of the left L5 spinal nerve, a control group (n=5), a naive rat without any procedures. Withdrawal threshold, activity, body weight and food intake were measured daily. At 8 days after neuropathic pain, all rats were anesthetized and the soleus and plantaris muscles were dissected from the both hindlimbs. Body weight, food intake, muscle weight and Type I and II fiber cross-sectional area of the dissected muscles were determined. Result: The neuropathic pain group showed a significant decreases (p<.05) as compared with the control rats, in diet intake, body weight, muscle weight and Type II fiber cross-sectional area of the left (affected side) soleus and plantaris muscles, and the right (unaffected side) muscle weight of plantaris and Type II fiber cross-sectional area of the soleus muscle. Conclusion: The hindlimb muscle atrophy occurs in both affected and unaffected side due to neuropathic pain by the peripheral nerve injury. The hindlimb muscle atrophy of the affected side is more pronounced than that of the unaffected side.

• Journal of Acupuncture Research
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• v.36 no.4
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• pp.238-244
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• 2019

Background: This study aimed to investigate the protective effects of Zanthoxylum bungeanum Maxim pharmacopuncture on disuse muscle atrophy in the gastrocnemius muscle of rats. Methods: Thirty male 250 g Sprague-Dawley rats were distributed randomly into 3 groups. The left hindlimb immobilization was performed with casting tape for 2 weeks, and no treatment was given to the right hindlimb. Rats received pharmacopuncture and were injected daily on the BL57 with either 2 mL of Zanthoxylum bungeanum Maxim aqueous extract (ZM-W group), 1 mL pharmacopuncture of Zanthoxylum bungeanum Maxim ethanol extract (ZM-E group), or 2 mL normal saline (control group). After 2 weeks of immobilization, the weight of the whole gastrocnemius muscle was measured, and the morphology of both the left and the right gastrocnemius muscles were assessed by Hematoxylin and Eosin staining. To investigate the immobilization-induced muscular apoptosis, the immunohistochemical analysis of BAX and Bcl-2 was carried out. Results: ZM-W and ZM-E significantly inhibited the reduction in weight of the left gastrocnemius muscle, the reduction in the left myofibrils, and the cross-sectional area of gastrocnemius, as compared with the control. Moreover, the ZM-W and ZM-E groups showed significantly reduced immunoreactivity for BAX, and increased immunoreactivity of Bcl-2 in left gastrocnemius muscle compared with the control group. Conclusion: These results suggest that Zanthoxylum bungeanum Maxim pharmacopuncture has protective effects against immobilization-induced muscle atrophy by regulating the activity of apoptosis-associated BAX / Bcl-2 proteins in the gastrocnemius muscle.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.593-599
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• 2005

An abattoir study on the abdominal fat necrosis in adult cattle was performed pathologically. Grossly, masses of fat necrosis were leekgreen in colour, lobulated on the cut surface, and saponificated in the texture. These necrotic adipose tissues infiltrated usually into neighboring parenchymal organs including intestines and pancreas, leading to fibrosis or atrophy of them. Histopathologically, necrotic fat cells contained acidophilic, opaque, amorphous substance or basophilic fibrillar or granular minerals in their cytoplasms. The lesions of fat necrosis were divided by fibroconnective tissue. With increase of the severity, necrotic fat cells fused each other and then formed fat cysts. In this severe lesion, necrotic fat cells were partialy or completely replaced by macrophages. Multinucleated giant cells were scattered in this lesion. Interestingly, small artery in the lesion of fat necrosis revealed severe thickening of internal elastic membrane. Severe fibrosis was observed in or between the outer longitudinal and inner circular muscular externas causing segregation, degeneration and necrosis of muscle fibers. The nerve cells of Auerbach's and Meissner's plexuses surrounded by fibrosis were degenerated or necrotic. In addition, necrotic fat cells infiltrated into the pancreas, resulting in pancreas atrophy. From these results, it is speculated that fat necrosis might compromise intestinal movement due to necrosis of muscular externa and ganglion cells of Auerbach's and Meissner's plexuses.

• Journal of Korean Academy of Nursing
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• v.41 no.4
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• pp.520-527
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• 2011

Purpose: The purpose of this study was to examine effects of nitric oxide synthase (NOS) inhibitor on muscle weight and myofibrillar protein content of affected and unaffected hindlimb muscles in rats with neuropathic pain induced by unilateral peripheral nerve injury. Methods: Neuropathic pain was induced by ligation and cutting of the left L5 spinal nerve. Adult male Sprague-Dawley rats were randomly assigned to one of two groups: The NOSI group (n=19) had NOS inhibitor (L-NAME) injections daily for 14 days, and the Vehicle group (n=20) had vehicle injections daily for 14 days. Withdrawal threshold, body weight, food intake and activity were measured every day. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected from hindlimbs. Muscle weight and myofibrillar protein content of the dissected muscles were determined. Results: The NOSI group showed significant increases as compared to the Vehicle group for body weight at 15 days, muscle weight and myofibrillar protein content of the unaffected soleus and gastrocnemius. The NOSI group demonstrated a higher pain threshold than the vehicle group. Conclusion: NOSI for 14 days attenuates unaffected soleus and gastrocnemius muscle atrophy in neuropathic pain model.

• Journal of Korean Biological Nursing Science
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• v.13 no.2
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• pp.179-184
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• 2011

Purpose: The purpose of this study was to examine the effect of short-term undernutrition on muscle weight and Type I and II fiber cross-sectional area of hindlimb muscles in undernourished rats. Methods: Adult male Sprague-Dawley rats were randomly assigned to one of two groups: The undernourished (UN) group (n=9) and the control (C) group (n=9). A control group was allowed to have water and pellet ad libitum for 5 days. Undernutrition was induced by providing 32% of total intake of the control group for 5 days. Body weight of two groups and food intake of the control group were measured every day. At 6 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles, and liver were dissected. Body weight, food intake, muscle weight, liver weight and cross-sectional area were determined. Results: The UN group at 6 days after undernutrition showed significant decreases, as compared to the control group in body weight, liver weight, muscle weight of soleus, plantaris, and gastrocnemius, and Type I fiber cross-sectional area of soleus and gastrocnemius muscles and Type II fiber cross-sectional area of plantaris and gastrocnemius muscles. Conclusion: Hindlimb muscle atrophy occurs from the short-term undernutrition.

• Journal of Microbiology and Biotechnology
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• v.8 no.6
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• pp.663-668
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• 1998

Several neurodegenerative diseases such as Huntington's disease, dentatorubralpallidoluysian atrophy, spinobulbar muscular atrophy, Machado-Joseph disease, and spinocerebellar ataxias type 1 are associated with the aggregation of expanded glutamine repeats within their proteins. Generally, in clinically affected individuals, the expansion of the polyglutamine sequences is beyond 40 residues. To address the length of polyglutamine that forms aggregation, we have constructed plasmids encoding glutathione S-transferase (GST) Machado-Joseph disease gene fusion proteins containing polyglutamine and investigated the formation of aggregates in E. coli. Surprisingly, even $(Gin)_8$, in the normal range as well as $(Gin)_{65}$ in the pathogenic range enhanced the formation of insoluble protein aggregates, whereas $(Ser)_8$, and $(Aia)_8$, did not form aggregates. Our results indicate that the formation of protein aggregates in GST-polyglutamine proteins is specifically mediated by the polyglutamine repeat sequence within their protein structure. Our study may contribute to the understanding of the molecular mechanism of the formation of protein aggregates in neurodegenerative disorders and the development of preventative strategies.

• The Journal of Korean Physical Therapy
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• v.22 no.3
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• pp.9-15
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• 2010

Purpose: To evaluate, in patients with degenerative disc disease (DDD), the efficacy of using spinal stabilizing exercises for the reversal? of atrophy of the multifidus and psoas major, reductions in pain and disability, and for increases in paraspinal muscle strength. Methods: Nineteen patients diagnosed with DDD participated for 10 weeks in a spinal stabilization exercise program. Pain and disability were measured before and after exercise using, respectively, a visual analogue scale (VAS) and the Oswestry Disability Index (ODI). Paraspinal muscular strength in four directions was evaluated using CENTAUR. Both before and after exercise we used computed tomography (CT) too measure cross-sectional areas (CSAs) of both the left and right multifidus and the psoas major at the upper & lower endplate of L4. Results: After 10 weeks of a spinal stabilization exercise program, pain was significantly decreased from $5.7{\pm}0.9$ to $2.5{\pm}0.9$ (p<0.01); the ODI score decreased from $16.7{\pm}4.9$ to $7.3{\pm}3.1$. Paraspinal muscle strength was significantly increased (p<0.01) and the CSAs of the left and right multifidus and psoas major muscles were significantly increased (p<0.01). Conclusion: Spinal stabilization exercise is effective in reversing atrophy in DDD patients, in reducing pain and disability, and in increasing paraspinal muscle strength. It is an effective treatment foro aiding rehabilitation in these cases.

• Journal of Electrodiagnosis and Neuromuscular Diseases
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• v.20 no.2
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• pp.124-129
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• 2018

Neuralgic amyotrophy (NA) is an idiopathic disease characterized by muscular atrophy accompanied by neuralgia, where acute pain in the limb, mostly including the shoulders, leads to muscle weakeness and atrophy in the limb days to weeks after the onset of pain. Although its exact pathogenesis is unknown, genetic and nongenetic factors, such as infection, surgery, and trauma are suspected contributors. We report this case as we diagnosed NA of the right lower limb via enhanced MRI as well as EMG and have followed up the patient's prognosis and radiologic changes for one and a half years. In addition, the patient had been diagnosed with neuropsychiatric disorders, such as major depressive disorder and somatic symptom disorder.

• Journal of Genetic Medicine
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• v.17 no.2
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• pp.89-91
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• 2020

Charcot-Marie-Tooth (CMT) disease can be divided mainly into demyelination and axonopathy based on the results of the electrophysiological study. Mitofusin 2, encoded by MFN2 gene, has a crucial role in the fusion of mitochondria, which is known to associate with CMT type 2A as one of the axonal forms. We describe a 44-year-old man with progressive weakness on bilateral legs after noticing foot drop in his early teen. When we examined him at 45 years of age, he presented atrophy on entire legs and with distal muscle weakness on limbs. The nerve conduction study revealed severely decreased amplitude on motor nerve ranging from 0.2 to 4.5 mV, while conduction velocity remained more than 30.4 m/s. The whole-exome sequencing revealed a novel variant c.2228G>T in MFN2 by efficient genetic analysis tool, MutationDistiller. This report will not only expand the mutation spectrum of CMT2A but also introduce a time-saving genetic analysis tool.