• Perspectives in Nursing Science
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• v.2 no.1
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• pp.19-36
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• 2005

Muscle atrophy is defined as a decrease in muscle mass, cross-sectional area, and myofibrillar protein content. Causes inducing muscle atrophy may be inactivity, denervation, undernutrition and steroid. Inactivity may decrease protein synthesis and increase protein breakdown of skeletal muscle. The muscle atrophy due to inactivity was induced by bed rest, hindlimb suspension, cast, total hip replacement arthroplasty, anterior cruciate ligament reconstruction. Denervated atrophy may be induced by the loss of innervation from lower motor neuron. The atrophy was apparent in the lower limb of hemiplegic patients following ischemic stroke and in the hindlimb of ischemic stroke rats. Protein breakdown of skeletal muscle in the undernourished state results in muscle atrophy. The atrophy due to undernutrition was evident in cancer and leukemia patients and in the undernourished rats. Steroids have been used to treat allergies, inflammatory diseases, autoimmune diseases and to inhibit immune function following transplantation. Steroids may induce muscle atrophy by protein breakdown of skeletal muscle. Muscle Physiology Laboratoryat College of Nursing, Seoul National University proved that dexamethasone may induce hindlimb muscle atrophy in rats and exercise and DHEA may attenuate hindlimb muscle atrophy induced by the steroid in rats. Nurses working with patients undergoing steroid treatment need to be cognizant of steroid induced muscle atrophy. They need to assess whether muscle atrophy is being occurred during and after the steroid treatment. Moreover, they need to apply exercise and DHEA to the patients undergoing steroid treatment in order to attenuate the steroid induced muscle atrophy.

• Biomolecules & Therapeutics
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• v.31 no.5
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• pp.573-582
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• 2023

Muscle atrophy is characterized by the loss of muscle function. Many efforts are being made to prevent muscle atrophy, and exercise is an important alternative. Methylglyoxal is a well-known causative agent of metabolic diseases and diabetic complications. This study aimed to evaluate whether methylglyoxal induces muscle atrophy and to evaluate the ameliorative effect of moderate-intensity aerobic exercise in a methylglyoxal-induced muscle atrophy animal model. Each mouse was randomly divided into three groups: control, methylglyoxal-treated, and methylglyoxal-treated within aerobic exercise. In the exercise group, each mouse was trained on a treadmill for 2 weeks. On the last day, all groups were evaluated for several atrophic behaviors and skeletal muscles, including the soleus, plantaris, gastrocnemius, and extensor digitorum longus were analyzed. In the exercise group, muscle mass was restored, causing in attenuation of muscle atrophy. The gastrocnemius and extensor digitorum longus muscles showed improved fiber cross-sectional area and reduced myofibrils. Further, they produced regulated atrophy-related proteins (i.e., muscle atrophy F-box, muscle RING-finger protein-1, and myosin heavy chain), indicating that aerobic exercise stimulated their muscle sensitivity to reverse skeletal muscle atrophy. In conclusion, shortness of the gastrocnemius caused by methylglyoxal may induce the dynamic imbalance of skeletal muscle atrophy, thus methylglyoxal may be a key target for treating skeletal muscle atrophy. To this end, aerobic exercise may be a powerful tool for regulating methylglyoxal-induced skeletal muscle atrophy.

• Biomedical Science Letters
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• v.18 no.1
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• pp.49-55
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• 2012

Numerous biochemical molecules have been implicated in the development of muscular atrophy. However, control mechanisms associated with muscular disease are not clear. The present study was conducted to investigate gene expression profiles of rat muscle during the denervation to atrophy transition processes. We isolated total RNA from rats suffering from partial muscle atrophy (P) and electromyostimulated atrophy (PE) and synthesized cDNA using annealing control primers. Using 20 ACPs for PCR, we cloned 18 DEGs using TOPO TA cloning vector, sequenced, and analyzed their identities using BLAST search. Sequences of 14 clones significantly matched database entries, while one clone was ESTs, and 3 clones were unidentified. Different expression profiles of selected DEGs between P and PE were confirmed. The troponin T, Fkbp1a, RGD1307554, Phtf1, Atp1a1 and Commd3 were highly expressed genes in the P and PE groups, while Krox-25 and TCOX2 were only expressed genes in the P group, the Sv2b and Marcks were only expressed genes in PE group. also, Cox8h was highly expressed genes in PE groups. The ASPH, ND1, and ARPL1 were highly expressed genes in the P and PE groups. List of genes obtained from the present study might provide an insight for the study of mechanism regulating muscle atrophy and electrostimulated muscle atrophy transitions. These data suggest that troponin T, Fkbp1a, RGD1307554, Phtf1, Atp1a1, and Commd3 are potentially useful as clinical biomarkers of age-related muscle atrophy and dysfunction.

• 대한상한금궤의학회지
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• v.4 no.1
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• pp.67-74
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• 2012

Objective : This research is to prove the effectiveness of Jinmutang in curing muscular atrophy Method : To achieve the goal of this research, we gave Jinmutang to the selected patients and observed the progress. Results & Conclusions: The results indicate the followings 1. After the treatment with Jinmu-tang, the symptoms of muscular atrophy were significantly improved. 2. JinmuTang based on sanghanron, as shown in the example above, has an effect on Muscle atrophy of the legs, But we need to study this pharmacologic and biological mechanism.

• Journal of Korean Medical classics
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• v.33 no.2
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• pp.1-12
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• 2020

Objectives : In this paper, lung atrophy syndrome[肺痿] in 『Huangdineijin(黃帝內經)』 and 『Jinguiyaolue(金匱要略)』 were compared, followed by examining its relation with upper wasting thirst[上消]. Also, ways in which psychological factors that contribute to lung atrophy syndrome could cause upper wasting thirst were studied. Methods : Verses from 『金匱要略·肺痿肺癰咳嗽上氣病脈證治』 and 『素問·痿論』 were analyzed based on various annotators's opinions to determine the cause and mechanism of lung atrophy syndrome and its relationship with upper wasting thirst. Results : In 『Jinguiyaolue(金匱要略)』, lung atrophy syndrome is described as the heat of the upper body entering the lungs to dry it out. The description in 『Suwen(素問)』 differs in that it accompanies atrophy symptoms, but the mechanism is the same. Lung atrophy syndrome in 『Jinguiyaolue』 could come from wasting thirst, while wasting thirst can be accompanied in deficiency caused by chronic lung atrophy syndrome. Heat in the lungs is caused by psychological factors where the person has lost its subject of possession or was unable to attain what was desired. When expanded to include heart atrophy syndrome[心痿] and lung atrophy syndrome[肝痿], the reason for upper wasting thirst could include immense sadness or excessive indulgence in pleasure due to unmet desires. Conclusions : Although diabetes and wasting thirst are not identical, application of wasting thirst pattern differentiation to diabetes treatment and management could lead to tailored treatment of each patient. Moreover, the five zhang pattern differentiation from the 『Suwen(素問)』 could increase treatment efficacy when applied to conditions caused by stress and emotional disorder, which are increasingly playing larger roles in causing wasting thirst, or diabetes.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.2
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• pp.200-205
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• 2014

Based on the way we have created to measure the brain atrophy of pons, frontal lobe, sylvian fissure, ventricle, cerebellum, we analyzed the correlation with age. We confirmed whether the brain atrophy due to hypertension, diabetes, hyperlipidemia, drinking, smoking is increasing. Brain deficiency(髓海不足), Brain dissatisfied(腦爲之不滿), Brain Consume(腦髓消烁) listed in Donguibogam(東醫寶鑑) have to be diagnosed with brain atrophy induced by developmental disorders, diseases, aging. Sylvian fissure is well reflected brain atrophy progressed by aging. And brain atrophy increased in hypertension, diabetes, hyperlipidemia, drinking, smoking is well reflected at Sylvian fissure.

• Journal of Yeungnam Medical Science
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• v.37 no.2
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• pp.133-135
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• 2020

Intercostal nerve injury is known to occur during thoracotomy; however, rectus abdominis muscle atrophy has rarely been reported. We describe a 52-year-old man who underwent primary closure of esophageal perforation and lung decortication via left thoracotomy. He was discharged 40 days postoperatively without any complications. He noticed an abdominal bulge 2 months later, and computed tomography revealed left rectus abdominis muscle atrophy. We report thoracotomy induced denervation causing rectus abdominis muscle atrophy.

• Journal of Oral Medicine and Pain
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• v.47 no.4
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• pp.217-221
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• 2022

Neurogenic muscular atrophy is muscle wasting and weakness caused by trauma or disease of the nerve that innervates the muscle. We describe a case of unilateral trigeminal neuropathy and neurogenic muscular atrophy of the masticatory muscle caused by a tumor in the foramen ovale. A 59-year-old man visited our clinic complaining of difficulty in right-sided mastication. There were no evident clinical signs and symptoms of temporomandibular disorder. However, severe atrophy of the right masseter and temporalis muscles and hypesthesia of the right side mandibular nerve area were confirmed. Through T1 and T2 signals on magnetic resonance imaging (MRI), a mass suspected of a neurogenic tumor was observed in the foramen ovale and cavernous sinus. Severe atrophy of all masticatory muscles on the right side was observed. This rare case shows trigeminal neuropathy caused by a tumor around the foramen ovale and atrophy of the ipsilateral masticatory muscles. For an accurate diagnosis, it is essential to identify the underlying cause of muscle atrophy with neurologic symptoms present. This can be done through a more detailed clinical examination, including sensory testing and brain MRI, and consider a referral to neurology or neurosurgery for the differential diagnosis of the intracranial disorder.

• The Journal of Internal Korean Medicine
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• v.39 no.4
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• pp.802-813
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• 2018

This case report describes a patient with olivopontocerebellar atrophy accompanied by sleep disorder and gait disturbance whose condition was improved by treatment with Korean medicine. The 61-year-old woman, who was diagnosed with olivopontocerebellar atrophy (Multiple Systemic Atrophy-Cerebellum), was admitted to hospital twice and treated with Korean medicine (acupuncture and herbal medicine) and rehabilitation. The Korean medicine was Gwibiondam-tang-gami and Jaeumgeonbi-tang-gami. Clinical symptoms were assessed by the Modified Bathel index, functional independent measurement, Berg balance scale, and Unified Multiple System Atrophy rating scale. A brain MRI at the one-year follow up after onset showed similar progress but clinical symptoms were improved after treatment, and the evaluation index score increased. Multiple system atrophy, a type of degenerative neurological disease, has no targeted treatment. In this situation, although this report describes a single case, Korean medicine treatment could provide a meaningful improvement in the sleep disturbance and gait disorder symptoms of patients with olivopontocerebellar atrophy.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.8 no.1
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• pp.33-37
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• 1997

Incomplete glottic closure of vocal cord atrophy is the common cause of dysphonia. Patients with vocal cord atrophy have complaints such as dysphonia, vocal fatigue, abnormal sensation in the throat, laryngeal pain, cough or sputum like functional voice disorders. Many investigators could not confirm the pathologic laryngeal structure because of their minute pathology. But recent advancements of laryngeal examinations made the many clinicians to detect minimal laryngeal pathology and to have mind the treatment for the vocal cord atrophy. But the results were less effective than their thoughts, the reasons of ineffectiveness were not known well. Authors have found the Hyperfunctional movement of the supraglottis during phonation before and after thyroplasty type I for vocal cord atrophy. Then we have applied the combined modality treatment with thyroplaty type I and voice therapy for relieve of hypefunctional movement of the supraglottis. These options have had more imporved results.