• Proceedings of the KSLP Conference
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• 1995.11a
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• pp.165-180
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• 1995

복잡한 음성장애를 이해하기 위해서는 음성관에 대한 여러 단계에서의 정량적인 검사가 이루어져야 한다. 이를 위하여 여러 가지 검사 법이 이용되고 있는데 예를 들면 음성의 인지적 검사(perceptual intelligibility), 음향음성학적검사(acoustic analysis), 공기역동학적 검사(aerodynamic study), 후두구조물의 운동 관찰, 그리고 근과 신경의 기능 검사(electromyographic study)등이 있다. 이중 인지적 검사는 청취자 동의 문제와 검사 법에 대하여 문제점이 제기 되기도 하며 발화 중 후두기능의 병태생리에 관한 추론적인 정보만을 제공한다는 문제점이 있다. 음향음성 검사는 이미 잘 알려진 상태로서 많은 parameter들이 측정되어온 것이 사실이나 그 유용성에 대해서도 아직 논란이 있으며 단지 성대의 진동에 의해 나타나는 현상만을 이용한 검사로서 일종의 정지성 연구에 불과한 것이 사실이다. (중략)

• Journal of Korean Foot and Ankle Society
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• v.18 no.3
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• pp.87-92
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• 2014

Acquired adult flatfoot is a deformity characterized by a decreased medial longitudinal arch and a hindfoot valgus with or without forefoot abduction. The etiologies of this deformity include posterior tibial tendon dysfunction, rheumatoid arthritis, trauma, Charcot's joint, neurologic deficit, and damage to the medial spring ligament complex or plantar fascia. Among these, posterior tibial tendon dysfunction is the most well-known cause. Although posterior tibial tendon dysfunction has been regarded as a synonym of acquired adult acquired flatfoot, failure of the ligaments supporting the arch can also result in progressive deformity even without a posterior tibial tendon problem. The authors describe the pathophysiology, diagnosis, and nonoperative treatment of acquired adult flatfoot, focusing on posterior tibial tendon dysfunction.

• The Academic Congress of Korean Shoulder and Elbow Society
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• 2006.11a
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• pp.59-68
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• 2006

회전근 개 질환의 병리기전의 연구과정은 과거에 형태학, 거시적 해부학 또는 방사선학적 연구를 통해 충돌 증후군에 대한 연구에 집중되었으나 그간의 병리조직학 및 생역학의 발전에 힘입어 좀 더 근본적인 원인에 대한 접근이 가능하게 되어 다양한 요인에 의해 복합적인 기전을 통해 발생함이 밝혀지고 있다. 그러나 아직 이와 같은 성과를 바탕으로 임상적으로 적절한 진단, 치료, 재활 및 예방에 대한 명확한 해답을 제시하기에는 부족함이 있으며 향후 건 내의 퇴행성 변화에 대한 분자 생물학적인 접근과 생체 내와 같은 조건에서의 역동성을 재현할 수 있는 견관절 모델의 개발을 통한 더욱 향상된 생역학적 연구가 필요할 것으로 생각된다.

• Korean Journal of Veterinary Research
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• v.36 no.4
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• pp.967-972
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• 1996

A study was carried on histopathology of LUTD. Based on this study, it was noted that a plural number of factors and some genetic mechanisms are participating in onset of this disease, which should have to be studied further in future in omnidirections.

• Journal of the Korean Society of Radiology
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• v.82 no.6
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• pp.1355-1365
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• 2021

Adhesive capsulitis, the so-called 'frozen shoulder', is one of the common causes of pain with a limited range of motion in the shoulder joint. The condition is usually diagnosed through the clinical course and physical examinations; however, several studies on imaging findings of adhesive capsulitis using sonography, MRI, and MR angiography have been reported. In this article, various imaging findings for the diagnosis of adhesive capsulitis-related anatomy are reviewed.

• Clinical and Experimental Pediatrics
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• v.51 no.1
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• pp.54-61
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• 2008

Purpose : This study was designed to clarify the mechanism of proteinuria in nephrotic syndrome patients by using puromycin aminonucleoside (PAN) nephrosis model. Methods : Following administration of various concentrations of PAN and antioxidants we observed the changes of podocyte cytoskeletons in cultured rat glomerular epithelial cells (GEpC) by method of scanning electron microscope, reactive oxyten species (ROS) analysis, permeability assay, confocal microscope, and Western blot assay. Results : PAN not only induced the ultrastructural changes of GEpC, such as shortening and fusion of microvilli, but also separated the intercellular gaps and linear ZO-1. PAN induced oxidative stresses in time and dose dependent manners and increases of intercellular permeability in anti-oxidants inhibitable manners. High concentration of PAN induced not only actin polymerization and disorganization, but also the conglomerulation and internal dislocation of ${\alpha}-actinin$ protein. The intensities of fluorescences of ZO-1 protein were diminished and internalized by PAN in a dose-dependent manner, which were inhibited by anti anti-oxidants. Conclusion : PAN induced the changes of podocytes cytoskeleton and junctional barriers by way of increasing ROS in GEpC that resulted in increasing their permeability in a antioxidatn-inhibitable manner. Glomerular hyperpermeability induced by PAN mediateing through oxidative stresses is thought to take part in the mechanism of proteinuria in nephrotic syndrome.

• Korean Journal of Psychosomatic Medicine
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• v.14 no.1
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• pp.39-46
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• 2006

Objectives: The study was intended to explore the relationships between temperament and premenstrual dysphoric disorder, to understand symptomatology of premenstrual dysphoric disorder and associated personality trait and to suggest therapeutic availability. Method : Twenty eight women, diagnosed as premenstrual dysphoric disorder by DSM-IV, were asked to complete the Korean version of Tridimensional Personality Questionnaire, and Shortened Premenstrual Assessment Form. The correlations between the severity of premenstrual symptoms and the scores of Tridimensional Personality Questionnaire were calculated. Results : The severity of symptoms of premenstrual dysphoric disorder was best explained by the harm-avoidance factor of the four dimensions of temperament. Conclusion : The symptoms of premenstrual dysphoric disorder are well explained by the harmavoidance factor and the reward-dependence factor of four dimensions of the temperament.

• Journal of radiological science and technology
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• v.32 no.4
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• pp.411-418
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• 2009

To evaluate the bone mineral density (BMD) and biochemical markers. We evaluated the BMD of femoral neck and lumbar spines of 998(male 568, female 430) persons who took a regular health screening in Woosuk University Hospital from September 2007 to March 2008 by dual energy bone mineral densitometry. Results of BMD are different in terms of biochemical markers. Especially aged people showed osteoporotic change progressively. Degree of osteoporosis increases with age. A steep decrease of BMD can be found in postmenopausal women who have low level of female hormone. More persistent effort is needed to find out the factors that can reduce BMD values for prevention of problems by osteoporosis. In essence, research on factors related to other biochemical markers must be studied continuously.

• Journal of Digestive Cancer Reports
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.

• Journal of Digestive Cancer Research
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.