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JYMS : Journal of Yeungnam Medical Science

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Hyun Do Kim 3 Articles
Identification of Interleukin 1-Responsive Genes in Human Chondrosarcoma SW1354 cells by cDNA Microarray Technology.
Jun Ha Jeon, Yong Wook Jung, Dae Young Yun, Hyun Do Kim, Chang Mo Kwon, Young Hoon Hong, Jae Ryong Kim, Choong Ki Lee
Yeungnam Univ J Med. 2007;24(1):24-40.   Published online June 30, 2007
DOI: https://doi.org/10.12701/yujm.2007.24.1.24
  • 1,429 View
  • 2 Download
AbstractAbstract PDF
BACKGROUND
Accumulating evidence shows that interleukin(IL)-1 plays a critical role in inflammation and connective tissue destruction observed in both osteoarthritis and rheumatoid arthritis. IL-1 induces gene expression related to cytokines, chemokines and matrix metalloproteinases by activation of many different transcription factors. MATERIALS AND METHODS: The chondrosarcoma cell line, SW1353, is known to be a valuable in vitro system for investigating catabolic gene regulation by IL-1beta in chondrocytic cells. To explore and analyze the changes in gene expression by IL-1 responsible for arthritis, SW1353 was treated with IL-1 for 1, 6 and 24 h and then total RNAs were purified for each time. The changes in gene expression were analyzed with 17k human cDNA microarrays and validated by semi-quantitative RT-PCR. RESULTS: Greater than a two-fold change was observed in 1,200 genes including metallothioneins, matrix metalloproteinases, extracellular matrix proteins, antioxidant proteins, cytoskeleton proteins, cell cycle regulatory proteins, proteins for cell growth and apoptosis, signaling proteins and transcription factors. These changes appeared to be correlate with the pathophysiological changes observed in early osteoarthritis. CONCLUSION: cDNA microarray analysis revealed a marked variability in gene expression, and provided insight into the overall molecular changes. The result of this study provide initial information for further studies to identify therapeutic targets in osteoarthritis pathogenesis.
A Case of Mercury Intoxication Associated with Pernicious Anemia.
Kyoung Ae Chang, Hyun Do Kim, Sun Jung Mun, Dong Hee Kim, Sung Ho Chun, Ha Young Lee, Dong Woon Bae, Hee Soon Cho, Kyung Hee Lee, Myung Soo Hyun
Yeungnam Univ J Med. 2006;23(1):103-107.   Published online June 30, 2006
DOI: https://doi.org/10.12701/yujm.2006.23.1.103
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AbstractAbstract PDF
Pernicious anemia is the frequent cause of megaloblastic anemia, and it is the result of a vitamin B12 deficiency due to the decrease or absence of intrinsic factor (IF) because of gastric mucosa atrophy or autoimmune destruction of IF-producing parietal cells. With the existence of a severe gastric atrophy, there is a decreased in acid and IF production and a further change in vitamin B12 absorption. Mercury is ubiquitous in nature and exists in 3 forms, elemental mercury, inorganic salts and organic compounds. Organic forms, specifically methyl mercury, are the most toxic of the 3 classes of mercurials. Methyl mercury exerts its most devastating effect on the central nervous system by causing psychiatric disturbances, ataxia, visual loss, hearing loss, and neuropathy. We report a case of mercury intoxication associated with pernicious anemia. The 77 years old patient was referred to Yeungnam University Hospital for tongue pain, somatitis, headache and aggressive behavior. He had taken an unevaluated medicine for a long time. After clinical evaluation, this case was diagnosed as a pernicious anemia and the unevaluated medicine was made up of mercury. After the administration of D-penicillamine and intramuscular injection of BAL and cobalamine, clinical symptoms and aggressive behavior were improved as well as laboratory findings.
A Case of Protein-losing Enteropathy Treated with High Dose Intravenous Glucocorticoid Therapy in Systemic Lupus Erythematosus.
Kyu Hyung Lee, Chang Mo Kwon, Hyun Do Kim, Dae Young Yun, Jae Yoong Lee, Yeong Hoon Hong, Choong Ki Lee
Yeungnam Univ J Med. 2005;22(2):253-258.   Published online December 31, 2005
DOI: https://doi.org/10.12701/yujm.2005.22.2.253
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  • 1 Crossref
AbstractAbstract PDF
Generalized edema and hypoalbuminemia are relatively common presenting manifestations in many clinical situations. The differential diagnosis of hypoalbuminemia include: Kwashiorkor, synthetic dysfunction of the liver, and excessive protein loss as in nephrotic syndrome. In systemic lupus erythematosus (SLE), hypoalbuminemia and generalized edema are most commonly due to protein loss associated with lupus nephritis; gastrointestinal involvement is uncommon, and therefore protein loss through the gastrointestinal tract is quite rare. We report a case of a protein losing enteropathy (PLE) associated with SLE. The patient was referred to our hospital for generalized edema, arthralgia and facial rash. After clinical evaluation, the patient met the criteria for the SLE diagnosis; hypoalbuminemia with general edema was consistent with a protein losing enteropathy. After two weeks of therapy with parenteral high dose glucocorticoid, the patients was improved in laboratory findings as well as clinical symptoms.

Citations

Citations to this article as recorded by  
  • A Case of Protein Losing Enteropathy as Only Clinical manifestation of Systemic Lupus Erythematosus
    Tae Hyun Kim, Yu Hee Choi, Lae Hyung Kang, Hyeong Jin Kim, Jin Ho Jang, Min Wook So
    Kosin Medical Journal.2017; 32(1): 84.     CrossRef
JYMS : Journal of Yeungnam Medical Science
© Yeungnam University College of Medicine, Yeungnam University Institute of Medical Science.