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- 저자 : 유순희 ( Soon Hee Yoo ) (검색결과 2 건)
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이베나 ( Be Na Lee ),유순희 ( Soon Hee Yoo ),조덕원 ( Duk Won Cho ) 한국정맥경장영양학회 2010 한국정맥경장영양학회지 Vol.3 No.1
Purpose: We wanted to compare the nutritional status of stroke patients who are in the acute state with that of stroke patients who are in the chronic state and to evaluate the factors that may affect stroke patients` nutritional status in Korea. Methods: This is a retrospective study. We reviewed the medical histories of stroke patients who were hospitalized in St. Paul`s hospital from January 2005 to February 2007.The applied measurements were the body mass index (BMI) and the biochemical findings such as albumin, the total lymphocyte count (TLC) and the hemoglobin level. We considered the factors that might affect the patient`s nutritional status, including the patient`s mobility, the mode of feeding, the type of medical insurance as an indicator of the socioeconomic status, diabetes mellitus, dysphagia and a medication for depression. Results: Thirty four males and 27 females were studied and the mean age of the patients was 60.13 years old. The mean follow up duration was 456.64 days. The BMI was decreased from 23.85 to 23.16 kg/m2 (P-value=0.049), the albumin was decreased from 4.09 to 3.88 g/dl (P-value=0.012) and the TLC was decreased from 2,056.6 to 1,772.3/L(P-value=0.034) in the chronic state. Specially, the nutritional imbalance was severe in the chronic patients who were undergoing tube feeding, in those who had poor mobility, in those who had dysphagia or those who were taking a medication for depression. Conclusion: Control of stroke patients` nutritional state is crucial for a better outcome, not only at the acute stage but also at the chronic stage. Therefore, medical personnels should be aware of and care for the nutritional state of stroke patients. (KJPEN 2010;3(1):33-39)
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이강욱,김영건,노흥규,송민호,김호,박은신,유순희,한희정,주원찬,원진호,임규,권오유 대한내분비학회 1998 Endocrinology and metabolism Vol.13 No.4
Background: The proinflammatory cytokine, IFN-y has been shown to exert pleiotropic effects in a variety of pathophysiologic conditions in autoimmune thyroid disease. The thyrocyte response to IFN-y is mediated two distinct classes of proteins, Janus kinases(Jakl and Jak2) and Signal Transducers and Activation of Transcription(STATl). The activation of STAT 1 is involved in the regulation of many interferon stimulated genes, such as MHC class II, intercellular adhesion molecules-1(ICAM-1) and MHC class II transactivator(CIITA) after the binding to the GASgFN- pactivated site) of the gene promoters. Recently we found TSH/forskolin inhibits IFN-y stimulated maximal expression of ICAM-1 in FRTL-5 cell. IFN-y action is localized between -175 bp and -97 bp from the start of translation of ICAM-1 gene which contains regulatory elements known to be involved in IFN-y action in other eukaryotic cells, palindromic IFN-y activated site(GAS)(5-TTTCCGGGAAA-3) which could bind STAT1, STAT3, STAT5, STAT6. Furthermore, the addition of TSH and forskolin causes a decrease in ICAM-1 promoter activity and its action was localized in GAS. These findings suggested TSH/cAMP signaling pathways downregulate IFN-y activated Janus kinase-STAT signaling path. We wanted to explore the possible involvement of elevated cAMP in the negative regulation of IFN-y induced STAT1 activation in thyroid cells. Method: We made several 5-deletion constructs of rat ICAM-1 promoter and analyzed the promoter activities by measuring the luciferase activity after tranfection into FRTL-5 cells. The protein/DNA complex was measured by electrophoretic mobility shift analysis using labeled oligonucleotide. We checked the level of total and phosphorylated STATl protein by immunoblot analysis using specific antibodies. Results: Stimulation of IFN-y in FRTL-5 cells resulted in rapid activation of STATl/DNA binding activity, which was apparent after several minute of stimulation, maintains its activity until 48 h. Incubation of cells with TSH result in suppression of IFN-p mediated STAT1/DNA binding activity throughout the time course of activation by IFN-y. Addition of TSH into 5H maintained FRTL-5 cells did not change the total amount of latent STAT1 amount and also not affect IFN-y mediated production of total STAT1 until 4 h. IFN-y(100 U/mL) rapidly induced phosphorylation of STAT1 within 30 min. and maintained its level without significant change until 48 hours. Cells treated with TSH dramatically lowered the level of IFN-y induced production and phosphorylation of STAT1 after 12 h, 24 h, 36 h, and 48 h but TSH had no effect on the level of phosphorylated STATl within 4 h after IFN-y stimulation. The proteasome inhibitor, MG132 and phosphatase inhibitor, sodium orthovanadate did not block the TSH or forskolin mediated downregulation of phosphorylated STAT1. Conclusion: These results indicate a regulatory mechanism which TSH signaling can modulate the prolonged activation of Jak/Stat by IFN-y. We identified one of mechanisms related to TSH mediated negative suppression of the ICAM-1 gene; TSH/cAMP signaling pathways downregulate the cytokine activated Janus kinase-STAT signaling path (J Kor Soc Endocrinol 13:536-553, 1998).
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