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당뇨병성 신증 : 아포지단백 E 제거 백서에서 장기적인 Deoxycorticosterone acetate 투여가 미치는 영향에 관한 연구
고강지 ( Gang Jee Ko ),강영선 ( Young Sun Kang ),송혜경 ( Hye Kyoung Song ),이미화 ( Mi Hwa Lee ),권오성 ( Oh Sung Kwon ),한금현 ( Kum Hyun Han ),한상엽 ( Sang Youb Han ),한지영 ( Jee Young Han ),김형규 ( Hyoung Kyu Kim ),차대룡 ( 대한신장학회 2008 춘계학술대회 초록집 Vol.28 No.1
Role of aldosterone in diabetic nephropathy
CHA, DAE RYONG,KANG, YOUNG SUN,HAN, SANG YOUB,JEE, YI HWA,HAN, KUM HYUN,KIM, HYOUNG KYU,HAN, JEE YOUNG,KIM, YOUNG SIK Blackwell Science Pty 2005 Nephrology Vol.10 No.suppl2
<P>SUMMARY: </P><P>In the last 10 years, many studies have focused on the non-classical action of aldosterone. One of the most important new aspects of aldosterone is its pathogenic role as proinflammatory and profibrotic molecules. It has been reported that aldosterone induces myocardial fibrosis and vascular inflammation through up-regulation of various proinflammatory and profibrotic cytokines. We investigated the effect of aldosterone and spironolactone, which is a non-selective mineralocorticoid receptor antagonist, on monocyte chemoattractant peptide (MCP-1) and collagen synthesis in cultured mesangial and tubular epithelial cells. In addition, to evaluate the effect of spironolactone on diabetic nephropathy, we used Otsuka Long-Evans Tokushima Fatty (OLETF) rats which are known type 2 diabetic animal models. Spironolactone treatment did not induce any significant change in blood glucose levels and blood pressure. However, spironolactone therapy significantly inhibited urinary albumin and MCP-1 excretion. Spironolactone treatment also suppressed renal mRNA expression for MCP-1, macrophage migration inhibitory factor (MIF) as well as intrarenal protein synthesis for ED-1 and MIF. Morphologically, spironolactone treatment significantly prevented glomerulosclerosis, collagen deposition and connective tissue growth factor (CTGF) expression in diabetic rats. In cultured cell experiments, aldosterone directly increased the MCP-1, collagen secretion and spironolactone treatment abolished aldosterone-induced MCP-1 and collagen synthesis. Surprisingly, aldosterone treatment did not induce any significant change in TGF&bgr;1 gene transcription. Finally, we found that NF-kB activity was increased after stimulation with aldosterone and spironolactone therapy inhibited their activation. In addition, prior treatment with pyrrolidine dithiocarbamate (PDTC), which is a NF-KB inhibitor, inhibited aldosterone-induced MCP-1 protein secretion. These results suggest that aldosterone blockade could play a role in preventing the progression of diabetic nephropathy via anti-inflammatory and antifibrotic mechanisms.</P>
Kang, Young Sun,Park, Yun Gyu,Kim, Bo Kyung,Han, Sang Youb,Jee, Yi Hwa,Han, Kum Hyun,Lee, Mi Hwa,Song, Hye Kyoung,Cha, Dae Ryong,Kang, Shin Wook,Han, Dae Suk Journal of Endocrinology (Ltd. by Guarantee) 2006 Journal of molecular endocrinology Vol.36 No.2
<P>Angiotensin II (Ang-II) and vascular endothelial growth factor (VEGF) have an important role in the pathogenesis of diabetic nephropathy, but the signaling cascade of VEGF regulation in response to Ang-II in podocytes is largely unknown. In these experiments, we looked at the effect of Ang-II on the production of VEGF, and investigated whether VEGF production depends on the p38 mitogen activated protein kinase (MAPK) pathway in cultured mouse podocytes. Incubation of podocytes with Ang-II induced a rapid increase in VEGF mRNA expression and protein synthesis as well as its transcriptional activity in an Ang-II dose-dependent manner. To further define the role of angiotensin type 1 (AT1) and type 2 (AT2) receptors involved in Ang-II-mediated VEGF synthesis, the effects of selective AT1 and AT2 receptor antagonists were evaluated. Prior treatment with losartan significantly inhibited VEGF mRNA and protein synthesis induced by Ang-II, which suggests that the AT1 receptor is involved in Ang-II-mediated VEGF synthesis. Furthermore, stimulation of the cells with Ang-II increased both phosphorylation of p38 MAPK and MAP kinase kinase 3/6 (MKK3/6). Additionally, Ang-II enhanced the DNA binding activity to cAMP response element binding protein (CREB) and phosphorylation of CREB. In addition, to investigate the role of p38 MAPK in Ang-II-induced VEGF synthesis, podocytes were pretreated with or without the p38 MAPK inhibitor, SB203580 for 24 h to observe whether Ang-II-mediated VEGF synthesis was inhibited by blocking p38 MAPK. The addition of SB203580 led to a marked inhibition of the increased VEGF mRNA and protein production induced by Ang-II in a dose-dependent manner. Taken together, these results suggest that Ang-II stimulates the synthesis of VEGF in podocytes and the production of VEGF induced by Ang-II is mediated, in part, through the activation of the p38 MAPK pathway.</P>
서금희 ( Kum Jee Seo ),김기영 ( Ki Young Kim ),문병문 ( Byung Moon Moon ) 한국주조공학회 2012 한국주조공학회지 Vol.32 No.3
A series of refractory mold coatings were applied to cast iron specimens, and their resistances to wear and spalling were investigated. Tests were carried out with own made measures, and also a calculation was tried for the comparison of a part of results like spalling. Worn width by scrubbing the indenter on the coating layer increased significantly at high temperature. Temperature increasing rate across the specimen when the coating side was exposed to 1,000oC was in the range of 14.5~75.8oC/sec·mm, and specimens with thicker coating layer showed lower temperature increase. Severe spalling of coated layer was observed after heating the specimen, and it was able to confirm by calculation using a commercial code.
( Jin Joo Cha ),( Young Youl Hyun ),( Yi Hwa Jee ),( Mi Jin Lee ),( Kum Hyun Han ),( Young Sun Kang ),( Sang Youb Han ),( Dae Ryong Cha ) 대한신장학회 2012 Kidney Research and Clinical Practice Vol.31 No.3
Background: Leptin is an adipokine that is recently reported to be a biomarker of systemic inflammation. Although atherosclerosis causes cardiovascular diseases, it is not clear whether leptin contributes to the acceleration of this process. In this study, we investigated whether alterations of plasma leptin levels were related to diabetic nephropathy and systemic inflammation. In addition, we examined the physiologic action of leptin in cultured vascular smooth muscle cells (VSMCs). Methods: A total of 126 type 2 diabetic participants and 37 healthy controls were studied. The diabetic participants were divided into three groups according to stage of nephropathy. We investigated whether leptin induced monocyte chemo- tactic peptide-1 (MCP-1) synthesis through the mitogen-activated protein kinase (MAPK) pathway using cultured VSMCs. Results: Plasma leptin concentrations were significantly higher in the diabetic group than in the controls. Plasma leptin levels were positively correlated with body mass index, fasting and postprandial blood glucose, hemoglobin A1c, total cholesterol, urinary albumin excretion, high-sensitivity C-reactive protein (hsCRP), and MCP-1 plasma levels, and negatively correlated with creatinine clearance values. In cultured VSMCs, leptin increased MCP-1 production in a dose-dependent manner, and this stimulating effect of leptin on MCP-1 expression was reversed by the MAPK (MEK) inhibitor PD98059. In addition, leptin stimulated the phosphorylation of MEK, extracellular signal-regulated kinase, and E26-like transcription factor, which are components of the MAPK pathway. Conclusions: Overall, these findings suggest that activation of leptin synthesis may promote MCP-1 activation in a diabetic environment via the MAPK pathway in VSMCs and that it possibly contributes to the acceleration of atherosclerosis.
김준우,안철우,남주영,김똘미,김영균,추적금,박종숙,박진아,조승현,김동연,김도연,윤수지,이경열,차봉수,김경래,임승길,이현철,허갑범 대한당뇨병학회 2002 임상당뇨병 Vol.3 No.2
본 저자들은 인위적인 인슐린 투여로 인한 인간성 저혈당증 1예에서 보존적인 치료로 의식기능은 회복하였으나, 현저한 인지능력 저하를 하였기에 문헌고찰과 함께 보고하는 바이다. Factitious hypoglycemia is a covert attempt to lower the blood glucose concentration with insulin or a sulfonylurea agent. This attempt is mainly performed by the patients themselves. In a large series of diabetics who had overdosed on drug, less than 5% had used insulin for suicidal or homicidal purposes. Additionally, 4 of 204 hypoglycemic episodes were due to a suicide attempt with insulin. The onset of insulin action, its peak level, and duration, and the degree of hypoglycemia, are determined by insulin's pharmacokinetics. However, the final outcomes are not associated with the amount of insulin used. The complications related to insulin overdose are cerebral damage and hypokalemia. Other complications include, pulmonary edema attributed to congestive heart failure and hypertensive crisis, as well as respiratory insufficiency. We report this case with a review of the literature.