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RISS 인기검색어
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- 저자 : ( Hi Bahl Lee ) (검색결과 99 건)
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장기투석을 받은 만성 신부전 환자에서 발생한 종양에 관한 고찰
황정화,이혜경,홍현숙,박재성,김대호,권귀향,최득린,황승덕,이희발 순천향의학연구소 1996 Journal of Soonchunhyang Medical Science Vol.2 No.2
The authors tried to evaluate tumor occurrence in long-term dialysis patients with chronic renal failure. Among 359 patients, 20 patients (about 5.6%) were diagnosed with malignancy during long-term dialysis from the period of 1983 to 1995 at our nephrology department. The ultrasonographic and computed tomographic findings including the clinical features of 20 patients that were retrospectively reviewed. The mean age of the patients was 53 (37-75)years old and the ratio of male to female was 9:1. Among the 20 cases, 7 cases of hepatoma (35%) were developed. Among them, urinary tract tumors such as renal and bladder cancer were developed in 4 (20%) and 2 (10%) of the cases. Other malignant tumors were lymphoma, stomach cancer, uterine cervical cancer, cholangiocarcinoma, lung cancer, meningioma, and acoustic neuroma one case of each (each of 5.3%). The most common tumor in patients with chronic renal failure, who were receiving long-term dialysis, was hepatoma and the second most common tumor was cancer of the urinary tract such as kidney and bladder.
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Lee, Hi-Bahl,Yu, Mi-Ra,Song, Jae-Sook,Ha, Hun-Joo 이화여자대학교 약학연구소 2004 藥學硏究論文集 Vol.- No.14
Background, We previously demonstrated that high glucose up'-regulates fibronectin mRNA and protein expression by human peritoneal mesothelial cells (HPMC) through activation of protein kinase C (PKC). PKC is known to induce cellular reactive oxygen species (ROS) and PKC-dependent activation of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase has recently been shown to be responsible. in part for increased oxidative stress in diabetes. On the other hand, high glucose-induced mitochondrial overproduction of superoxide anion was found to activate PCK. We, therefore hypothesized that high glucose-induced activation of PCK in HPMC may increase cellular ROS and ROS, in turn, may activate PKC and thus provide: signal amplification in high glucose-induced fibronectin up-regulation in HPMC. Methouds. The role of ROS in high glucose and PKC-induced fibronectin expression was examined by quantification of cellular ROS after stimulation with high glucose and phorbol 12-myristate 13-acetate (PMA), by the effect of hydrogen peroxide (H₂O₂) and PMA on fibronectin expression, and final1y by inhibition of ROS and PKC. The source of cellular ROS was further examined by inhibition of NADPH oxidase and mitochondrial metabolism. Results. D-glucose increased dichlorofluorescein (DCF)-sensitive cellular ROS in HPMC in a dose-dependent manner. L-glucose did not induce ROS generation and cytochalasin B completely blocked high glucose-induced ROS generation, suggesting that glucose uptake, but not media hyperosmolality, is required in ROS generation in HPMC. PMA increased cellular ROS and fibronectin secretion, A single dose of H₂O₂ or H₂O₂ continuously generated by glucose oxidase fibronectin expression. Antioxidants trolox and catalase inhibited high glucose- and PMA-induced fibronectin mRNA and protein expression. Inhibition of PKC inhibited high glucose and H₂O₂-induced fibronectin secretion. NADPH oxidase inhibitors (diphenyleneiodinium and apocynin) and an inhibitor of mitochondrial electron transport chain subunit I (rotenone) all effectively inhibited high glucose-induced cellular ROS generation and fibronectin secretion. Conclusion. The present data demonstrate that high glucose increases cellular ROS in HPMC through activation of PKC, NADPH oxidase, and mitochondrial metabolism and that ROS, thus generated, up-regulate fibronectin expression by HPMC. ROS are not only downstream but also upstream signaling molecules to PKC and provide signal amplification in high glucose-induced fibronectin expression by HPMC. The present data imply that cellular ROS may he potential therapeutic targets in progressive accumulation of extracellular matrix in the peritoneal tissue of long-term peritoneal dialysis patients using high glucose-containing peritoneal dialysis solutions.
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Lee, Hi Bahl,Ha, Hunjoo 이화여자대학교 약학연구소 2004 藥學硏究論文集 Vol.- No.13
Background: Advanced glycation end products (AGEs) have been implicated in the pathogenesis of diabetic complications including nephropathy. Aminoguanidine prevents formation of AGEs and protein cross linking and has been shown to delay the onset and the progression of glomerular injury in experimental diabetic animals. Long-term exposure of mesangial cells to high glucose significantly increases transforming growth factor (TGF)-β1 and extracellular matrix mRNA and protein expression, which are two prominent features of diabetic glomerulopathy. However, the role of AGEs in mesangial cell activation induced by long-term exposure to high glucose has not been elucidated. Methods: The effects of aminoguanidine on the synthesis of TGF-β1 and fibronectin by rat mesangial cells cultured under high glucose for 2 weeks were examined and compared with the effects of N^(G)-nitro-L-arginine methyl ester (NAME), a selective nitric oxide synthase inhibitor, because aminoguanidine also inhibits the inducible nitric oxide synthase. Results: Culture of mesangial cells in 30 mM (high) glucose for 2 weeks induced 1.5-fold (ELISA) and 1.9-fold (Western blot analysis) increase in AGEs in the culture media. Northern blot analysis revealed 1.5-fold increase in TGF-β1 and 1.7-fold increase in fibronectin mRNA expression in cells cultured under high glucose compared to 5.6 mM (control) glucose. Increases in mRNA expression were followed by increased protein synthesis. Mink lung epithelial cell growth inhibition assay revealed 1.4-fold increase in TGF-01 protein in high glucose media compared to control. Fibronectin protein also increased 2.1-fold that of control glucose by Western blot analysis. Administration of aminoguanidine suppressed AGE formation in a dose dependent manner and at the same time suppressed TGF-β1 and fibronectin synthesis by mesangial cells cultured in both control and high glucose. In contrast, NAME did not affect high glucose-induced changes. Conclusion: These findings support a role for AGEs in high glucose-induced upregulation of TGF-β1 and fibronectin synthesis by mesangial cells.
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Hi Bahl Lee,하헌주 대한의학회 2007 Journal of Korean medical science Vol.22 No.6
A growing body of evidence indicates that epithelial-mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMC) may play an important role in the development and progression of peritoneal fibrosis during long-term peritoneal dialysis (PD) leading to failure of peritoneal membrane function. Here, we review our own observations and those of others on the mechanisms of EMT of HPMC and suggest potential therapeutic strategies to prevent EMT and peritoneal fibrosis during long-term PD. We found that high glucose and H2O2 as well as transforming growth factor- 1 (TGF- 1) induced EMT in HPMC and that high glucoseinduced EMT was blocked not only by inhibition of TGF- 1 but also by antioxidants or inhibitors of mitogen-activated protein kinases (MAPK). Since MAPKs are downstream target molecules of reactive oxygen species (ROS), these data suggest that high glucose-induced generation of ROS and subsequent MAPK activation mediate high glucose-induced EMT in HPMC. We and others also observed that bone morphogenetic protein-7 (BMP-7) prevented EMT in HPMC. Glucose degradation products (GDP) were shown to play a role in inducing EMT. Involvement of a mammalian target of rapamycin (mTOR) in TGF- 1-induced EMT has also been proposed in cultured HPMC. A better understanding of the precise mechanisms involved in EMT of HPMC may provide new therapeutic strategies for inhibiting peritoneal fibrosis in long-term PD patients.
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이철우,이현아,박민선,김진국,김원배,이희발,황승덕,이유경,강문수,추원석 대한신장학회 1999 Kidney Research and Clinical Practice Vol.18 No.1
A 44-year-old man treated with azathioprine, cyclosporine and prednisolone for 7.5 years after allogeneic renal transplantation was admitted because of exertional dyspnea, fatigue and pancytopenia which were found 3 months ago. He had been on hemodialysis for renal failure of unknown cause for 8 months before the renal transplantation. Bone marrow examination showed hypercellularity, erythroid hyperplasia and 7% of myeloblast, consistent with the diagnosis of myelodysplastic syndrome. Cytogenetic study showed chromosomal abnormalities:deletion of chromosome 5, monosomy 7, trisomy 8, monosomy 14 and deletion of chromosome 17. Immunosuppressive agents were discontinued and he was treated with transfusion, G-CSF, and combination chemotherapy including topotecan and Ara-C. Graft kidney function was normal before and after the treatment, but the clinical course was fatal because of leukemic transformation and eventually sepsis. Although therapy induced myelodysplastic syndrome was rare in renal allograft recipients, thorough evaluations including bone marrow biopsy and cytogenetic study are recommended in patients with anemia of unknown etiology.
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