- Epidermal Cyst in the Renal Pelvis: A Case Report with Review of the Literature.
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Sun Zoo Kim, Tae In Park, Sang Han Lee, Jung Sik Kwak
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Korean J Pathol. 2004;38(4):270-272.
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- We report here on a case of an epidermal cyst arising in the kidney. This cyst occurred in a 61-year-old woman with a past history of several attacks of ureteral stones and she received treatments of extracoporeal shock wave lithotripsy and open nephrolithostomy. On the intravenous pyelogram, a relatively well demarcated, 5x5 cm-sized lesion with calcification was detected in the renal pelvis and calices.
The lesion was removed by percutaneous nephrolithotomy.
Histologically, the lesion had the same morphologic feature as a typical epidermal cyst arising in the skin. It has been postulated that the intrarenal epidermal cyst arises either from epidermal remnants or it results from traumatic implantation of transformed epithelium. Considering the past history of the patient, it might well be suspected that the present case occurred as a result of traumatic implantation of metaplastic squamous epithelial cells. We report here on a very interesting case of an epidermal cyst in the renal pelvis with a review of the relevant literatures.
- The Effects of Ginsenoside Rb1 on the Apoptosis and the Production of Nitric Oxide in Rat C6 Glioma Cells.
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Joo Hyeon Park, Yoon Hee Lee, Ku Seong Kang, Soo Kyoung Lee, Sun Zoo Kim, Ji Young Park, Eun Kyoung Kwak, Yoon Kyung Sohn
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Korean J Pathol. 2004;38(1):1-7.
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Abstract
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- BACKGROUND
Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production.
METHODS
Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)-gamma , and tumor necrosis factor (TNF)-alpha on the culture medium to investigate the effects of ginsenoside Rb1.
RESULTS
Compared with C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha, C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells.
CONCLUSIONS
These results suggest that the induction of iNOS expression and subsequent
- Sudden Death from Cardiac Sarcoidosis: A Case Report.
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Soo Kyoung Lee, Sun Zoo Kim, Yoon Seup Kum, Tae In Park, Sang Han Lee, Jong Min Chae, Jung Sik Kwak
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Korean J Pathol. 2003;37(5):358-361.
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Abstract
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- Sarcoidosis is a systemic granulomatous inflammation with an unknown cause. The commonly involved sites are the lymph nodes, lungs, skin, eyes, and heart. Although cardiac involvement in sarcoidosis is rarely detected clinically, it is reported in 20-50% of autopsied sarcoidosis patients.
Cardiac involvement is one of the most severe conditions of sarcoidosis and may cause sudden death. We report a case of a sudden death due to a massive cardiac sarcoidosis in a 43-year-old man. The microscopic examination revealed an extensive noncaseating granulomatous inflammation in the mediastinal lymph nodes and the heart with no evidence of myocyte necrosis. A special stain and molecular study excluded the possibility of other causes such as fungi or mycobacterium. The authors concluded that the cause of death was attributed to arrhythmia due to a cardiac sarcoidosis with massive involvement of the conduction system.
- Lipopolysaccharide/Interferon-gamma Induced Nitric Oxide Production in C6 Glioma Cells: Modulation by Dexamethasone.
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Jong Heun Shin, Ku Seong Kang, Ji Yeoun Kim, Sun Zoo Kim, Ji Young Park, Eun Kyoung Kwak, Yoon Kyung Sohn
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Korean J Pathol. 2002;36(6):406-411.
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Abstract
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- BACKGROUND
Glial cell-derived nitric oxide (NO), and its regulation has significant implications for central nervous system pathophysiology. The aim of the present study was to see the production of NO in lipopolysaccharide (LPS)/interferon-gamma (IFN-)-treated C6 glioma cells and the effect of dexamethasone on NO production and apoptosis of LPS/IFN--treated C6 glioma cells.
METHODS
The apoptosis of LPS/IFN- treated C6 glioma cell was examined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method and the production of NO in culture medium was measured. The expression of iNOS mRNA was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The effect of the N-monomethyl L-arginine (NMMA) and dexamethasone on the apoptosis and NO production was also examined.
RESULTS
Inducible nitric oxide synthase (iNOS) mRNA and NO production were markedly increased in LPS/IFN--treated C6 glioma cells. The expression of iNOS mRNA arose at 3 hours, peaked at 12 hours, and declined 24 hours after LPS/IFN--treatment. Accumulation of NO derivatives in the culture media was increased at least upto 48 hours after LPS/IFN-. The induction of iNOS expression and NO production in LPS/IFN--treated C6 cells was correlated with apoptotic cell death judged by TUNEL staining. After treatment of NMMA, one of the NOS inhibitors, NO production and apoptosis were markedly decreased. Dexamehasone treatment suppressed the NO production by concentration depenedent manner.
CONCLUSIONS
From the above results it is concluded that the LPS/IFN- induced apoptosis of C6 cells is mediated by iNOS-derived NO and NO production and apoptosis was suppressed by dexamethasone.
- The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B.
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Kum Yoon Seup, Soo Kyoung Lee, Sun zoo Kim, Eun Kyoung Kwak, Ji Young Park, Tae In Park, Han Ik Bae, Yoon Kyung Sohn, In Soo Suh
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Korean J Pathol. 2002;36(4):238-242.
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Abstract
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- BACKGROUND
A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation.
METHODS
We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA.
RESULTS
Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group.
CONCLUSIONS
We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.
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