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특정적 광과민성 피부증상 없이 우울증으로 입원한 전신성 홍반성 낭창 1례
최석채,이상열,박민철,나용호 圓光大學校 醫科學硏究所 1998 圓光醫科學 Vol.14 No.2
We experienced a 22-years-old female patient with systemic lupus erythematosus (SLE) who was admitted with major depressive disorder symptoms such as a depressive mood, loss of appetite, weight loss, insomnia, and fatigue. She did not show any characteristic photosensitive cutaneous symptoms of SLE when she came to the hospital. Antidepressants and psychotherapy under hospitalization did not show any improvements in her depressive symptoms. Her past history revealed Raynaud's phenomenon and arthralgia, leukopenia, normochronic normocytic anemia and elevated erythrocyte sedimentation rate were detected on her routine laboratory examinations. We considered an autoimmune connective tissue disease and performed specific hematologic and immunologic tests. We confirmed that her systemic symptoms and results of specific tests were fitted to a case of SLE, so we started prednisolone medication. After treating the patient with prednisolone for 2 weeks, her psychiatric and systemic symptoms of SLE were improved. We concluded that psychiatrists have to pay attention to SLE that can manifest depressive symptoms without characteristic photosensitive cutaneous symptoms of SLE.
Choi, Suck-Chei,Kim, Beom-Su,Yoon, Kwon-Ha,Song, Moon-Young,Oh, Hyun-Mee,Han, Weon-Cheol,Kim, Tae-Hyeon,Kim, Eun-Cheol,Jun, Chang Duk The Korean Society for Integrative Biology 2002 Korean journal of biological sciences Vol.6 No.2
Nitric oxide has high affinity for iron, and thus it can cause intracellular iron loss. We tested the idea that intracellular iron can be the primary target of NO toxicity by comparing the signaling mechanisms involved in cell death caused by iron depletion and that caused by NO. Treatment of HL-60 cells with a NO donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP), decreased the intracellular iron level rapidly as that observed with the iron chelator deferoxamine (DFO). Iron chelators such as DFO and mimosine could induce death of human leukemic HL-60 cells by a mechanism requiring activation of p38 kinase, c-Jun N-terminal kinase, caspase-3 and caspase-8. DFO and SNAP also caused release of cytochrome c from mitochondria. Inhibition of p38 kinase by a selective inhibitor, SB203580, abolished the NO and DFO-induced cell death, release of cytochrome c, and activation of caspase-3 and caspase-8, thus indicating that p38 kinase lies upstream in the cell death processes. In a parallel situation, the cells that are sensitive to NO showed similar sensitivity to DFO. Moreover, simultaneous addition of ferric citrate, an iron-containing compound, inhibited the SNAP and DFO-induced activation of caspases and also blocked the NO-mediated cell cycle arrest at $G_1$ phase. Collectively, our data implicate that the NO-induced cell death of tumor cells including HL-60 cells is mediated by depletion of iron and further suggest that activation of p38 kinase lies upstream of cytochrome c release and caspase activation involved in this apoptotic process.
Choi, Eun-Young,Park, Zee-Yong,Choi, Eun-Ju,Oh, Hyun-Mee,Lee, SungGa,Choi, Suck-Chei,Lee, Kang-Min,Im, Sin-Hyeog,Chun, Jang-Soo,Jun, Chang-Duk Wiley Subscription Services, Inc., A Wiley Company 2007 Journal of cellular biochemistry Vol.102 No.6
<P>We have shown that the bacterial iron chelator, deferoxamine (DFO), triggers inflammatory signals including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs) by activating the ERK1/2 and p38 kinase pathways. In this study we investigated the mechanisms involved in IL-8 generation by DFO, focusing on the transcription factors involved and the roles of both mitogen-activated protein kinases (MAPKs) in the transcription factor activation. Treatment of human epithelial HT-29 cells with DFO markedly up-regulated the expression of the essential components of the transcription factor AP-1 at a transcriptional level, while it minimally affected the expression of the NF-κB subunits. DFO also induced AP-1-dependent transcriptional activity in HT-29 cells, and this activity was further augmented by the wild-type c-Jun transfection. In contrast, the AP-1 activity by DFO was markedly decreased by the dominant-negative c-Jun transfection. Electrophoretic mobility shift assays revealed that DFO increases the specific binding of AP-1 but not of NF-κB. Such AP-1 binding and transcriptional activities were blocked by the inhibitors of the ERK1/2 and p38 kinase pathways, suggesting that both mitogen-activated protein kinases (MAPKs) lie upstream of AP-1. Besides its action on AP-1, DFO also induced the specific binding of other transcription factors such as CREB and Egr-1. In summary, our results indicate that iron chelator-induced IL-8 generation in IECs involves activation of ERK1/2 and p38 kinase and downstream activation of AP-1. A possible link between iron status and two additional transcription factors, that is, CREB and Egr-1, rather than NF-κB, was also suggested. J. Cell. Biochem. 102: 1442–1457, 2007. © 2007 Wiley-Liss, Inc.</P>
Choi, Suck-Chei,Lee, Eun-Kyung,Lee, Sung-Ga,Chae, Soo-Cheon,Lee, Myeung-Su,Seo, Geom-Seog,Kim, Sang-Wook,Yeom, Joo-Jin,Jun, Chang-Duk The Korean Association of Immunobiologists 2005 Immune Network Vol.5 No.4
Background: We examined global gene expression profiles of peripheral blood mononuclear cells (PBMCs) in patients with ulcerative colitis (DC), and tested whether the identified genes with the altered expression might be associated with susceptibility to UC. Methods: PBMCs from 8 UC and 8 normal healthy (NH) volunteers were collected, and total RNAs were subjected to the human 8.0K cDNA chip for the micro array analysis. Real time-PCR (RT-PCR) was performed to verify the results of micro array. One hundred forty UC patients and 300 NH controls were recruited for single nucleotide polymorphism (SNP) analysis. Results: Twenty-five immune function-related genes with over 2-fold expression were identified. Of these genes, two chemokines, namely, CXCL1 and CCL20, were selected because of their potential importance in the evocation of host innate and adaptive immunity. Four SNPs were identified in the promoter and coding regions of CXCL1, while there was no significant difference between all patients with UC and controls in their polymorphisms, except minor association at g.57A>G (rs2071425, p=0.02). On the other hand, among three novel and one known SNPs identified in the promoter region of CCL20, g. -1,706 G>A (p=0.000000055), g. -1,458 G>A (p=0.0048), and g. -962C>A (p=0.0006) were found to be significantly associated with the susceptibility of Uc. Conclusion: Altered gene expression in mononuclear cells may contribute to IBD pathogenesis. Although the findings need to be confirmed in other populations with larger numbers of patients, the current results demonstrated that polymorphisms in the promoter region of CCL20 are positively associated with the development of Uc.
Choi, Suck-Chei,Han, Weon-Cheol,Park, Do-Sim,Kim, Eun-Cheol,Oh, Hyun-Mee,Oh, Jung-Mi,Jun, Chang-Duk The Korean Society for Microbiology 2002 Journal of Bacteriology and Virology Vol.32 No.1
Intercellular adhesion molecule-1 (ICAM-1) is a membrane protein, exists as a dimer on the cell surface, and interacts with leukocyte function associated antigen-1 (LFA-1), a member of ${\beta}_2$-integrin family. A soluble circulating form of ICAM-1 (sICAM-1) is also detected in human serum, and has been implicated as a regulator for LFA-1-dependent cell-cell interaction in vivo. However, previous reports demonstrated that sICAM-1 shows little inhibitory effect on LFA-1 binding to ICAM-1, indicating that sICAM-1 is unlikely to antagonize LFA-1/ICAM-1-mediated cellular events in vivo. Here, we investigated the property of the dimeric sICAM-1 as an inhibitor of LFA-1 interaction with ICAM-3, since the lower avidity of LFA-1 for ICAM-3 compared with ICAM-1 or ICAM-2 had been speculated. Using recently constructed heterodimeric sICAM-1 joined at the C terminus via an ${\alpha}$-helical coiled coil (ACID-BASE) (Jun, CD. et al., 2001, Proc Natl Acad Sci 98, 6830-6835), we also tested whether the structural integrity in dimer could affect the inhibitory action of sICAM-1. Engineered sICAM-1 dimer that contained intact ectodomain (E34/E34) significantly blocked SKW3 cell (LFA-$1^+$) binding to ICAM-3, but not to ICAM-1 and ICAM-2, indicating the lower avidity of LFA-1 to ICAM-3 than that of both ICAM-1 and ICAM-2. A one binding site knock out mutant (E34/K34) showed ${\sim}2$-fold reduction in efficiency compared with E34/E34 to inhibit cell binding. Interestingly, a one binding domain deletion mutant (E34/${\Delta}D1$-D2) showed significant reduction (${\sim}5$-fold) compare with E34/K34, suggesting that structural integrity, which is precluded in E34/${\Delta}D1$-D2, is necessary for optimal binding of dimeric sICAM-1 to LFA-1, thereby inhibiting LFA-1/ICAM-3-dependent adhesion. Furthermore, BIAcore affinity measurements revealed that E34/${\Delta}D1$-D2 bound to immobilized soluble open LFA-1 I domain with an ${\sim}3$-fold reduced affinity compared with E34/K34. Overall, our results demonstrate that maintaining the structural integrity in dimer is necessary for optimal binding of sICAM-1 to LFA-1, and further suggest the therapeutic potential of dimeric sICAM-1 to antagonize LFA-1/ICAM-3-mediated cellular events in vivo.
Choi, Suck-Chei,Choi, Eun-Ju,Oh, Hyun-Mee,Lee, SungGa,Lee, Jeong-Kun,Lee, Meung-Su,Shin, Yong-Il,Choi, Suck-Jun,Chae, Jeong-Ryong,Lee, Kang-Min,Lee, Won-Jung,Park, Jae-Sik,Shin, Chang-Yell,Oh, Tae-You WJG Press 2006 WORLD JOURNAL OF GASTROENTEROLOGY Vol.12 No.30
<P>To investigate whether, or how, DA-9601, which is a new gastroprotective agent, inhibits TNF-alpha-induced inflammatory signals in gastric epithelial AGS cells.</P>