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홍승재,양형인,윤휘중,이명수,강효종,김완욱,이상헌,조철수,김호연,Hong, Seung-Jae,Yang, Hyung-In,Yoon, Hwi-Joong,Lee, Myoung-Soo,Kang, Hyo-Jong,Kim, Wan-Uk,Lee, Sang-Heon,Cho, Chul-Soo,Kim, Ho-Youn 대한면역학회 2003 Immune Network Vol.3 No.1
Background: Celecoxib, a COX-2 specific inhibitor, has recently been used for the treatment of rheumatoid arthritis. However, the molecular and cellular mechanisms of celecoxib against RA inflammation remain to be defined. To elucidate the action mechanism of celecoxib on inflammatory cells, we investigated the effect of celecoxib on the production of two important mediators of inflammation, nitric oxide and PGE2 Methods: RAW 264.7 cells stimulated with LPS were preincubated with various concentrations of celecoxib (from $10^{-8}$ to $10^{-5}$ M) and $10{\mu}M$ hydrocortisone, respectively. The production of NO and PGE2, the end products of iNOS and COX-2 genes, were estimated in culture supernatants by Greiss method and EIA, respectively. The expression of iNOS gene, COX-2 gene, $NF-{\kappa}B$, and $I-{\kappa}B$ were determined by RT-PCR and western blot analysis. Results: Celecoxib and hydrocortisone inhibited the production of NO and PGE2 in dose dependent manner, when RAW 264.7 cells were stimulated with LPS. The expression of iNOS was also down-regulated by celecoxib and hydrocortisone. Interestingly, COX-2 gene differentially expressed according to the dose of celecoxib, a decrease with lower dose ($10^{-8}$ M) but an increase with higher dose ($10^{-5}$ M). $NF-{\kappa}B$ binding activity was decreased by lower dose of celecoxib, whereas was not affected by higher dose of it. The expression of $I-{\kappa}B$ was suppressed by higher dose of celecoxib. Conclusion: The celecoxib strongly suppressed the production of NO and PGE2 in LPS-stimulated RAW264.7 cells. The decrease of NO seems to be linked to the inhibition of iNOS by celecoxib. The lower and higher dose of celecoxib differentially regulated the COX-2 expression and $NF-{\kappa}B$ activity.
Bortezomib과 Radiotherapy 혼합요법으로 호전을 보인 피부형질세포종
정기헌 ( Ki Heon Jeong ),윤휘중 ( Hwi Joong Yoon ),이무형 ( Mu Hyoung Lee ) 대한피부과학회 2009 대한피부과학회지 Vol.47 No.4
Multiple myeloma is a hematologic malignancy characterized by the proliferation of monoclonal plasma cells that produce monoclonal immunoglobulins. Cutaneous involvement is very uncommon in patients with multiple myeloma. It usually appears late in the course of the disease. Bortezomib is a potent proteasome inhibitor, recently introduced in the treatment of multiple myeloma. It has proven to be safe and effective in the treatment of refractory or relapsed multiple myeloma. In this study, we show the high efficacy of a concurrent therapeutic approach with bortezomib and radiation in a patient with a cutaneous plasmacytoma. (Korean J Dermatol 2009;47(4):483~486)
만성골수성백혈병 및 급성임파구성혈병에서 Breakpoint Cluster Region ( bcr ) 유전자 재배열 관찰
김시영(Si Young Kim),윤휘중(Hwi Joong Yoon),조경삼(Kyung Sam Cho),최영길(Young Kil Choi) 대한내과학회 1990 대한내과학회지 Vol.39 No.1
N/A molecular genetic features in 14 CML patients and four acute lymphoblastic leukemia (ALL) patients. Genomic DNA was isolated from the cells of peripheral blood or bone marrow aspirates and digested with Bgl II and BamH I restriction endonuclease. A 5', 1.95-kb bcr (BglII/HindIII) probe and a 3, 1.2 kb bcr (Hind III/Bgl II) plasmid probe were used for hybridization. The results were as follows.: 1) In 14 CML patients, the bcr rearrangenment was detected in 13 patients, 2) The bcr rearrangement was detected in all seven Ph positive CML patients. 3) In five Ph1 negative CML patients, the bcr rearrangement was detected in four patients. 4) The bcr rearrangement was not detected in all four ALL patients, 5) One Ph1 positive ALL patient did not have ber rearrangement. In conclusion, the bcr DNA probe assay can determine the responses to therapy and the prognosis. It also can be used as a tumor marker in CML and ALL patients. In the future, this assay can be helpful for understanding the machanism of tumoriaenesis.