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심정연,변원철,홍정수,문희범,홍수종 ( Jung Yeon Shim,Won Chul Byun,Jeong Soo Hong,Hee Bom Moon,Soo Jong Hong ) 대한천식알레르기학회 1998 천식 및 알레르기 Vol.18 No.3
Objective .' To evaluate the basophil histamine releasability in response to IgE- and non- IgE-mediated stimuli in children with atopic asthma. Met: Basophil histamine releasability was measured in Dermatophagoides farinae (D. farinae) -sensitive atopic asthmatics, D.farinae -sensitive healthy atopics, non-atopic asthmatics, and healthy non-atopics. Basophils were stimulated with D.farinae, goat antihuman IgE antibody, formyl-Met-Leu-Phe(fMLP), and Calcium ionophore A23187. Histamine was measured by automated fluorometric technique. Results '. Sponianeous histamine release was higher in atopic asthmatics compared to healthy non-atopics. Histamine release by D.farinae and by anti-IgE antibody was higher in atopic asthmatics compared to the other groups. There was no difference in histamine release by fMLP among all groups. Histamine release by Calcium ionophore was higher in healthy atopics and non-atopic asthmatics compared to healthy non-atopics. The atopics showed correlation between histamine release by D.farinae, by anti-IgE antibody and total serum IgE levels. Conclusions '. Spontaneous and IgE-mediated histamine release were related to the presence of both atopy and asthma, whereas non-IgE mediated histamine release was different depending on the stimuli.
TGF-β1과 IL-1β에 의한 류마티스 관절염 활막세포 자사(apoptosis)의 억제
김성호 ( Seong Ho Kim ),변원철 ( Won Chul Byun ),임미경 ( Mi Kyoung Lim ),조유숙 ( You Sook Cho ),김찬 ( Chan Kim ),김미정 ( Mi Jung Kim ),유빈 ( Bin Yoo ),문희범 ( Hee Bom Moon ) 대한류마티스학회 1999 대한류마티스학회지 Vol.6 No.2
Objective: To investigate the proliferative and anti-apoptotic effects of TGF-β1 and IL-1β on rheumatoid synovial cells. Methods: Synovial cells obtained from surgical procedure of the rheumatoid joint were cultured with TGF-β1 and IL-1. The proliferative response of synovial cells was examined by non-radioactive cell proliferation assay. Fas-mediated apoptosis of synovial cells was measured by flowcytometry after addition of anti-Fas antibody. Results: TGF-β1 and IL-1β proliferated synovial cells in a dose-dependent manner. They also made synovial cells resistant to anti-Fas antibody induced apoptosis. Conclusion: TGF-β1 and IL-1β promotes synovial cell proliferation possibly through interference with Fas-mediated apoptosis, suggesting their role in synovial hyperplasia in rheumatoid arthritis.