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      • KCI등재후보

        그레이브스병 환자의 Suppressor Induction Factor ( SIF ) 의 활성도

        양인명(I . M . Yang),윤휘중(H . J . Yoon),조경삼(K . S . Cho),김진우(J . W . Kim),김광원(K . W . Kim),최영길(Y . K . Choi) 대한내과학회 1986 대한내과학회지 Vol.31 No.1

        N/A Autologous mixed lymphocyte culture reaction (AMLCR) has been known to represent the generation of suppressor T cell without direct evidence that the proliferating cell is suppressor T cell itself. Our previous study had demonstrated that the proliferative response of T cell during AMLCR in the patients with Graves' disease is not different from that in normal control, The recent studies showed that suppressor induction factor(SIF) which induce suppressor T cell is produced during the AMLCR. We observed the SIF activity in the patients with Graves disease by measuring the suppression of normal allogeneic MLCR by the normal T cell incubated with the supernatant of AVLCR, and also observed the proliferative response of T cell incubated with the supernatant of AMLCR proliferate to determine whether the suppressor T cell proliferate or not during AMLCR. T cells incubated with the supernatant of AMLCR suppressed the allogeneic MLCR prominently in normal controls(55±11%), and the supernatant of patients' AMLC induced the suppressor T cells which successfully suppressed the allogeneic MLCR(50±9%). T cells incubated with the supernatant of AMLCR did not proliferate. These data indicate that the proliferating cells during AMLCR are the self-antigen recognizing T cells which secrets SIF, a kind of lymphokines, to induce the suppressor T cells, It is suggested that the process of self antigen recognization is normal in Graves' disease.

      • KCI등재후보

        말단비대증 환자의 박동빈도에 따르는 임상적 내분비학적 특성

        이규춘(G . C . Lee),양인명(I . M . Yang),우정택(J . T . Woo),김성운(S . W . Kim),김진우(J . W . Kim),김영설(Y .S .Kim),최영길(Y . K . Choi) 대한내과학회 1997 대한내과학회지 Vol.52 No.4

        N/A Objectives: Pulsatile secretion of GH are present in acromegalics and normal men. GH concentration profiles in patients with acromegaly are characterized by rapid GH pulsatility and high interpulse concentrations. There is also variations of GH pulse frequency in individual acromegalic patients. We performed this study to investigate any correlation between GH pulse frequency and clinical or endocrinological findings. Material and Methods: We have studied pulse frequency in 18acromegalic patients by modified Santen and Bardin Method through blood sampling every 1hour for 24hours. TRH stimulation test, LHRH stimulaton test, Somatostatin suppression test and bromocriptine suppression test was done in this patients. We sequenced from cordon 184 to cordon 251 of Gsa gene in pituitary tumor tissue of this acromegalic patients. Clinical findings or endocrinological test results studied above matched to GH pulse frequency to find any correlation by simple regression analysis or Chi-square test. Results: There is no correlation between GH pulse frequency and age, sex, grade of tumor, size of tumor or GH fluctuations. We can not find any difference at incidence of gsp oncogene by pulse frequency of acromegalic patients. GH pulse frequency of acromegalic patients in our study did not identified any difference in paradoxical response to TRH or LHRH and % suppression of GH by somatostatin or bromocriptine. Conclusions: There is no correlation between GH pulse frequency and clinical or endocrinological test. This suggest that GH pulse frequency is not correlated with the expression of various hormone receptors such as dopamine receptor, TRH receptor, LHRH receptor and SSTR.

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