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소화성 위장질환에 사용하는 Cimetidine , Ranitidine , Proglumide 및 Clebopride 의 면역반응조절
김대곤(Dae Ghon Kim),허영상(Yeong Sang Heo),안관용(Kwan Yong Ahn),이용기(Yong Gi Lee),안득수(Deuk Su Ahn) 대한내과학회 1987 대한내과학회지 Vol.33 No.1
N/A It has been reported that among many drugs used for the treatment of peptic gastrointestinal disorder, a few drugs exerts a variety of modulating effects on immune responsiveness. This study was undertaken to investigate the effect of four of the drugs on immune response of mice to sheep red blood cells (SRBC). Four drugs used in this experiment are cimetidine, a imidazole derivative of histamine type 2 (H₂) receptor antagonist; ranitidine, a furan derivative of H₂, antagonist; proglumide, a gastrin antagonist; and clebopride, a dopamine antagonist. Mice were pretreated with daily oral administration of varying concentration of each drugs for 30 days and were immunized with 10(8) SRBC. Each mouse was challenged 4 days after the sensitization, Immune response were evaluated by measuring footpad swelling reaction at 3 hr (Arthus reaction) and 24hr (delayed type hypersensitivity, DTH) after challenge, rosette forming reaction, hemagglutinin (HA) and hemolysine (HE) titers to SRBC. The pretreatment of mice with cimetidine inhibited Arthus and rosette forming reactions, but enhanced DTH to SRBC. The pretreatment of mice with proglumide suppressed both DTH and rosette forming reaction. The pretreatment of mice with clebopride enhanced DTH, but decreased rosette forming reaction. In contrast to cellular immune response, there was not any significant difference between the drug treated and untreated control groups in HA and HE reactions. These results suggest that cimetidine, ranitidine and clebopride enhance cellular immune response, but proglumide suppress the above response and all of the drugs do not significantly change the humoral immune response.
항인체 사이클린 B2 항체를 이용한위점막 상피세포의 역동성
김대곤 ( Dae Ghon Kim ),김형식 ( Hyung Sik Kim ),문우성 ( Woo Sung Moon ),이승옥 ( Seong Ok Lee ),김정권 ( Jeong Kwon Kim ),양두현 ( Doo Hyun Yand ) 전북대학교 의과학연구소 2002 全北醫大論文集 Vol.26 No.2
인간의 B형 cyclin B1과 B2는 대부분의 분열세포들에서 발현된다. cyclin B1은 세포분열에 필수 유전자로 알려졌으나 cyclin B2는 그 기능이 잘 알려져 있지 않다. 따라서 그 기능을 파악하기 위하여 인간 cyclin B2 유전자를 분리하여 다양한 조직에 cyclin mRNA 발현을 관찰하였으며 폴리클론 항체를 제작하여 위장의 각 질환별 면역화학염색을 실시하였다. 정상 위 유문부에는 음성이었으나 intestinal metaplasia에서는 대부분에서 양성이었으며 선종 및 선암 등의 상당 예에서 양성 면역염색이 관찰되었으며 이는 MUC2 면역염색과 유사하였다. 이러한 결과로 인간의 cyclin B2는 전구위암질환인 intestinal metaplasia에 발현되며 선종이나 선암에서는 감소하는 경향을 보였다. 따라서 cyclin B2는 점액분비형성에 관련되며 일부 위암의 발암과정에 연관된다고 추정되었다.
김대곤 ( Dae Ghon Kim ) 대한췌장담도학회 2015 대한췌담도학회지 Vol.20 No.4
Different ligands can lead to the activation of epidermal growth factor receptor, and the subsequent signal transduction leads to an increase in cellular motility, proliferation, invasion, and blocking of apoptosis, and all of this contributes to the development and progression of cancer. Our studies clarified; 1) The EGFR expression level is reduced during tumor progression or during ligand-induced EGFR activation. 2) ANXA8 and its regulatory pathway may well be alternative, strategic targets for inhibiting tumor metastasis. 3) The molecular pathway of EphA2 signaling and provide insight into the mechanisms that control cancer progression and metastatic spread in cholangiocarcinoma (CC). Therefore, therapeutic strategies that target EphA2 and its downstream effectors may be useful to control CC.
Hep G2 간암세포주에서 Retinoic Acid 가 p53 단백 , Ki - 67 및 PCNA / Cyclin 발현에 미치는 효과
김대곤(Dae Ghon Kim),임수일(Soo Il Im),안득수(Deuk Soo Ahn) 대한내과학회 1995 대한내과학회지 Vol.49 No.1
N/A Ol4ctlves: Retinoic acid(RA), known to have antiproliferative and differentiation-inducing effects on cancer cells, was examined to evaluate its potential as a chemotherapeutic agent for hepatocellular carcinoma. Methods: We examined the level of expressions of the p53 protein, the Ki-67 antigen, and the proliferation cell nuclear antigen(PCNA) in cultured Hep G2 hepatocelluar carcinoma cells before and after RA treatment. The mutant p53 is thought to be involved in development of human cancers, and the expressions of the Ki-67 and the PCNA are used to evaluate tumor cell kinetics. Results: The expression of p53 protein was significantly inhibited in Hep G2 cells by treatment with 10-5 M RA, from 61.1±1.3 to 53.3±0.8% in G0/G1 phase fraction(p=0.001), as detected by immunocytochemical staining using the monoclonal antibody PAb 1801 which recognizes both the wild type and the mutant p53 protein. The significant decrement of expression was also demonstrated using the monoclonal antibody PAb 240 which binds only the mutant p53 protein, from 55.6±0.4% to 50.8±1.2% in G0/G1 phase fraction(p=0.019) and 18.2±0.6% to 8.9±1.3%(p=0.0003) in S phase fraction Also RA treatment increased Go unstained fraction from 0.6±0.1% to 5.9±0.7% and decreased Ki-67 antigen expression significantly from 4.0±1.4% to 10.2±1.5% in S phase, PCNA expression was also dropped by RA treatment in every cell cycle fraction, from 57.0±0.7% to 47.3±1.9% in G0/G1 from 15.2±0.7 % to 10.6±0.6% in S, from 20.5±0.85% to 13.6±0.7% in G2/M phase. Conclusion: RA appeared to have anticancer effect through the inhibition of p53 protein expression, Ki-67 and PCNA expression in Hep G2 cells in similar but not coincident proliferating mode. In addition cell cycle anaysis suggested that RA induced an arrest of G0 progression to G1 and S phase.
B 형 간염 바이러스 ( HBV ) 감염 후 B 형 간염 바이러스 표면 항원 ( HBsAg ) 에 대한 세포 면역성 반응
김대곤(Dae Ghon Kim),이남심(Nam Sim Lee),류완희(Wan Hee Yoo),안득수(Deuk Su Ahn),양두현(Doo Hyun Yang),조백환(Baik Hwan Cho) 대한내과학회 1996 대한내과학회지 Vol.51 No.1
N/A Objectives: The immune reaction of host, esp., cell-mediated, is provided as an important factor to determine the progression of disease after hepatitis H virus infection. The change of suppressor cell that control T cells, decrease of lymphocytic proliferation, or production of IL-2 production in PBMC is reported. Thus we were undertaken this study to investigate cell-mediated immunopathogenic mechanism in hepatitis B virus infection. Methods: 5 groups were studied; non-immune donors, immune donors, asymptomatic HBsAg carriers, patients with chronic active hepatitis (CAH) and patients with acute hepatitis (AH). The present study was tried to estimate the proportional variation of T cell subsets of the peripheral blood mononuclear cells (PBMC), proliferative responses of PBMC which was cultured with rIL-2, concanavalin (Con A) and phytohemagglutinin (PHA), or hepatitis B surface antigen (HBsAg), and changes of HLA-DR and IL-2R expression of stimulated lymphocytes as lymphocyte-activation markers in each groups. Results: There were no proportional changes of CD3 positive cells in subjects of each group, but the proportion of CD4 positive cells (18.4±2.9%) was signifiantly(p<0.01) reduced in patients with CAH. The CD4: CDH ratio was significantly decreased in carriers, in patients with CAH, and in patients with AH. Also the proliferative responses of cultured lymphocyes after stimulation with exogenous rIL-2 were not significantly changed in above three groups compared with that of unstimulated control culture. Enhanced HBsAg-specific proliferation was not detected after stimu1ation with rI1-2+HBsAg. HLA-DR and IL-2R expression of unstimulated lymphocytes were significantly decreased in patients with CAH and patients with AH. The HBsAg-specific HLA-DR expression was not demonstrated in subjects of each group. But, increased HLA-DR expressions after stimulation with rIL-2+HBsAg were observed, 48±6.2% in asymptomatic carriers, 34.5±5.0% in patients with CAH and 43.7±3.3% in patients with AH, compared with that of nonimmune donors. A weak HBsAg-specific IL-2R expression was demonstrated in patients with CAH, but there were no HBsAg-specific IL-2R expression in subjects of other 8 groups. After stimulation with rIL-2 or rIL-2+ HBsAg, there were increased IL-2R expression in asymptomatic HBsAg carriers, in patients with CAH, and in patients with AH, compared with that of nonimmune donors. Conclusion: These results suggested that impaired HLA-DR and IL-2R expression would be associated with HBsAg immunogenicity or/and IL-2 activity, and may be important immunogenetic role in the course of post-HRV infection.