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오도연 ( Do Yeun Oh ) 대한간학회 2011 Clinical and Molecular Hepatology(대한간학회지) Vol.17 No.2(S)
Patients with chronic liver disease frequently show hemostatic abnormalities with complex mechanism. Patients with chronic liver disease may be in hemostatic rebalance by concomitant changes in prohemostatic and antihemostatic pathways. Because the rebalanced hemostatic conditions in patients with chronic liver disease can be only detected by sophisticated tests, results from current routine laboratory tests do not well correlated with clinical findings in patients with chronic liver disease. More studies are required for proper management of hemostatic abnormalities in patients with chronic liver disease.
Phosphorylation of 44-kilodalton Proteins in Peripheral T-lymphocyte of Rat
안영수,주일로,오도연,임승욱,박경선,Ahn, Young-Soo,Jou, Il-O,Oh, Do-Yeun,Lim, Seung-Wook,Park, Kyung-Sun The Korean Society of Pharmacology 1991 대한약리학잡지 Vol.27 No.2
Using T-lymphocytes obtained from rat peripheral blood, we found that the 44kD/pI6.8 protein was the major phosphoprotein of T-lymphocytes under basal condition, and that the 44kD/pI6.3 protein was a new phosphoprotein appeared in T-lymphocytes stimulated with ${\beta}-agonist$. The phosphorylation of the 44kD/pI6.3 protein was also induced by forskolin but inhibited by H-8 pretreatment. To clarify the character of the 44kD/pI6.3 protein, we used Con-A and kinase inhibitors, H-7 and W-7. Con-A stimulation induced phosphorylation of 44kD/pI 6.3 protein but that was inhibited by W-7 pretreatment. The phosphorytation of 44kD/pI6.3 protein was not induced by the PKC activator, PMA. Instead, the phosphorylation of 44kD/pI6.8 protein was reduced by H-7, a PKC inhibitor. From the above results,it can be concluded that the 44kD/pI6.3 protein can be a common substrate for A-kinase and CaM kinase. The two dimensional tryptic peptide mapping revealed that the 44kD/pI6.8 and 44kD/pI6.3 proteins are different. 흰쥐 말초혈액에서 얻은 T 림프구를 아드레날린성 ${\beta}-$수용체 효현제 및 concanavalin A(Con-A)로 자극해 다음과 같은 결과를 얻었다. 자극이 없는 상태에서의 주 인산화 단백은 분자량 44kD, 등전점 6.8의 단백이었으며 효현제로 자극시키면 분자량 44kD, 등전점 6.3의 단백이 새로이 인산화되어 나타났다. 이 분자량 44kD, 등전점 6.3의 단백은 forskolin에 의해 역시 인산화되며 A-kinase 억제제인 H-8을 전처치하면 인산화의 억제가 나타났다. 또한 Con-A로 자극시키면 44 kD/pI 6.3 단백의 인산화가 증가되었으며 이 인산화의 증가는 CaM kinase 억제제인 W-7 전처치에 의해 억제되었다. H-7은 분자량 44 kD, 등전점 6.8 단백의 인산화를 감소 시켰다. 이상의 결과로 분자량 44 kD 등전점 6.3의 단백은 A-kinase와 CaM kinase 모두에 의해 인산화 되는 기질단백으로서 tryptic peptide map상에서 44 kD/pI 6.8 단백과 44 kD/pI 6.3 단백은 서로 다른 단백임을 알 수 있었다.
정정욱,박정미,최병옥,김남근,오도연,정우상,Jung, Jung-Uk,Park, Jung-Mi,Choi, Byung-Ok,Kim, Nam-Keun,Oh, Do-Yeun,Jung, Woo-Sang 대한한방내과학회 2002 大韓韓方內科學會誌 Vol.23 No.1
Objective : Hyperhomocysteinemia has been proven to be an independent risk factor for stroke. The genetic mutation of methylenetetrahydrofolate reductase(MTHFR) elevates serum homocysteine level, but it still remains controversial whether the MTHFR gene mutation could be a predictor of ischemic stroke. Therefore, we studied if this genetic defect could cause ischemic stroke independently. Methods : We gathered ischemic stroke subjects and age, sex-matched controls. Age, gender, past medical history, smoking habit, serum homocysteine level, and the MTHFR genotype were recorded. General characteristics of ischemic stroke subjects were compared to the controls. We classified the stroke according to the related vessels(small and large artery infarction) and single lesion and multiple infraction. Relevant risk of the MTHFR genotype was evaluated in each stroke subtype with multiple logistic regression analysis. Results : When the controls were compared to the whole ischemic stroke, there was no specific difference except some medical histories. However, further analysis based on stroke subtypes showed important results. The small artery infarction group, multiple infraction group had significant odds ratio of the MTHFR TT genotype adjusted for age, gender, medical history and smoking habit. Conclusions : The MTHFR TT genotype is an independent risk factor for certain types of ischemic stroke, small artery infarction and multiple infarction.
흰쥐 말초 혈액 림프구의 분자량 44 kD 단백의 인산화
안영수(Young Soo Ahn),주일로(I-Lo Jou),오도연(Do Yeun Oh),임승욱(Seung Wook Lim),박경선(Kyung Sun Park) 대한약리학회 1991 대한약리학잡지 Vol.27 No.2
흰쥐 말초혈액에서 얻은 T 림프구를 아드레날린성 β-수용체 효현제 및 concanavalin A(Con-A)로 자극해 다음과 같은 결과를 얻었다. 자극이 없는 상태에서의 주 인산화 단백은 분자량 44kD, 등전점 6.8의 단백이었으며 효현제로 자극시키면 분자량 44kD, 등전점 6.3의 단백이 새로이 인산화되어 나타났다. 이 분자량 44kD, 등전점 6.3의 단백은 forskolin에 의해 역시 인산화되며 A-kinase 억제제인 H-8을 전처치하면 인산화의 억제가 나타났다. 또한 Con-A로 자극시키면 44 kD/pI 6.3 단백의 인산화가 증가되었으며 이 인산화의 증가는 CaM kinase 억제제인 W-7 전처치에 의해 억제되었다. H-7은 분자량 44 kD, 등전점 6.8 단백의 인산화를 감소 시켰다. 이상의 결과로 분자량 44 kD 등전점 6.3의 단백은 A-kinase와 CaM kinase 모두에 의해 인산화 되는 기질단백으로서 tryptic peptide map상에서 44 kD/pI 6.8 단백과 44 kD/pI 6.3 단백은 서로 다른 단백임을 알 수 있었다. Using T-lymphocytes obtained from rat peripheral blood, we found that the 44kD/pI6.8 protein was the major phosphoprotein of T-lymphocytes under basal condition, and that the 44kD/pI6.3 protein was a new phosphoprotein appeared in T-lymphocytes stimulated with β-agonist. The phosphorylation of the 44kD/pI6.3 protein was also induced by forskolin but inhibited by H-8 pretreatment. To clarify the character of the 44kD/pI6.3 protein, we used Con-A and kinase inhibitors, H-7 and W-7. Con-A stimulation induced phosphorylation of 44kD/pI 6.3 protein but that was inhibited by W-7 pretreatment. The phosphorytation of 44kD/pI6.3 protein was not induced by the PKC activator, PMA. Instead, the phosphorylation of 44kD/pI6.8 protein was reduced by H-7, a PKC inhibitor. From the above results,it can be concluded that the 44kD/pI6.3 protein can be a common substrate for A-kinase and CaM kinase. The two dimensional tryptic peptide mapping revealed that the 44kD/pI6.8 and 44kD/pI6.3 proteins are different.
반복자연유산에서 Methylenetetrahydrofolate Reductase 돌연변이에 대한 분석
남윤성,차광렬,김남근,김선희,임진우,강금덕,강명서,김세현,오도연,Nam, Yoon-Sung,Cha, Kwang-Yul,Kim, Nam-Keun,Kim, Sun-Hee,Lim, Jin-Woo,Kang, Geum-Duk,Kang, Myung-Seo,Kim, Se-Hyun,Oh, Do-Yeun 대한생식의학회 2001 Clinical and Experimental Reproductive Medicine Vol.28 No.3
Objective: To analyze the methylenetetrahydrofolate reductase (MTHFR) mutation in patients with recurrent spontaneous abortion. Material and Method: The blood samples of patients with recurrent spontaneous abortion were tested by PCR-RFLP method. Results: Of 51 cases of study group, 14 (27.5%) were normal, 25 (49.0%) were heterozygosity, and 12 (23.5%) were homozygosity. Of 58 cases of control group, 20 (34.5%) were normal, 30 (51.7%) were heterozygosity, and 8 (13.8%) were homozygosity. But the difference between two groups was not significant (p=0.190). Conclusion: Hyperhomocysteinemia due to MTHFR mutation is a cause of recurrent spontaneous abortion. Therefore, the study for MTHFR mutation should be included in the workup of recurrent spontaneous abortion.
5,10-Methylenetetrahydrofolate Reductase (MTHFR C677T와 A1298C) 유전자 돌연변이의 반복자연유산 관련성 연구
김남근,남윤성,이수만,김선희,신승주,장성운,김세현,차광렬,오도연,Kim, Nam-Keun,Nam, Yoon-Sung,Lee, Su-Man,Kim, Sun-Hee,Shin, Seung-Joo,Chang, Sung-Woon,Kim, Se-Hyun,Cha, Kwang-Yul,Oh, Do-Yeun 대한생식의학회 2002 Clinical and Experimental Reproductive Medicine Vol.29 No.3
Objective : Previous studies have suggested that hyperhomocysteinemia and methylenetetrahydrofolate reductase (MTHFR C677T) mutations are associated with increased risk of recurrent spontaneous abortion (RSA). Recently, a second site polymorphism in MTHFR, 1298A-->C, which changes a glutamic acid into an alanine residue, was shown to be associated with a decreased enzyme activity. We tested whether the variant alleles of MTHFR C677T and A1298C are risk factor (biomarker) for RSA. Materials and Methods: We analyzed DNA from a case-control study in the Korean DNA was extracted from blood samples of 118 patients with RSA and 123 healthy fertile patients as the controls. MTHFR variant alleles were determined by a PCR-restriction fragment length polymorphism assay. Results: We found no evidence for an association between 677TT genotype and risk of RSA (OR=1.95, 95% CI=$0.84{\sim}4.50$, p=0.12). However, the MTHFR 1298AC (OR=0.36, 95% CI=$0.20{\sim}0.63$, p=0.0004) and 1298AC+CC (OR=0.35, 95% CI=$0.20{\sim}0.61$, p=0.0002) genotypes were lower among 118 RSA cases compared with 123 controls, conferring a 2.8-fold decrease in risk of RSA, respectively. Moreover, the combined genotypes of MTHFR 677CC/1298AC (OR=0.30, 95% CI=$0.10{\sim}0.88$, p=0.029) and 677CT/1298AC (OR=0.77, 95% CI=$0.60{\sim}0.99$, p=0.043) also showed significantly lower risk than those with MTHFR 677CC/1298AA type. Conclusion: MTHFR 1298AC, MTHFR 677CC/1298AC and 677CT/1298AC genotypes may represent genetic markers for the protection of RSA at least in Korean women.
증례 : 혈액종양 ; 다발골수종 환자에서 보르테조밉(bortezomib) 투여 후 발생한 심부전 1예
송지현 ( Ji Hyun Song ),김희경 ( Hee Kyung Kim ),신석표 ( Suk Pyo Shin ),김인재 ( In Jai Kim ),오도연 ( Do Yeun Oh ),정소영 ( So Young Chong ) 대한내과학회 2015 대한내과학회지 Vol.88 No.4
이 증례는 다발골수종으로 진단 후 보르테조밉, 멜팔란 및 프레드니솔론 항암 치료를 시행 중 심부전이 악화되었던 사례이다. 심부전 악화 원인을 감별하기 위해 문진 및 혈액 검사를 시행했으나 특별한 소견은 없었다. 심독성이 보고된 보르테조밉이 그 원인일 가능성도 있다고 판단되어 보르테조밉 중단 및 보존적 치료 후 심부전이 호전되었다. 기존에 심장 질환이 있는 환자는 보르테조밉 투여 이후에 심장 질환이 악화될 수 있으므로 이에 유의해야 하겠다. Bortezomib (Velcade®) came into the spotlight as a target therapy for multiple myeloma. It acts through reversible inhibition of intracellular proteasomes, which triggers apoptosis, with relative selectivity for malignant cells. It has been hypothesized that the accumulation of damaged proteins in myocytes impairs cardiac function. Cardiotoxicity is a rare side effect of bortezomib treatment. We report a case of reversible systolic heart failure that probably occurred after bortezomib treatment in a patient with multiple myeloma. Patients being treated with bortezomib who have previously had cardiac comorbidities should undergo routine cardiac monitoring.
한국인 위암 환자에서 Thymidylate Synthase와 Methylenetetrahydrofolate Reductase 유전자 다형성의 임상 의의
이준 ( Jun Lee ),정철권 ( Cheol Kweon Jeong ),홍성표 ( Sung Pyo Hong ),정소영 ( So Young Chong ),오도연 ( Do Yeun Oh ),황성규 ( Seong Gyu Hwang ),안대호 ( Dae Ho Ahn ),김세현 ( Se Heun Kim ),한진희 ( Jin Hee Han ),김남근 ( Nam Ke 대한소화기학회 2005 대한소화기학회지 Vol.46 No.1
김선주(Sun Joo Kim),황성규(Seong Gyu Hwang),이문호(Moon Ho Lee),김순길(Soon Kil Kim),오도연(Do Yeun Oh),김창진(Chang Jin Kim) 대한소화기학회 1990 대한소화기학회지 Vol.22 No.3
Leiomyoblastoma is an uncommon intrarnural tumor of the stomach. It was first described in 1960 by Martin et al.. Stout reported a series of 69 simiIar cases and propoaed the term leiomyoblastoma in 1962. A 65 year old female patient presented with epigastric pain for two years. She took several episodes of transfusion for recent 2 years. UGI, gastrofiberscopy and abodinal CT showed a submucosal mass, located at anterior wall. Subtotal gastrectomy was perfomed under the impression of leiomyosarcoma, The final hiatologic diagnosis was leiomyoblastoma. The smooth muscle origin of this tumor was conffrmed positive staining for MaaSons trichrome and by intracellular myofibrils on electron microscopic studly. Cytoplaamic clear zonee, previously thought to be typical of the light microscopic moryhology of leiomyoblastoma, was not observed by electron microscopy, suggesting that they may be an artifact of fixation. The pragnosie of leiomyoblastoma may be related to tumor size, the numbers of mitotic figures and most impurtantly cellular characteristics.
증례 : 혈액종양 ; 항암 치료 후 발생한 급성B림프모구백혈병 2예
신석표 ( Suk Pyo Shin ),송상희 ( Sang Hee Song ),고은정 ( Eun Jung Ko ),김지수 ( Ji Su Kim ),박치영 ( Chi Young Park ),오도연 ( Do Yeun Oh ),정소영 ( So Young Chong ) 대한내과학회 2013 대한내과학회지 Vol.85 No.1
치료관련 골수성 백혈병은 잘 알려져 있으며 치료와의 연관성이 정립되어 있으나 치료관련 급성B림프모구백혈병은 드물고 이전의 악성 종양의 항암 치료와 방사선 치료가 급성B림프모구백혈병 발생에 영향을 미치는지는 아직 논란이 많다. 최근에 세포독성 치료와 연관된 급성B림프모구백혈병의 보고가 있으며 국내에서도 드물게 보고되고 있다. 이에 저자들은 과거 세포독성 치료를 한 뒤 급성B림프모구백혈병이 발병한 증례 2예를 경험하였기에 보고하는 바이다. Therapy-related myeloid neoplasms have been well characterized. However, precursor B-cell acute lymphoblastic leukemia in patients with prior malignancies is uncommon, and the effect of prior cytotoxic therapy on development of precursor B-cell acute lymphoblastic leukemia is controversial. Therapy-related precursor B-cell acute lymphoblastic leukemia has been reported occasionally. However, cytotoxic therapy-related precursor B-cell acute lymphoblastic leukemia has been reported in Korea only rarely. We herein describe two cases of therapy-related precursor B-cell acute lymphoblastic leukemia. (Korean J Med 2013;85:96-100)