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김배영(Bai Young Kim),김효종(Hyo Jong Kim),정형근(Hyung Keun Chung),김영관(Young Kwan Kim),동석호(Seok Ho Dong),김병호(Byung Ho Kim),이정일(Jung Il Lee),장영운(Young Woon Chang),장린(Rin Chang) 대한내과학회 1993 대한내과학회지 Vol.45 No.5
N/A Background: According to the rapid changes in social environment such as increasing alcohol consumption and the marked improvement in diagnostic technique, we expect that there have been major changes in various aspects of acute pancreatitis during the recent 12 years in Korea. Methods: The medical records of 317 patients with acute pancreatitis diagnosed from 1980 through 1992 were reviewed about clinical, laboratory and radiological findings in the three different time period. Results: 1) There has been an increasing incidence in male sex about three folds. 2) There has been an increasing trends in the duration of hospitalization. 3) A significant increase was observed in the proportion of patients with alcoholic pancreatitis in the three different time period; 26.9%, 45.7%, 50.7% respectively. 4) The complication rates have been slightly increased in the three different time period; 46.3%, 47.1%, 59.1% respectively. But, the type of complications has not been changed. 5) There is increasing severity in non-gallstone group, but no significant differences in gallstone group. There is a declining trends in the number of patients with muld severity index, but increasing trend in the number of patients with moderate severity index in non-gallstone group. 6) There was no significant differences in mortality rate. Conclusions: There has been major changes in the etiology ans severity of acute pancreatitis from 1980 through 1992. Especially, significant increase in the proportion of patients with alcoholic pancreatitis was observed in the three differnt time period. These results might be due to socioeconomic changes.
속박 (束縛) 과 침수 (浸水) 로 유도된 흰쥐의 스트레스성 급성 (急性) 위점막병변 (胃粘膜病變) 발생에 있어서 위산분비의 (胃酸分泌) 역할
민영일(Young Il Min),박충기(Choong Kee Park),장린(Rin Chang),김병호(Byung Ho Kim),장영운(Young Woon Chang),이정일(Jung Il Lee),박승준(Seung Joon Park),정주호(Joo Ho chung),정지창(Jee Chang Jung) 대한소화기학회 1989 대한소화기학회지 Vol.21 No.1
N/A The possible roles of gastric acid secretion in the pathogenesis of stress ulcers induced by restraint with water-immersion for 7 hours in pylorus-ligated rats were investigated. Control rats with pylorus-ligation only did not show any gastric mucosa} lesion, and their mean gastric acid output was 449.2 ± 36.1 umol/rat. In contrast, the stressed rats, group II, showed multiple, punctate and hemorrhagic erosions in gastric mucosa, and mean gastric acid output was decreased to the level of 253.7 ± 27.3 umol/rat. Subcutaneous administration of histamine(40 mg/kg every 2.5 h for a total three times) to stressed rats augmented the lesion with severe multiple, linear and hemorrhagic erosions and mean acid output increased significantly (328.1 ± 31.5 umol/, p<0.005) compared with group II. Pretreatment with rantidine(20 mg/kg) or prostaglandin E2 (30 ug/kg) before exposure to stress reduced gastric lesion formation slightly with no significance. In ranitidine pretreated rats, mean gastric acid output was decreased significantly (120.1 ± 15.3 umol/rat, p<0.005) compared with group II. However, in prostaglandin pretreated rats, mean gastric acid output showed no significant changes. Therefore, it is suggested that increased gastric acid secretion seems to be an aggravating or a permissive factor rather than a major factor in the pathogenesis of stress-induced gastric mucosal lesions.
정성훈 ( Sung Hoon Jung ),김병호 ( Byung Ho Kim ),김영일 ( Young Il Kim ),심재준 ( Jae Jun Shim ),황보영 ( Bo Young Hwang ),장재영 ( Jae Young Jang ),동석호 ( Seok Ho Dong ),김효종 ( Hyo Jong Kim ),장영운 ( Young Woon Chang ),장 대한내과학회 2010 대한내과학회지 Vol.78 No.1
목적: PPAR gamma 배위자의 항암 효과는 다양한 암세포에서 보고되었으나 담관암에 대한 연구는 부족한 실정이다. 본 연구에서는 한국인 간내담관암에서 확립한 암세포주를 대상으로 내인성 PPAR gamma 배위자인 15-deoxy-PGJ2의 항암 효과와 그 기전에 관하여 알아보았다. 방법: Cho-CK, Choi-CK, JCK, SCK의 네 가지 간내담관암 세포주를 사용하였다. RT-PCR 방법으로 PPAR gamma, bcl-2, bax 각 유전자의 mRNA 발현을 측정하였다. 세포증식 분석은 MTT assay, 세포주기 분석은 flow cytometry, 세포자 멸사 분석은 cell death detection ELISAplus kit를 사용하였다. 또한 Caspase 활성도 측정을 위해 caspase colorimetric assay kit를 사용하였고, MTT assay를 통해서 caspase 억제제가 15-deoxy-PGJ2의 암세포증식 억제를 차단하는지 알아보았다. 결과: 모든 담관암세포주에서 PPAR gamma mRNA가 발현 되었다. 15-deoxy-PGJ2를 5, 10, 25, 50, 100 mM 농도로 투여하여 72시간 배양하였을 때 모든 세포주에서 용량 및 시간 의존적으로 세포증식이 억제되었다. 세포주기 분석 결과 25 mM 15-deoxy-PGJ2 투여 48시간 후 모든 세포주에서 세포자멸사 분획이 증가하였으며 세포자멸사 유도 효과는 용량 의존적이었다. 25 mM 15-deoxy-PGJ2를 투여한 후 48시간까지 caspase 활성도를 측정하였는데, caspase 3 활성도는 모든 세포주에서 caspase 9 활성도는 JCK를 제외한 나머지 세포주에서 유의하게 증가하였으며 caspase 8 활성도는 별 변화가 없었다. Pancaspase 억제제인 Z-VAD-FMK와 caspase-3 억제제인 Z-DEVD-FMK를 투여한 경우 15-deoxy-PGJ2의 암세포증식 억제 효과가 48시간 이후 농도 의존적으로 차단되었으며, 이러한 효과는 모든 세포주에서 나타났다. 각 세포주에 15-deoxy-PGJ2를 투여 한 후 48시간까지 bcl-2 및 bax gene의 발현 유무를 관찰하였는데, bcl-2 mRNA는 Cho-CK, Choi-CK, SCK 세포 주에서 유의하게 감소하였으나 bax의 경우 모든 세포주에서 유의한 변화를 보이지 않았다. 결론: 한국인 간내담관암세포주 모두에서 PPAR gamma mRNA가 발현됨을 알 수 있었고, 내인성 PPAR gamma 배위 자인 15-deoxy-PGJ2가 세포자멸사 유도를 통해 담관암세포 증식을 용량 및 시간 의존적으로 억제하였다. Background/Aims: Peroxisome proliferator-activated receptor (PPAR)-γ ligand is known to inhibit the growth of several kinds of cancer cells, yet its effect on cholangiocarcinoma is indecisive. We investigated the effect of an endogenous ligand of PPAR-γ, 15-deoxy-δ (12,14)-prostaglandin J2 (15-deoxy-PGJ2) on cholangiocarcinoma cells that were established from intrahepatic cholangiocarcinoma tissue of Korean patients. Methods: Four cholangiocarcinoma cell lines, Cho-CK, Choi-CK, JCK and SCK, were studied. The mRNA expression of PPAR-γ, bcl-2, and bax were examined by RT-PCR. Cell viability was determined by MTT assay. The cell cycle was analyzed by flow cytometry, and apoptosis by cell death detection ELISA kit. Caspase activity was measured by colorimetric assay. The effect of caspase inhibitors on 15-deoxy-PGJ2-induced apoptosis was determined by measuring cell viability using the MTT assay. Results: PPAR-γ mRNA was expressed in all cholangiocarcinoma cells. 15-deoxy-PGJ2 inhibited proliferation of all cells in a dose- and time-dependent manner. All cells treated with 15-deoxy-PGJ2 showed increased dose-dependent apoptosis. Caspase 3 was activated in all cells and caspase 9 was activated in all but JCK cells after 15-deoxy-PGJ2 treatment. Caspase 8 activity showed no significant change. The pan-caspase inhibitor, Z-VAD-FMK, and the caspase-3 inhibitor, Z-DEVD-FMK, blocked 15-deoxy-PGJ2-induced apoptosis in all cells dose-dependently. The expression of bcl-2 was decreased in Cho-CK, Choi-CK and SCK cells, and bax expression was not changed significantly after 15-deoxy-PGJ2 treatment. Conclusions: PPAR-γ mRNA was expressed in all Korean cholangiocarcinoma cells. Our data suggest that 15-deoxy-PGJ2 exerts an antineoplastic effect against cholangiocarcinoma cells by inducing apoptosis through caspase activation. (Korean J Med 78:75-86, 2010)
SV40 T 항원의 온도조건부 변이형 유전자가 포함된 Amphotropic Retrovirus 에 의한 사람 태아 간세포의 불멸화
이정일(Joung Il Lee),동석호(Seok Ho Dong),김효종(Hyo Jong Kim),김병호(Byung Ho Kim),장영운(Young Woon Chang),장린(Rin Chang),성세라(Se Ra Seong),박재경(Jae Kyung Park),김승보(Seung Bo Kim),이상목(Sang Mok Lee) 대한내과학회 1999 대한내과학회지 Vol.57 No.1
N/A Human cells are almost never spontaneously immortalized in vitro. We tried to immortalize human fetal hepatocytes (h-FH) and evaluate the differentiational status and its change. Methods : Hepatocytes were isolated from a liver fragment of 20 week old fetus and infected with amphotropic recombinant retrovirus containing a temperature- sensitive mutant of SV40 large T antigen and neomycin phosphotransferase gene. G418 resistant colonies were cloned and expanded. The cells which were able to divide more than 30 times were used to analyze various functions. Results : The immortalization rate was 3.3 x 10-8 and two cell lines (C11, D21) were established. C11-60, C11-80, D21-30 and D21-60 (suffix number means the cell division counts) were evaluated. D21-30 was thougt to be imcompletely immortalized because a considerable portion of cells died during culture. The morphology was similar to that of epithelial cells except for D21-30 which looked like fibroblast. The cells grew rapidly at 33oC but stopped growing at 39oC. T antigen and p53 was expressed at 33oC but disappeared at 39oC, which suggest that T antigen binds to p53. Chromosomal changes were so marked that it was impossible to discriminate exact number. Albumin was secreted as about 1/10 as that of h-FH, but alpha-fetoprotein secretion stopped after immortalization. Telomerase was activated in both cell lines except for the incompletely immortalized cells D21-30. Telomere was elongated in competely immortalized cell lines, but it was rather shortened in D21-30 compared to that of h-FH. Macroscopic colonies did not develop in soft agar assay. Conclusions : We successfully immortalized human fetal hepatocytes. Although the cells are not likely to have oncogenicity, the functions are not so good, possibly due to marked chromosomal changes which are thought to occur before telomerase is activated during immortalization step.
흰쥐의 출혈성 쇼크로 유도된 위점막 손상에 있어서 재수혈과 산소 유리기의 역할
장영운(Young Woon Chang),김효종(Hyo Jong Kim),김병호(Byung Ho Kim),이정일(Jung Il Lee),장린(Rin Chang),박승준(Seung Joon Park),정주호(Joo Ho Jung),고계창(Gye Chang Ko) 대한내과학회 1990 대한내과학회지 Vol.39 No.6
N/A We studied the separate roles of ischemia, retransfusion, and oxygen free radicals on gastric lesion formations in rat hemorrhagic shock mode1s. 1n this model, the systemic arterial pressure was reduced to 30-40mmHg for 20 min by withdrawal of blood via the carotid artery, and then the shed blood was retransfused. In rats subjected to ischemia alone, there were very few gastric erosions on both gross and histologic evaluation. In contrast, ischemia followed by retransfusion caused severe gastric injury. Pretreatment with either superoxide dismutase or allopurinol significantly reduced gastric lesion formation (p<0.005). Therefore, oxygen-free radicals formed during retransfusion may play an important role in the pathogenesis of hemorrhagic shock-induced gastric injury. In addition, superoxide dismutase and allopurinol are effective against hemorrhagic shock-induced gastric injury.
장영운 ( Young Woon Chang ) 대한내과학회 2014 대한내과학회지 Vol.86 No.6
Antiplatelet therapies have been widely used to prevent cardiovascular diseases. However, antiplatelet agents cause gastrointestinal (GI) damage and are associated with a greater risk of gastroduodenal ulcers and life-threatening ulcer complications. The first step to reduce the GI risk of antiplatelet therapy is to assess whether the patient requires continuous antiplatelet therapy. The second step is to eliminate risk factors that may place the patient at greater GI risk such as Helicobacter pylori infection, NSAID use, steroid ingestion, and smoking. Continuous aspirin therapy plus a powerful proton pump inhibitor (PPI) is the choice of treatment for antiplatelet-related peptic ulcers. The risk of cardiovascular complications and risk of gastric complication using antiplatelet agents should be evaluated individually. (Korean J Med 2014;86:673-677)