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Enteropathogenic E. coli가 肺臟組織에 미치는 組織學的 및 組織化學的 變化에 關한 硏究
최삼임,전영경,김영선,김복이,윤병택,김상호 의과학연구소 1989 全北醫大論文集 Vol.13 No.4
Bacterial endotoxin(lipopolysaccharide, LPS) induces pulmonary hypertension and edema, but the mechanism is not clearly known. So we have to study for this mechanism and morphological changes of the lung. LPS was injected intravenously to mice with or without pretreatment with sheep erythrocytes. Twenty four hours after injection of LPS, histologic(HE stain) and histochemical(PAS, reticulin, and van Gieson stains) examinations for the pulmonary tissue were done. The results were as follows. 1. Histologically, LPS induced edema of interalveolar septa, infiltration of inflammatory cells such as segmented neutrophils, lymphocytes, and macrophages, especially around the vessels and small bronchial trees, and formation of granulomas in the lung. Occasionally, sever vasculitis was also noted. 2. These histological changes were more marked in the sheep erythrocyte-pretreated group, so completely occluded vessels with thrombi and cental necrosis of the granulomas were noted. 3. histochemically, reticulin fibers were increased in amount in interalveolar septa and granuloma, and disruption of continuity of collagen fibers of blood vessels was noted These results suggest that LPS induces inflammatory reaction in the lung and pulmonary circulatory disturbance, especially it induces increase of the vascular permeability.
Enteropathogenic E. coli가 肝臟組織에 미치는 形態學的 變化에 關한 硏究
崔三任,李東根,金洙烈,金福伊,崔湖烈,金象皓 의과학연구소 1988 全北醫大論文集 Vol.12 No.3
Enteropathogenic E.coli(EPEC) induce a number of reactions in experimental animals, so we need to study for the mechanism of action of EPEC. EPEC was administered to mice intravenously, with or whitout pretreatment with sheep erythrocytes. Twenty four hours after administration of EPEC, histologic(HE) and histochemical(PAS, methylgreen pyronin, and reticulin stains) examinations for the liver tissue were done. The results were as follows. 1.Kupffer cells were markedly proliferated and showed PAS-positive phagocytic material in the cytoplasm. 2.Inflammatory cells were infiltrated in the hepatic sinusoids in diffuse or nodular patterns, and formation of granulomas was also noted. 3.Coagulative necrosis of hepatocytes were more prominent and diffuse in sheep erythrocytes-pretreated group. 4.Histochemically, marked reduction of PAS-positive granules and pyroninophilia in the cytoplasm of hepatocytes was noted. From these results, EPEC is cleared by Kupffer cells, and general metabolic changes induced by EPEC are followed by hepatic lesion.
Immunopotentiator(OK-432)가 마우스 淋巴節 組織學的 變化에 미치는 影響
崔三任,趙南杓,宋熹鍾,文俊一,崔湖烈,金象皓 의과학연구소 1988 全北醫大論文集 Vol.12 No.3
To investigate the mechanism of action of the OK-432 as a immunopotentiator, morphological studies of the lymph nodes were carried out in mice. OK-432 was administered intravenously in single(0.1 KE/100 g body weight) or sequential(0.01, 0.025, and 0.05KE/100 g body weight for succesive 3 days) doses to mice sensitized with sheep erythrocytes(SRBC) and nonsenstized mice. One, 3,5,7, and 10 days after OK-432 administration, histological and histochemical examinations were performed by H&E, methylgreen pyronin(MGP), and reticulin stains. The results were as follows: 1. In control group(treated with SRBC only), follicular structures of primary lymph follicles with indistinct germinal center were partially disrupted. The parafollicular area consisted mostly of pyrninophilic cells. 2. In OK-432 administered group, especially in sequentially administered group, secondary lymph follicles with distinct germinal center were developed. 3. In OK-432 administered group, and the development of secondary lymph follicles with enlarged and prominent germinal center were noted in the sequentially-administered groups. According to these results, immunopotentiator OK-432 affected not only parafollicular area of the T-cell area, but also germinal center of the B-cell area. This suggest that OK-432 may potentiate the humoral immunity as well as the cellmediated immunity.
최삼임,김영준,이호,이동근,최호열,김상호 의과학연구소 1995 全北醫大論文集 Vol.19 No.1
To investigate the proliferative activity and relation to malignancy using proliferating cell nuclear antigen(PCNA)-labeled indices and number of silver stained nucleolar organizer regions(AgNORs) per cell in gastric cancer versus precancerous lesion, PCNA immunohistochemistry and AgNORs silver staining was performed in cases of gastric cancer(30 cases), flat adenoma(5 cases), adenomatous polyp(5 cases), and control(15 cases).
X線 照射가 白鼠 肝臟의 形態學的 變化에 미치는 影響에 關한 硏究
최삼임,임채상,김복이,최호열,김상호 의과학연구소 1991 全北醫大論文集 Vol.15 No.1
To investigate the effects if ionizing radiation on the hepatic tissue, various doses of X-ray(1,000 rads, 1,400 rads, 1,800 rads) were irradiated to the left upper quadrant of abdomen of rats(source-skin distance, 1m;field size 23X23mm), by means of linear accelerator. At 1, 2, 3, and 4 weeks after single exposure to each dose, histological(hematoxylin-eosin) and histochemical(PAS, trichrome, and reticulin) stains for the left lobe of the liver. Then inflammatory cell index, fibrosis index, nuclear index, and vascular index were estimated in the hepatic tissue specimens. The results were as follows. 1. dilatation and congestion of the hepatic sinusoids were the most prominent at 1 week after 1,400 and 1,800 rads-irradiated liver tissue. 2. Inflammatory cell indices were increased in all irradiated livers, in comparison with that of control. The increase was most prominent in 1,800 rads-irradiated group. 3. Fibrosis indices were progressively increased from 2 weeks after irradiation, but withour dose-dependency. 4. Nuclear indices were begun to increase at 2 weeks after 1,400 and 1,800 rads-irradiation. The increase was prominent at 3 and 4 weeks after irradiation. 5. Vascular indices were not changed during 3 weeks after irradiation, and the gradual increasing-pattern was noted. From these results, one could finds out changes of the hepatic tissue exposed to ionizing radiation are dilatation and congestion of sinusoids as an early response, and increased fibrosis and nuclear poikilosis as subsequent resoponses. The early changes might be a part of general inflammatory reaction and autoimmune reaction resulting from early tissue damage, and the subsequent changes are secondary to vascular injury induced by radiation.
Ehanol에 依하여 損傷된 胃粘膜 上皮의 回復에 關한 實驗的 硏究
최삼임,이혜수,고범권,장성강,강명재,조남표,조성남,김상호 의과학연구소 1992 全北醫大論文集 Vol.16 No.2
This study aimed to investigate muoosal damage and restitution in the rat stomach after absolute ethanol instillation. Four me. of absolute ethanol was instilled to stomach and gastric mucosa was exposed to it for 30 and 45second , and then examined at immediately, 10 minute, 30 minutes, 60 minutes and 6 hours. Morphological studies of gastric tissue were performed by means of epon-toluidine blue section, H&E, and periodic acid Schiff(pAS) stains. The results were as follows. 1. Immediately after exposure to absolute ethanol far 30· seconds(time 0), surface mucous cells and the cells lining the gastric pits were damaged and exfoliated, but the gastric gland cells were not damaged. 2. Immediately after exposure to absolute ethanol for 45 seoends(time 0), superficial epithelium was necrotic and cellular damage was evident in the gastric glands beneath the damaged surface and gastric pits. Some inflammatory reaction was also noted. 3. Hyperemia and hemorrhage in the gastric mucosa were evident in almost all experimental groups 4. Epithelial restitution was begun to observe at 30 minutes in both 30 and 45 seconds-exposure groups, and almost completely restituted at 60 minutes after ethanol exposure. Surface mucous cells in restituted area were somewhat different from normal mucous cells morphologically. 5. According to damage of surface mucous cells, cytoplasmic PAS-positive granules were markedly decreased, but the PAS-positivity was also restored with restitution of mucous cells(even if weaker reaction than in normal mucous cell). It is thought that absolute ethanol-induced mocosal damage is striking even if the exposure time is brief, and epithelial restitution is achieved for 30 or 60 minutes after ethanol exposure. The mechanism of epithelial restitution might be resulting from migration of undamaged epithelial cells.