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      • KCI등재

        흰쥐에서 허혈시간에 따라 재관류후 나타나는 근조직의 미세구조 변화에 allopurinol이 미치는 영향

        백두진,전재홍,Paik, Doo-Jin,Chun, Jae-Hong 한국현미경학회 1995 Applied microscopy Vol.25 No.3

        It has been well known that ischemia and reperfusion injury to skeletal muscle following an acute arterial occlusion causes significant morbidity and mortality. The skeletal muscle, which contains high energy phosphate compounds, has ischemic tolerance. During the ischemia, the ATP is catalyzed to hypoxanthine anaerobically and hypoxanthine dehydrogenase is converted to xanthine oxidase. During reperfusion, the hypoxanthine is catalyzed to xanthine by xanthine oxidase under $O_2$, presence and that results in production of cytotoxic oxygen free radicals. These cytotoxic free radicals, $O_2^-,\;H_{2}O_2,\;OH^-$, are toxic and make lesions in skeletal muscle during reperfusion. The authors perform the present study to investigate the effects of allopurinol, the inhibitor of xanthine oxidase, on reperfused ischemic skeletal muscles by observing the ultrastructural changes of the muscle fibers. A total of 48 healthy Sprague-Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under urethane(3.0mg/kg., IP) anesthesia, lower abdominal incision was done and the left common iliac artery were ligated by using vascular clamp for 1, 2 and 6 hours. The left rectus femoris muscles were obtained at 6 hours after the removal of vascular clamp. In the allopurinol pretreated group, 50mg/kg of allopurinol was administered once a day for 2 days and before 2 hours of ischemia. The specimens were sliced into $1mm^3$ and prepared by routine methods for electron microscopic observations. All preparations were stained with uranyl acetate and lead citrate, and then observed with Hitachi -600 transmission electron microscope. The results were as follows: 1. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats, decreased glycogen particles and electron density of mitochondrial matrix and dilated terminal cisternae are seen. In 2 hours ischemia/6 hours repersed rectus femoris muscles of rats, mitochondria with electron lucent matrix, irregularly dilated triad and spheromembranous bodies are observed. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats, irregularly arranged myofibrils, and many spheromembranous bodies, fat droplets and lysosome are seen. 2. In 1 hour ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, decreased glycogen particle and dilated cisternae of sarcoplasmic reticulum and triad are observed. In 2 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol decreased electron density of mitochondrial matrix and spheromembranous bodies are seen. In 6 hours ischemia/6 hours reperfused rectus femoris muscles of rats pretreated with allopurinol, mitochondria with electron lucent matrix, spheromembranous bodies and dilated cisternae of sarcoplasmic reticulum and terminal cistern are observed. The results suggest that the allopurinol attenuates the damages of the skeletal muscles of rats during ischemia and reperfusion.

      • 출생후 성숙에 따라 나타나는 흰쥐 십이지장 및 공장 점막의 alkaline phosphatase 활성에 대한 연구

        백두진 한양대학교 의과대학 1994 한양의대 학술지 Vol.14 No.2

        The alkaline phosphatase, which is the hydrolytic enzyme of the phosphate salt in alkaline solution, acts on differentiation and maturation of cells and tissues, absorption and metabolism of nucleic acid and proteins. The author has investigated the change in the activity of alkaline phosphatase of the duodenal and jejunal mucosa of the rats according to biochemical and physiological maturation during early postnatal life. The experimental animals, which were obtained from litters deliveried, normally and randomly sampled adults, were sacrificed at the 1st, 5th, 10th, 20th, and 30th day after birth. The specimens of duodenum and jejunum were fixed in 10%-neutral formalin at 4℃ and sectioned 10㎛ thickness in cryostat. The activity of the alkaline phosphatase was evaluated histochemically by Gomori's method and the incubation time of sliced specimens was 30 minutes. The results were as follows. 1. In the neonatal rats of the 1st day after birth, the activities of the alkaline phosphatase were moderately positive in the epithelium and lamina propria of villi and weakly positive in the intestinal glands and its surrounding lamina propria of the duodenal mucosa. ANd the activities of alkaline phosphatase in the mucosa of the jejunum were moderately positive in the epithelium of the villi and weakly positive in the intestinal glands and lamina propria. 2. In the neonatal rats of the 5th day after birth, the activities of the alkaline phosphatase were moderately positive in the epithelium of apical and middle portion of villi. traceablely positive in the epithelium of basal portion and lamina propria of the mucosa of the duodenum. And the activities of alkaline phosphatase were moderately positive in the epithelium of apical and basal portion of the villi and weakly positive in the epithelium of middle portion of the villi. the intestinal glands and lamina propria of the jejumum. 3. In the neonatal rats of the 10th day after birth, the activities of alkline phosphatase were moderately or strong positive in the epithelium of the villi and weakly positive in the epithelium of the villi and weakly positive in the intestinal gland and lamina propria of jejunal mucosa. 4. In the rats of the 20th day after birth, the activities of alkaline phosphatase were strong or moderately positive in the epithelium of the villi, moderately positive in lamina propria of the core of the villi and the weakly positive in the intestinal glands and its surrunding lamina propria of duodenum. And the activities of alkaline phosphatase in the mucosa of the jejunum were strong positive in the epithelium of basal portion of the villi, intestinal gland and lamina propria of the villi and weakly positive in the lamina propria surrounding intestinal glands. 5. In the rats of the 30th day after birth, the activities of alkaline phosphatase were moderately or strong positive in the epithelium of the villi, modereate positive in the lamina propria of the villi and weakly positive in the intestinal glands and its surrounding lamina propria of the duodenal mucosa. And the activity of alkaline phosphatase was strong positive in the epithelium of apical portion of villi of the mucosa of the jejunum. Activity was decreased gradually and in the epithelium of basal portion of the villi activity was weakly positive. The activities were moderately positive in the intestinal glands and weakly positive in surrounding lamina propria of the glands and weakly positive in surrounding lamina propria of the glands of the jejunal mucosa. 6. In the rats of the adulthood, the activities of the alkaline phosphatase were strong positive in the epithelium of the villi and weakly positive in the intestinal glands and lamina propria of the duodenum. And the activities of alkaline phosphatase were moderately positive in the epithelium of the villi and weakly positive in the intestinal glands and lamina propria of the mucosa of the jejunum. Consequently, it is suggested that the activities of the alkaline phosphatase in the mucosa of duodenum and jejunum were increased by differentiation, growth, maturation and the changes of diet during early postnatal life, of the rats.

      • KCI등재

        SOD, DMTU및 허혈양상화 처치가 허혈 및 재관류에 의한 흰쥐 넙다리곧은근의 미세구조 변화에 미치는 영향

        백두진,임재현,정호삼,Paik, Doo-Jin,Lim, Jae-Hyun,Chung, Ho-Sam 한국현미경학회 1997 Applied microscopy Vol.27 No.3

        The ischemia and reperfusion injury of the skeletal muscles is caused by generation of reactive oxygen during ischemia and reperfusion. It is well known that over 4 hours of ischemia injures the skeletal muscles irreversibly. The author has demonstrated the effects of SOD (superoxide dismutase), DMTU (dimethyl thiourea) and ischemic preconditioning on ultrastructural changes of the muscle fibers in the rectus femoris muscles after 4 hours of ischemia and 1 day and 3 days of reperfusion. A total of 72 healthy Sprague-Dawley rats weighing from 200 gm to 250 gm were used as experimental animals. Under urethane(1.15 g/kg, IP, 2 times) anesthesia, lower abdominal incision was done and the left common iliac artery was occluded by using vascular clamp for 4 hours. The left rectus femoris muscles were obtained at 1 and 3 days after the removal of vascular clamp. The SOD (15,000 unit/kg) or DMTU (500 mg/kg) were administered intraperitoneally at 1 hour before induction of ischemia. The ischemic preconditioned group underwent three episodes of 5 minutes occlusion and 5 minutes reperfusion followed by 4 hours of ischemia and 1 day and 3 days of reperfusion. The specimens were sliced into $1mm^3$ and prepared by routine methods for electron microscopic observation. All specimens were stained with uranyl acetate and lead citrate and then observed with Hitachi-600 transmission electron microscope. The results were as follows: 1. SOD or DMTU alone did not affect the ultrastructure of muscle fibers in the rectus femoris muscles. The electron density of mitochondrial matrix was decreased by ischemic preconditioning. 2. Dilated cisternae of sarcoplasmic reticulum, triad, mitochondria and the loss of myofilament in the sarcomere were observed in the 4 hours ischemia and 1 day reperfused rectus femoris muscles. Markedly changed sarcoplasmic reticulum, triad, disordered or loss of myofilament, indistinct A-band and I-band, and irregular electron lucent M -line and Z-line are seen in the 4 hours ischemia and 3 days reperfused rectus femoris muscles. 3. SOD reduced the changes of organelles in the muscle fibers of the 4 hours ischemia and 1 day reperfused rectus femoris muscles of the rats, but SOD did not affect the changes of muscle fibers in the 4 hours ischemia and 3 days reperfused muscles. On the other hand, DMTU markedly attenuated considerably the ultrastructural change of the 4 hours ischemia and 1 day or 3 days reperfused rectus femoris muscles. 4. By the ischemic preconditioning, the change was attenuated remarkably in the 4 hours ischemia and 1 day reperfused rectus femoris muscles. As the ischemic reperfused changes of muscle fibers were regenerated or recovered by ischemic preconditioning, the ultrastructures of them were similar to those of normal control in the 4 hours ischemia and 3 days reperfused rectus formoris muscles. Consequently, it is suggested that DMTU is stronger inhibitor to ischemic reperfused change than SOD. The ischemia and reperfusion-induced muscular damage is remarkably inhibited by ischemic preconditioning.

      • KCI등재

        Superoxide dismutase 및 Dimethyl thiourea가 흰쥐 위샘 으뜸세포에서 Adriamycin 투여 후 나타나는 미세구조의 변화에 미치는 영향

        백두진,장형심,정호삼,Paik, Doo-Jin,Chang, Hyung-Shim,Chung, Ho-Sam 한국현미경학회 1998 Applied microscopy Vol.28 No.2

        Adriamycin is a one of anthracyclin antibiotics isolated from the culture media of Streptomyces peucetius var casius. The formation of reactive oxygen metabolite by redox cycling during the metabolism and the inhibition of DNA synthesis results in antineoplastic effects of adriamycin. The authors have demonstrated the effects of SOD(superoxide dismutase) or DMTU (dimethyl thiourea), which are used as an antioxidant, on the ultrastructural changes of the gastric chief cells after the administration of adriamycin in the rat. Adriamycin (30 mg/kg) was administered intraperitoneally to the Sprague-Dawley rats weighing about 220 gm and SOD (15000 unit/kg) or DMTU (500 mg/kg) were administered intraperitoneally to the rats 30 minutes after the administration of adriamycin. The gastric chief cells 24, 48 and 72 hours after the administration of adriamycin were observed with Hitachi-600 electron microscope. The results were as follows. 1. SOD or DMTU alone did not affect the ultra structures of the gastric chief cells in the rat. 2. Dilation, sacculation and segmentation of the cisternae of rough endoplasmic reticulum, dilation of the saccules of Golgi complex and dilated mitochondria with electron lucent matrix were seen in the adriamycin treated rats. In the course of time, the ultrastructures of the chief cell changed markedly. 72 hours after drug administration, severely dilated cisternae of rough endoplasmic reticulum, with clumping of chromatin around the nuclear envelope and mitochondria with electron lucent matrix and dilated cristae were seen in the chief cell. 3. The treatment of SOD is more effective than DMTU to attenuated the ultrastructural changes of the chief cells in the adriamycin administered rat. Consequently it is suggested that adriamycin would induce the degenerative changes of the organelles of the chief cell. The treatment of SOD is more effective than DMTU to attenuate the adriamycin induced damage.

      • KCI등재

        흰쥐에서 cisplatin에 의한 위벽세포의 미세구조변화에 미치는 SOD의 영향

        백두진,박규완,정호삼,Paik, Doo-Jin,Park, Kyu-Wan,Chung, Ho-Sam 한국현미경학회 1996 Applied microscopy Vol.26 No.3

        This study aims to demonstrate the effect of SOD (superoxide dismutase), one of the antioxidant enzymes, on the ultrastructural changes in the parietal cells caused by the administration of cisplatin in the rat. A total of 60 healthy Sprague-Dawley rats weighing about 200 gm were used as experimental animals. Cisplatin (6 mg/kg) was administered intraperitoneally to rats pretreated with 15,000 unit/kg of SOD or rats without the pretreatment. The experimental animals were sacrificed at 6 hours, 12 hours, 24 hours and 3 days after the administration of cisplatin. The results were as follows: 1. SOD alone did not affect the ultrastructural changes in the gastric parietal cells in the rat. 2. Irregular shaped mitochondria, mitochondria with dim cristae, dilated cristae, ruptured outer membrane, electron lucent matrix and degenerative mitochondria were seen in cisplatin treated rat. Whorled membranous body, many lysosomes and large vacuole were observed in the gastric parietal cells in cisplatin treated rat. 3. Mitochondria with dilated cristae and electron lucent matrix and irregular shaped mitochondria were observed in the gastric parietal cells of the cisplatin treated rat with pretreatment of SOD. These results suggest that SOD attenuates the toxic effect of the cisplatin in the gastric parietal cells of the rat.

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