• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.185-191
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• 2008

Activation of c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is an important cellular response that modulates the outcome of the cells which are exposed to the tumor necrosis factor (TNF) or the genotoxic stress including DNA damaging agents. Although it is known that JNK is activated in response to genotoxic stress, neither the pathways to transduce signals to activate JNK nor the primary sensors of the cells that trigger the stress response have been identified. Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-${\beta}$-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation. Our findings revealed that this sustained JNK activation was not mediated by the TNF (tumor necrosis factor) receptor signaling, but it required a functional ATM (ataxia telangiectasia) activity. In addition, JNK inhibitor SP-600125 significantly blocked the Adr-induced cell death, but it did not affect the cell death induced by MNNG. These findings suggest that the sustained activation of JNK mediated by RIP plays an important role in the DNA damage-induced cell death, and that the duration of JNK activation relays a different stress response to determine the cell fate.

• Journal of radiological science and technology
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• v.26 no.2
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• pp.29-35
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• 2003

The purpose of this study was to compare the compression force and thickness of the compressed breast between mediolateral oblique and craniocaudal mammography. This population consisted of 204 paired mediolateral oblique and craniocaudal mammography obtained on one mammographic unit by certified mammography technologists during 2 month period. The women examined were $30{\sim}59$ years old with breast implants, the patients were classified into 3 groups according to age, $30{\sim}39$, $40{\sim}49$, and $50{\sim}59$, prior breast cancer, mastectomy or breast deformity were excluded. The digital readout of compressed breast compression force and thickness was recorded. Mammographic positioning was assessed using standard criteria. The mean compression force of the compressed breast on the craniocaudal projection was less than the mean compression force on the mediolateral projection(14 versus 13.88 daN, p<0.05). The mean thickness of the compressed breast for mediolateral projection was 41.46 mm and that for the craniocaudal projection was 39.50 mm(p<0.05). The compressed breast is higher or thicker on mediolateral oblique than on craniocaudal mammography.

• Journal of Preventive Medicine and Public Health
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• v.41 no.6
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• pp.373-379
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• 2008

Objectives ; The objective of this study was to evaluate the prevalence of atrophic gastritis and intestinal metaplasia according to gender, age and Helicobacter pylori infection in a rural population in Korea. Methods: Between April 2003 and January 2007, 713 subjects (298 men and 415 women, age range: 18-85) among the 2,161 adults who participated in a population-based survey received gastrointestinal endoscopy. All the subjects provided informed consent. Multiple biopsy specimens were evaluated for the presence of atrophic gastritis and intestinal metaplasia. The presence of Helicobacter Pylori was determined using CLO and histology testing. Results ; The age-adjusted prevalence of atrophic gastritis was 42.7% for men and 38.1% for women and the prevalence of intestinal metaplasia was 42.5% for men and 32.7% for women. The prevalence of atrophic gastritis and intestinal metaplasia increased significantly with age for both men and women (p for trend<0.001). The age-adjusted prevalence of Helicobacter pylori was similar for men (59.0%) and women (56.7%). The subjects with Helicobacter pylori infection showed a significantly higher prevalence of intestinal metaplasia (44.3%) compared with that (26.8%) of the noninfected subjects (p<0.001). However, the prevalence of atrophic gastritis was not statistically different between the Helicobacter pylori-infected subjects and the noninfected individuals. Conclusions : Our findings suggest that the prevalence of atrophic gastritis and intestinal metaplasia is higher for a Korean rural population than that for a Western population; this may be related to the high incidence of gastric cancer in Koreans. Especially, the prevalence of intestinal metaplasia was high for the subjects with Helicobacter pylori infection. The multistep process of gastric carcinogenesis and the various factors contributing to each step of this process need to be determined by conducting future follow-up studies.

• Journal of the Korean Society of Radiology
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• v.11 no.1
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• pp.49-54
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• 2017

As the Radiofrequency(RF) increases with the magnetic field strength, the wavelength of the RF excitation field becomes smaller, which leads to more the thermal effect in the human-body placed in the electric field. MRI scanner used was GE signa 1.5T, HDx 3.0T and Philips 3.0T with same routine clinical sequence protocol. Therefore temperature was measured before and after each scan. Taken the temperatures in the ear with ear infra-red type thermometer(Braun co). 3.0T were temperature increases more than $0.15^{\circ}C$ and GE 3.0T MRI equipment about $0.14^{\circ}C$ higher than the Philips 3.0T MRI(p<0.012). Psychogenic status was investigated by the survey respondents about their status can not just answer therefore, a little different from the expected. In our study of Thermal effect of clinical MRI with clinical protocol sequence, we found that the 3.0T in the body-temperature rise was greater than the 1.5T. Therefore, in clinical 3.0T examine the dangerous situation caused by the temperature rise occurred (burns, impaired thermoregulatory mechanism in patients with high-temperature damage, exhaustion occurs due to excessive sweating), not to appear the more watched the patient's condition with procedure.

• Korean Journal of Veterinary Research
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• v.30 no.4
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• pp.447-457
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• 1990

In order to observe the distribution of mast cell on the stages of the mammary carcinogenesis, the numerical changes of mast cells in the mammary tumor development in rats treated with DMBA and compound 48/80 have been investigated by the light microscope. The results observed were summarized as follows: The appearance of tumor were not observed during the whole experimental period in the rats of the control group received injection of sterile saline, but tumors appeared in 100% of the animals, the tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days and the mean number of tumor masses per rat was $3.4{\pm}1.2$ in the DMBA treated group. And the majority of the DMBA-induced mammary neoplasms were appeared cervical mammary gland and thoracic mammary gland. The histological findings of mammary carcinoma were recognized adenocarcinoma in the DMBA treated group. Mast cells were distributed within the adipose tissues and the interglandular connective tissue in the control, but found to be randomly dispersed within the tumor cell masses, in the connective tissues adjacent to the periphery of the tumor, the adipose tissues and the subcutaneous tissues contiguous to the region of tumor development in the DMBA treated group. Numerical alterations of mast cells were observed in the mammary tumors that separated into three major classes of tumors: hyperplasia, atypical hyperplasia and carcinoma. The number of mast cells were distributed in the connective tissues adjacent to the mammary gland was $45.3{\pm}3.4$ cells in the control group, but was $50.2{\pm}4.9$ cells, $126.7{\pm}10.5$ cells and $340.3{\pm}19.2$ cells according to each stages of mammary tumorigenesis in the DMBA treated group.

• Journal of Chest Surgery
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• v.5 no.1
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• pp.45-56
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• 1972

Esophageal perforation is one of the most grave prognostic problems among thoracic and general surgical emergencies which necessitate urgent operative measures. In Korea,there are still many persons ingesting lye for suicidal attempt and thoracic surgeons in Korea have more chances to deal with lye burned esophagus with or without instrumental perforation than those in Western countries. Main cause of esophageal perforation in Korea is instrumental perforation in patients with lye stricture of the esophagus during diagnostic endoscopy or therapeutic bouginage. Other causes are corrosion of the esophagus due to ingestion of caustic agents, pathologic perforation, surgical trauma, stab wound and spontaneous rupture of the esophagus in our series. Therapeutic measures are various,and depend on duration of perforation, severity of its complications, pathology of perforated portion of the esophagus and degrees of inflammation at the point of perforation. The most important therapeutic measures are prevention of this grave condition during esophagoscopy, bouginage and surgical procedures on lungs and mediastinal structures and to make early diagnosis with prompt therapeutic measures. During the period of January, 1959, to December, 1971, the authors experienced 65 cases ofesophageal perforation including acquired esophagorespiratory fistula at Dept. of Chest Surgery, the National Medical Center in Seoul, and obtained following results in the series. 1. Female were 35 cases, and peak age incidence was 2nd and 3rd decades of life. 2. Among 65 cases, 43 were corrosive esophagitis or benign stricture of the esophagus due to caustic agents, 7 were patients with esophageal cancer. and there were 5 cases of esophageal perforation developed after pneumonectomy or pleuropneumonectomy. 3. Causes of perforation are instrumental perforation in 45, acute corrosion in 7, pathologic perforation in 7, surgical trauma in 3, stab wound in 2 cases, and one spontaneous rupture of the esophagus. 4. Most frequent sites of esophageal perforation were upper and mid thoracic esophagus, and 8 were cases with cervical esophageal perforation. 5. Complications of esophageal perforation were mediastinitis in 42, empyema or pneumothorax in 35, esophagorespiratory fistula in 12, retroperitoneal fistula or abscess in 5,pneumoperitoneum in 3, and localized peritonitis in 1 case. 6. Cases with malignant esophagorespiratory fistula were only 3 in the series which is predominant cause of acquired esophagorespiratory fistula in Western countries. 7. Various therapeutic measures were applied with mortality rate of 27.7% in the series. 8. In usual cases early treatment gave better prognosis, and least mortality rate in cases with perforation in mid thoracic esophagus. 9. Main causes of death were respiratory complications,acute hemorrhage with asphyxia, and septic complications. 10. Esophageal perforation developed after pneumonectomy gave more difficult therapeutic problems which were solved in only 1 among 5 cases.

• Korean Journal of Veterinary Research
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• v.31 no.1
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• pp.77-87
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• 1991

In order to know the influence of mast cells on the mammary tumor development, the growth of the mammary carcinoma, the numerical changes and the morphological findings of mast cells appeared in the tumor were microscopically observed in the rat treated with DMBA and each chemical of histamine, heparin, pyrilamine or cimetidine. The results observed were summarized as follows: The tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days, and the mean number of tumor mass per rat was $3.4{\pm}1.2$ in the DMBA-treated group. No significant difference was apparent in the tumor induction time of the histamine-treated group, heparin-treated group or pyrilamine-treated group compared with the control group, but in the cimetidine-treated group the tumor induction time was $61.8{\pm}10.6$ days (p<0.005). The mean number of tumors per rat was $2.1{\pm}0.9$ in the cimetidine-treated group in contrast to $3.4{\pm}1.3$ in the control group (p<0.005). Numerical changes of mast cells were observed according to the development of DMBA induced mammary tumors that were separated into three major classes of tumors. The numbers of mast cells in all the experimental group were inclined to increase significantly according to the mammary tumor development (p<0.005), and the histamine-treated group, heparin-treated group, or pyrilamine-treated group were nearly similar to the control group. But the mast cells in the each stage of tumor development were more numerous in the cimetidine-treated group than in the control group (p<0.005). There were not significant in the numerical changes of mast cells among the experimental groups on each stage of carcinomas separated by early stage, middle stage and late stage. In the morphological characteristics of mast cells, the degranulation was not detectable from the hyperplasia stages to the early stage of carcinoma, but its degranulation was observed at the middle stage of carcinoma. Most mast cells were nearly degranulated at the late stage of carcinoma. The histamine treated group, pyrilamine-treated group and cimetidine treated group did not differ from the control group in morphological changes of mast cells, but the degranulation was shown mild in the heparin-treated group. And the degranulation gave rise to the depletion of intercellular matrix via exocytosis all the experimental group. From above results, it is supposed that mast cells inhibit the tumor development and that the inhibition is not caused by a single-factor, but by a complex activities of mast cell mediators.

• Korean Journal of Veterinary Research
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• v.31 no.3
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• pp.343-353
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• 1991

In order to investigate the histopathological, mechanism of Rompun-induced shock, the development of mammary carcinoma, the numerical changes and the morphological findings of the mast cells appeared in the carcinoma were microscopically observed in the rat treated with DMBA and each chemical of compound 48/80 and Rompun. Also mast cell degranulation induced by Rompun was observed with electron microscope. The results observed were summarized as follows: Tumor appeared in 100% of the animals. Tumors grew more rapidly to $10{\times}10mm$ in rats depleted of mast cells ($37.7{\pm}4.2$ days) than was observed in the control group ($42.5{\pm}4.7$ days) (p<0.005). The mean number of tumors per rat was $2.8{\pm}1.3$ in the compound 48/80- treated group in contrast to $3.4{\pm}1.3$ in the control group. No significant difference was apparent in the tumor induction time of Rompun treated group compared with the compound 48/80-treated group, but the tumor measuring at least $10{\times}10mm$ appeared more quickly in the Rompun treated group than in the control group (p<0.005). The numbers of mast cells in the control group were inclined to increase significantly according to the mammary tumor development (p<0.005). In contrast, the mast cells were fewer significantly in the compound 48/80-treated group and Rompun-treated group than in the control group (p<0.005). The numbers of mast cells in the compound 48/80-treated group and Rompun-treated group were inclined to reduce significantly according to the stages of the mammary carcinoma growth in contrast to the control group respectively. The ultrastructural morphologies of mast cells at 30 minutes after Rompun injection were appeared many normal granules in the cytoplasm, but many normal and degranulated granules were scattered along the cell membrane. And at 1 hour after Rompun injection mast cell granules were disappeared nearly or rarely seen. many long cytoplasmic projections were folded back to adhere to their own surface membrane. and mast cells resulted in a reduced size of these cells. Otherwise. compound 48/80 caused extensive degranulation of mast cells by disrupting cell membrane. but mast cell degranulation by Rompun was observed exocytosis of granules through a channel. From the above results. it is concluded that the Rompun may give rise to the dealth of animals as a shock caused by mast cell degranulation.

• Korean Journal of Psychosomatic Medicine
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• v.16 no.2
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• pp.120-124
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• 2008

Objectives : The current study aimed at assessing clinical symptoms and personality characteristics on MMPI of patients in Hwa-Byung clinic. Methods : Thirty-one female patients($45.4{\pm}8.4$ years old) who visited to the Hwa-Byung Clinic in Ewha womans Dongdaemoon hospital were recruited. Semistructured interviews and laboratory tests for symptoms were performed for the patients group. Patients group and control group($42.9{\pm}8.0$ years old) completed MMPI. Results : All patients had symptoms of chest tightness or chest pain. 19(61.3%) out of 31 patients had gastrointestinal complaints. There were respiratory symptoms in 13(41.9%) patients. 12 patients(38.7%) suffered from difficulties in their sleep. 12 patients(38.7%) had psychiatric symptoms including anxiety or depressed mood. 8 patients(27.6%) were diagnosed as gastrointestinal diseases by the laboratory test. After controlling age and education, scores of Hs, D, Hy, Pt on MMPI in patients group were significantly higher than control group (p=0.001, p=0.049, p=0.000, and p=0.029, ANCOVA, respectively). Conclusion : In the current study, patients who have visited Hwa-Byung clinic showed various somatic symptoms including chest tightness, gastrointestinal symptoms, complaints in respiratory system and psychiatric symptoms. Based on laboratory tests, considerable proportion of patients was diagnosed as physical illnesses. Additionally, patients in Hwa-Byung clinic have a tendency to be more hypochondriatic, depressed, hysteric and anxious.

• Journal of Life Science
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• v.16 no.7 s.80
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• pp.1235-1242
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• 2006

Sulforaphane, an isothiocyanate derived from hydrolysis of glucoraphanin in broccoli and other cruciferous vegetables, was shown to induce phase II detoxification enzymes and inhibit chemically induced mammary tumors in rodents. Recently, sulforaphane is known to induce cell cycle arrest and apoptosis in human canter cells, however its molecular mechanisms are poorly understood. In tile present study, we demonstrated that sulforaphane acted to inhibit proliferation and induce morphological changes of human hepatocarcinoma HepG2 cells. Treatment of HepG2 cells with $10{\mu}M\;or\;15{\mu}M$ sulforaphane resulted in significant G2/M cell cycle arrest as determined by DNA flow cytometry. Moreover, $20{\mu}M$ sulforaphane significantly induced the population of sub-G1 cells suggesting that sulforaphane induced apoptosis. This anti-proliferative effect of sulforaphane was accompanied by a marked inhibition of ryclin A, cyclin 31 and Cdc2 protein. However, the levels of tumor suppressor p53 and Cdk inhibitor p21 mRNA and protein expression were significantly increased by sulforaphane treatment in a concentration-dependent manner. Although further studies are needed, the present work suggests that sulforaphane may be a potential rhemoprevetiveichemotherapeucc agent for the treatment of human cancer cells.