• Radiation Oncology Journal
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• v.12 no.2
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• pp.143-150
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• 1994

The damage which radiation produces in tissues such as the lungs can be discussed at the molecular, biophysical, cellular, and organ levels. The cellular effects of irradiating the lungs are related to the histologic and clinical sequelae. In the present study the right lung of rabbits were exposed to single dose of 20 Gy of X-irradiation. Animals from each group were sacrificed monthly for 6 months postexposure. Sections of lung were examined by light microscopy(LM) and by transmission electron microscopy(TEM). Multiple exudative lesions were seen at 2 months after the 20Gy irradiation,and they progressed to a proliferative and then reparative fibrotic lesion by 6 months. Changes in epithelial lining of lung components, particulary the presence of type II pneumocytes were found by both LM and TEM. Capillary endothelial damages were less pronounced. The possible implication of cellular components in radiation pneumonitis and fibrosis is discussed.

• Journal of Radiation Industry
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• v.17 no.4
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• pp.533-542
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• 2023

We developed an emergency national manual for preservation of cultural heritage using irradiation disinfection technic under flood disaster. And we examined its practicality with a critical radiation dose on fungi that occur at water-logged event in order to prevent fungal damage that occurs during submersion. The X-ray irradiation for this experiment was conducted at the Production Technology Research Institute located in Yeongcheon, Gyeongsangbuk-do. A disinfection critical dose of 12 kGy was selected for two types of fungi known to spread rapidly and are resistant to radiation to submerged cultural properties, and this experiments were conducted by setting a target dose of 12kGy at 8.37mA at 5MeV. Under the above conditions, only continuity of irradiated samples were completely disinfected. This suggests that continuity of irradiation is important for fungal disinfection.

• Clinical Endoscopy
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• v.55 no.1
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• pp.22-32
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• 2022

Radiotherapy (RT) is a treatment modality that uses high-energy rays or radioactive agents to generate ionizing radiation against rapidly dividing cells. The main objective of using radiation in cancer therapy is to impair or halt the division of the tumor cells. Over the past few decades, advancements in technology, the introduction of newer methods of RT, and a better understanding of the pathophysiology of cancers have enabled physicians to deliver doses of radiation that match the exact dimensions of the tumor for greater efficacy, with minimal exposure of the surrounding tissues. However, RT has numerous complications, the most common being radiation proctitis (RP). It is characterized by damage to the rectal epithelium by secondary ionizing radiation. Based on the onset of signs and symptoms, post-radiotherapy RP can be classified as acute or chronic, each with varying levels of severity and complication rates. The treatment options available for RP are limited, with most of the data on treatment available from case reports or small studies. Here, we describe the types of RT used in modern-day medicine and radiation-mediated tissue injury. We have primarily focused on the classification, epidemiology, pathogenesis, clinical features, treatment strategies, complications, and prognosis of RP.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.80-80
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• 2003

${\beta}$-lapachone(${\beta}$-Lap), a natural o-naphthoquinone, presents in the bark of the Lapacho tree. ${\beta}$-Lap is cytotoxic against a variety of human cancer cells and it potentiates the anti-tumor effect of Taxol. In addition, ${\beta}$-Lap has been reported to radiosensitize cancer cells by inhibiting the repair of radiation-induced DNA damage.In the present study, we investigated the cytotoxicity of ${\beta}$-Lap against RKO human colorectal cancer cells as well as the combined effect of ${\beta}$-LaP and ionizing radiation. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h killed almost 90％ of the clonogenic cells. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h or longer also caused massive apoptosis. Unlike other cytotoxic agents, ${\beta}$-Lap did not increase the expression of p53 and p21 and it suppressed the NFkB expression. The expression of Caspase 9 and 3 was minimally altered by ${\beta}$-Lap. Radiation and ${\beta}$-Lap acted synergistically in inducing clonogenic cell death and apoptosis in RKO cells when ${\beta}$-Lap treatment was applied after but not before the radiation exposure of the cells. Interestingly, a 4 h treatment with 5 ${\mu}$M of ${\beta}$-Lap starting 5 h after irradiation was as effective as that starting immediately after irradiation. The mechanisms of ${\beta}$-Lap-induced cell killing is controversial but a recent hypothesis is that ${\beta}$-Lap is activated by NAD(P)H: quinone-onidoreductase (NQO1) in the cells followed by an elevation of cytosolic Ca$\^$2+/ level and activation of proteases leading to apoptosis. It has been reported that NQO1 level in cells is markedly up-regulated for longer than 10 h after irradiation. Indeed, using immunological staining of NQO1, we observed a significant elevation of NQO1 expression in RKO cells 5h after 2-4 Gy irradiation. Such a prolonged elevation of NQO1 level after irradiation may be the reasons why the ${\beta}$-Lap treatment applied S h after irradiation was as effective as that applied immediately after irradiation in killing the cells. In view of the fact that the repair of radiation-induced damage is usually completed within 1-2 h after irradiation, it is highly likely that the ${\beta}$-Lap treahment applied 5 h after irradiation could not inhibit the repair of radiation-induced damage. For in vivo study, RKO cells were injected S.C. into the hind-leg of Nu/Nu mice, and allowed to grow to 130 mm3 tumor. The mice were i.p. injected with ${\beta}$-lapachone or saline 2 h after irradiation of tumors with 10 Gy of X-rays. The radiation induced growth delay was increased by 2.4 $\mu\textrm{g}$/g of ${\beta}$-lapachone. Taken together, we may conclude that the synergistic interaction of radiation and ${\beta}$-Lap in killing cancer cells is not due to radiosensitization by ${\beta}$-Lap but to an enhancement of ${\beta}$-Lap cytotoxicity by radiation through an upregulation of NQO1. The fact that NQO1 is elevated in tumors and that radiation causes prolonged increase of the NQO1 expression may be exploited to preferentially kill tumor cells using ${\beta}$-Lap in combination with radiotherapy.

• Journal of Korean Ophthalmic Optics Society
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• v.7 no.2
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• pp.229-234
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• 2002

The human eye and skin is exposed daily to solar energy. Expecially, the ultraviolet radiation (UVR) exposure has been damaged as an important causative factor in corneal disease. These damage of cornea was effected the retina. Therefore the eye function was effected very significant damage. As a results the protect of UVR in the eye is very important in ocular health. Therefore in living the intensive ultraviolet radiation environment by solar energy, human eye have protected the cornea and eyeball by the UV-blocking sunglass, eyeglass, goggles, and contact lens. Finally the specific UV-blocker lens devices available to the primary care for the subjects by optician. Of course, in the future these specific lenses have to development and study by fellowship.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2012.05a
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• pp.880-883
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• 2012

In this paper, CMOS logic device, the INVERTER, NAND, NOR were designed and fabricated using 0.18um CMOS process for analyzing the effect of transient radiation damage. Fabricated logic devices were measured by applying a 1kHz input at 1.8V supply. As a result, the current consumption of less than 70uA and Rising time, Falling time was within a 4us. Experimental results transmission delays occurred when using a 50M cable for pulse radiation experiments.

• Journal of Environmental Health Sciences
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• v.32 no.5 s.92
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• pp.492-498
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• 2006

Ultraviolet(UV) radiation causes a variety of biological effects on the skin, including inflammation, pigmentation, photoaging and cancer. Free radicals are involved in inflammatory skin reactions induced by UVB radiation. In this study, we investigated the effects of antioxidants(Tea, Korean red ginseng, Ginkgo biloba extract) on UVB-induced skin damage. Tea, KRG and EGb 761 were topically treated to dorsal skin of ICR mouse. The mice were also treated soon after IMED ($1.4KJ/m^{2}$) of UVB irradiation. Skin pigmentation of irradiated mouse was observed by a chromameter after 2 weeks. Topical application of Tea, KRG and EGb 761 for 2 weeks decreased skin pigmentation compared to DVB control group(p<.05). Tea, KRG and EGb 761 also reduced UVB-induced infiltration of inflammatory cells. These results showed that Tea, KRG and EGb 761 as a topical application may have preventive effect against UVB-induced skin damage.

• Biomolecules & Therapeutics
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• v.24 no.1
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• pp.75-84
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• 2016

This study was designed to investigate the cytoprotective effect of rosmarinic acid (RA) on ultraviolet B (UVB)-induced oxidative stress in HaCaT keratinocytes. RA exerted a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuated UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increased the expression and activity of superoxide dismutase, catalase, heme oxygenase-1, and their transcription factor Nrf2, which are decreased by UVB radiation. Collectively, these data indicate that RA can provide substantial cytoprotection against the adverse effects of UVB radiation by modulating cellular antioxidant systems, and has potential to be developed as a medical agent for ROS-induced skin diseases.

• Radiation Oncology Journal
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• v.3 no.1
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• pp.1-8
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• 1985

To determine the dose·survival and repair characteristics of the jejunal crypt cells, experimental study was carried out using total 70 mice. Single or split irradiations of 1,100 to 2,200 rad were delivered to whole bodies of $C_{57}$ BL mice, using a cesium 137 animal irradiator and those mice were sacrificed after 90 hours. The number of regenerating crypts per jejunal circumference was counted by a jejunal crypt cell assay technique and dose·response curve was measured. The results were as follows : 1. The average number of jejunal crypts per circumference in control group was 140. In a single irradiation group, the number of regenerated jejunal crypts was, 125, 56, 2 in each subgroup of 1,100 rad, 1,400 rad and 1,800 rad respectively. In split irraiation group, it was 105,44,2 in each subgroup of 1,400rad 1,800rad and 2,200rad respectively. 2. Mean lethal dose of mouse jejunal crypt cell was 167 and 169 rad respectively in a single and split irradiation. 3. Repair dose of sublethal damage was 280 rad. 4. Sublethal damage was completely repaired within 4 hours between the split dose of irradiation.

• Journal of Radiation Protection and Research
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• v.45 no.1
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• pp.11-15
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• 2020

Background: There have been various studies to investigate the mechanisms of DNA damage from low-energy electrons. To understand the mechanism of these strand breaks, it is necessary to investigate the dissociation mechanism of the DNA constituents, that is, bases, sugars, and phosphates. Materials and Methods: We studied the dissociation of thymine base upon interaction with low-energy electrons. For this experiment, thymine powder was pressed onto the indium base and irradiated by 5 eV electrons. Results and Discussion: Non-irradiated and irradiated thymine samples were compared and analyzed using the X-ray photoelectron spectroscopic technique to analyze the dissociation patterns of the molecular bonds after low-energy electron irradiation of thymine. Conclusion: With 5 eV electron irradiation, C-C and N-C = O bonds are the primary dissociations that occur in thymine molecules.