• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• International Journal of Reliability and Applications
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• v.18 no.1
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• pp.1-8
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• 2017

In this paper, we study an extended warranty model under minimal repair-replacement warranty (MRRW) which is suggested by Park, Jung and Park (2013). Under MRRW policy, the manufacturer is responsible for providing the minimal repair-replacement services upon the system failures during the warranty period. And if the failure occurs during the extended warranty period, only the minimal repair is conducted. Following the expiration of extended warranty, the user is solely responsible for maintaining the system for a fixed length of time period and replaces the system at the end of such a maintenance period. During the maintenance period, only the minimally repair is given for each system failure. The main purpose of this article is to suggest the extended warranty and replacement model with MRRW. Given the cost structures incurred during the life cycle of the system, we formulate the expected cost and the expected length of life cycle to obtain the expected cost rate.

• International Journal of Reliability and Applications
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• v.12 no.2
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• pp.117-122
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• 2011

In this paper, we suggest the optimal replacement policy following the expiration of repair warranty when the cost of minimal repair depends on the age of system. To do so, we first explain the replacement model under repair warranty. And then the optimal replacement policy following the expiration of repair warranty is discussed from the user's point of view. The criterion used to determine the optimality of the replacement model is the expected cost rate per unit time, which is obtained from the expected cycle length and the expected total cost for our replacement model. The numerical examples are given for illustrative purpose.

• Environmental Mutagens and Carcinogens
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• v.11 no.2
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• pp.107-117
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• 1991

The effect of 3-aminobenzamide (3AB), an inhibitor of poly (ADP-ribose) polymerase, on ethyl methanesulfonate (EMS)-or bleomycin (BLM)-induced DNA repair synthesis and chromosome aberrations was examined during the cell cycle of Chinese hamster ovary (CHO)-K$_1$ cells. The synchronized cells were obtained by using thymidine double block method and mitotic selection method. Three assays were employed in this study: unscheduled DNA synthesis, alkaline elution and chromosome aberrations. 3AB alone did not induce DNA repair and chromosome aberrations in all phases. The post-treatment with 3AB inhibited DNA repair synthesis induced by EMS or BLM in G$_2$ phase, whereas 3AB did not affect chromosome aberrations induced by EMS or BLM in all phases. These results suggest that 3AB aggravates the cell cycle disturbance which occur after DNA damage, and leads to an accumulation of cells at G$_2$ phase, and inhibits DNA repair synthesis, while the effect 3AB on chromosome aberrations may need reevaluated.

• Journal of Photoscience
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• v.10 no.2
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• pp.195-198
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• 2003

In the cellular response to DNA damaging agents, cells undergo cell cycle arrest or apoptosis against irrepairable DNA damage. RpS3 is known to function as UV DNA repair endonuclease III and ribosomal protein S3. In this study, we used normal and rpS3-overexpressed 293T cells to examine the role of rpS3 in response to DNA damaging agents. When 293T cells transfected with rpS3 were irradiated with UV, the pattern of cell cycle was dramatically changed in comparison with un-transfected 293T cells. We also found that the expression of rpS3 in normal cells was increased by treatment with DNA damaging agents. By means of Western and Northern blot analyses in rat tissues, we showed the expression pattern of rpS3 protein and its mRNA. These data suggest that DNA repair and cell cycle arrest are interrelated to each other through rpS3, and the increased expression of rpS3 seems to regulate the cell cycle arrest by DNA damaging agents.

• Journal of Korean Society for Quality Management
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• v.48 no.1
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• pp.201-214
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• 2020

Purpose: The purpose of this paper is to determine an optimal number of cycle times for the replacement under the circumstance where the system is replaced at the periodic time and the multiple number of working cycles whichever occurs first and the system is minimally repaired between the replacements if it fails. Methods: The system is replaced at periodic time () or cycle time, whichever occurs first, and is repaired minimally when it fails between successive replacements. To determine the optimal number of cycle times, the expected total cost rate is optimized with respect to the number of cycle times, where the expected total cost rate is defined as the ratio of the expected total cost between replacements to the expected time between replacements. Results: In this paper, we conduct a sensitivity analysis to find the following results. First, when the expected number of failures per unit time increases, the optimal number of cycle times decreases. Second, when the periodic time for replacement becomes longer, the optimal number of cycle times decreases. Third, when the expected value for exponential distribution of the cycle time increases, the optimal number of cycle times increases. Conclusion: A mathematical model is suggested to find the optimal number of cycle times and numerical examples are provided through the sensitivity analysis on the model parameters to see the patterns for changes of the optimal number of cycle times.

• Proceedings of the Korean Institute of Building Construction Conference
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• 2014.05a
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• pp.162-163
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• 2014

Operation and maintenance stage consists the largest portion of project life cycle cost. Appropriate management and analysis of such stages have massive effect on the total project cost. The effective prediction of optimized repair period is one of main factors in ㅌ management. However, it has been analyzed that the prediction of appropriate repair period revealed limitations in reliability. Therefore, this study suggests a methodology of repair period prediction by dividing finished projects into similar groups with same properties to be compared with the target project using quantitative variables.

• Korean Management Science Review
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• v.26 no.1
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• pp.209-223
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• 2009

In this paper, an analysis problem of repair levels and spare part allocation for MIME(Multi indenture multi echelon) systems is studied using simulation and meta-heuristics. We suggest a method to determine simultaneously repair levels and spare parts allocation to minimize the life cycle cost of MIME system under availability constraint. A simulated annealing method is used to analyze the repair levels and genetic algorithm is used to obtain the optimal allocation of spare parts. We also develop a simulation system to calculate the life cycle cost and system availability. Some numerical examples are also studied.

• Environmental Mutagens and Carcinogens
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• v.9 no.1
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• pp.23-32
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• 1989

Chinese hamster ovary (CHO)-K1 cells echibited a differential sensitivity in the process of DNA repair synthesis induced by ethyl methanesulfonate (EMS) or bleomycin (BLM) in relation to cell cycle. Two assays were employed in this study: alkaline elution and unscheduled DNA synthesis. The post-treat-ment with aphidicolin (APC), an inhibitor of DNA polymerase alpha, inhibited DNA repair synthesis induced by EMS in G2 phase, while APC did not show any effect on BLM-induced DNA repair synthesis in all phases. On the other hands, the 2', 3'-dideoxythymidine (ddTTP), an inhibitor of DNA polymerase beta, inhibited DNA repair synthesis induced by EMS or BLM in both of G1 and G2 phases. These results suggested that the involvement of DNA polymerase alpha and beta in DNA repair was dependent on cell stage or used chemical agent.

• Proceedings of the Korean Institute of Building Construction Conference
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• 2012.05a
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• pp.149-150
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• 2012

According to the increase of demand of the deteriorated building. The interest of the building's maintenance is continually increased, so studies about how to increase building's stability & prolonged life span are increased. This study's purpose is to maintain building's function, so we suggest a protocol type system of UI to estimate reasonable planning of demand of repair & replacement and to distribute budget.