• Molecules and Cells
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• 제26권1호
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• pp.5-11
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• 2008

Stalled DNA replication forks activate specific DNA repair mechanism called post-replication repair (PRR) pathways that simply bypass DNA damage. The bypassing of DNA damage by PRR prevents prolonged stalling of DNA replication that could result in double strand breaks (DSBs). Proliferating cell nuclear antigen (PCNA) functions to initiate and choose different bypassing pathways of PRR. In yeast, DNA replication forks stalled by DNA damage induces monoubiquitination of PCNA at K164, which is catalyzed by Rad6/Rad18 complex. PCNA monoubiquitination triggers the replacement of replicative polymerase with special translesion synthesis (TLS) polymerases that are able to replicate past DNA lesions. The PCNA interaction motif and/or the ubiquitin binding motif in most TLS polymerases seem to be important for the regulation of TLS. The TLS pathway is usually error-prone because TLS polymerases have low fidelity and no proofreading activity. PCNA can also be further polyubiquitinated by Ubc13/ Mms2/Rad5 complex, which adds an ubiquitin chain onto monoubiquitinated K164 of PCNA. PCNA polyubiquitination directs a different PRR pathway known as error-free damage avoidance, which uses the newly synthesized sister chromatid as a template to bypass DNA damage presumably through template switching mechanism. Mammalian homologues of all of the yeast PRR proteins have been identified, thus PRR is well conserved throughout evolution. Mutations of some PRR genes are associated with a higher risk for cancers in mice and human patients, strongly supporting the importance of PRR as a tumor suppressor pathway.

• 한국콘크리트학회:학술대회논문집
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• 한국콘크리트학회 1996년도 봄 학술발표회 논문집
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• pp.323-327
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• 1996

Reinforced concrete(R/C) structures need repair and rehabilitation due to the deterioration such as a crack, spalling and disintergration. Numerous repair materials which are currently used in construction fields without any regulation are examined in terms of their serviceabilities and effectiveness. In this paper section of existing R/C beams are enlarged with repair materials, that is, epoxy, latex or premix. And then they are strengthened with rebar, steel poate of CFRP on the tension face. Structural behaviors of strengthened beams are investigated both statically and dynamically and they are compared with each. This paper summarizes the overall research plan.

• 한국환경성돌연변이발암원학회지
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• 제10권1호
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• pp.1-10
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• 1990

The regulation of DNA repair genes expression was investigated using fused genes, in which the promoter of repair genes was hybridized with the lacZ structural gene. The activities of beta-galactosidase expressed from the fused gense were highly increased when the host cells were exposed to methylating agents, such as methyl methansulfonate (MMS), N-methyl-N'-nitro-nitrosoguanidine (MNNG) and methyl nitrosourea (MNU). On the other hand, the enzyme activities from the fused genes were not induced when the cells were treated with ethylating or nonalkylating agents, such as ethyl methansulfonate (EMS), 4-nitroquinoline-1-oxide (4NQO), Bleomycin, and Benzo(a)pyrene (BP).

• 한국독성학회:학술대회논문집
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• 한국독성학회 2006년도 추계학술대회
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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.

• 한국건설관리학회:학술대회논문집
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• 한국건설관리학회 2002년도 학술대회지
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• pp.283-286
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• 2002

공동주택의 양적인 팽창에 주력하는 과정에서 품질관리 미비로 발생하는 하자문제는 입주자에게 정신적${\cdot}$ 경제적 피해를 끼치고 건설업에 대한 불신을 가중시켜, 주택공급자와 주택소비자간에 분쟁을 빈번하게 발생시키고 있다. 공통주택 관리령에 명시된 하자의 범위와 책임보증기간은 정량적 개념이 부족하고, 하자보증의 개념도 포괄적으로 구성되어 있어서 하자여부와 보수범위에 대한 견해차가 크다. 이로 인해 하자보수 종료처리가 원활하게 이루어지지 못하고 사회적 소모비용만 증가시키고 있다. 이에 대해 본 연구에서는 주택공급자 측면과 주택소비자 측면에서 하자보수 종료에 대한 합리적인 방안을 제시하고자 하였다. 아울러 원활한 하자보수 종료를 위하여 각 주체별 업무와 역할을 제시함으로써 하자보수 종결후의 유지관리를 향상시키는데 기여하고자 하였다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권12호
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• pp.7439-7444
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• 2013

Aim: ATF3, a member of the ATF/CREB family of transcription factors, has been found to be selectively induced by calcineurin/NFAT inhibition and to enhance keratinocyte tumor formation, although the precise role of ATF3 in human skin cancer and possible mechanisms remain unknown. Methods: In this study, clinical analysis of 30 skin cancer patients and 30 normal donors revealed that ATF3 was accumulated in skin cancer tissues. Functional assays demonstrated that ATF3 significantly promoted skin cancer cell proliferation. Results: Mechanically, ATF3 activated Stat3 phosphorylation in skin cancer cell through regulation of p53 expression. Moreover, the promotion effect of ATF3 on skin cancer cell proliferation was dependent on the p53-Stat3 signaling cascade. Conclusion: Together, the results indicate that ATF3 might promote skin cancer cell proliferation and enhance skin keratinocyte tumor development through inhibiting p53 expression and then activating Stat3 phosphorylation.

• 토지주택연구
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• 제7권1호
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• pp.43-51
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• 2016

장기수선계획은 공동주택 수선공사의 시행 기준으로서 장기수선충당금의 적립과 예방보전을 통한 효과적인 시설물관리의 기반을 제공하는 것이며 정부에서는 장기수선계획의 중요성을 감안하여 공동주택의 장기수선공사를 위한 대상항목과 수선주기, 수선율을 법으로 정하고 있다. 그러나 수립기준에 포함된 수선공사의 항목이 최근의 공법 등을 반영하여 적기에 개정되지 못함에 따라 실제 아파트 단지에서 장기수선계획의 빈번한 변경, 수선공사를 둘러싼 논란, 충당금 사용 상의 어려움을 가져오고 있다. 이러한 문제를 해결하기 위해서는 실태분석을 통해 계획수선 항목의 적정성을 평가하여 수립기준을 조정하는 것이 요구된다. 본 연구에서는 장기수선계획과 수선공사 데이터를 통해 파악할 수 있는 현황을 바탕으로 주요 수선항목을 도출하고 수립기준을 조정하는 방안을 제안함으로써 장기수선계획의 운영을 담당하는 관리주체의 부담을 저감함과 동시에 적정수준의 수선충당금 적립을 유도하여 건물 내구연한의 연장과 수선공사 실질화를 위한 방안을 제안하고자 하였다. 이를 위해 광범위하게 장기수선계획 사례를 수집하여 계획에의 항목 채택률을 검토하고, 장기수선충당금 사용내역과 관리비 상의 수선유지비 내역을 분석하였다. 주요 항목을 도출함에 있어서는 보수적인 방식으로서 불필요한 항목만을 최소한으로 삭제하는 배제방식과 각 항목의 계획 반영률이 일정 수준 이상이면서 공사내역이 있는 항목만을 가려내는 선택방식 등 두 가지 방식으로 접근하였다. 그 결과 현재의 147개 항목 중 118개와 73개 항목이 배제방식과 선택방식을 통해 각각 주요 항목으로 정리되었다. 장기수선계획 수립을 위한 법적기준은 실제 적용되는 공법과 재료의 현황을 주기적으로 반영하는 것이 필요하다는 점에서 본 연구의 결과는 기준의 실용성 제고에 기여할 것으로 기대된다.

• BMB Reports
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• 제35권2호
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• pp.194-198
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• 2002

Eukaryotic replication protein A (RPA) is a single-stranded(ss) DNA binding protein with multiple functions in DNA replication, repair, and genetic recombination. The 70-kDa subunit of eukaryotic RPA contains a conserved four cysteine-type zinc-finger motif that has been implicated in the regulation of DNA replication and repair. Recently, we described a novel function for the zinc-finger motif in the regulation of human RPA's ssDNA binding activity through reduction-oxidation (redox). Here, we show that yeast RPA's ssDNA binding activity is regulated by redox potential through its RPA32 and/or RPA14 subunits. Yeast RPA requires a reducing agent, such as dithiothreitol (DTT), for its ssDNA binding activity. Also, under non-reducing conditions, its DNA binding activity decreases 20 fold. In contrast, the RPA 70 subunit does not require DTT for its DNA binding activity and is not affected by the redox condition. These results suggest that all three subunits are required for the regulation of RPA's DNA binding activity through redox potential.

• 한국건축시공학회지
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• 제11권6호
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• pp.597-608
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• 2011

공동주택의 건설 분쟁(Claim)발생 시 지속적으로 발생하는 하자의 보수비용 산정 방안에 대한 객관적 기준이 없어 건설전문가들도 각자의 경험과 성향에 따라 다양하게 판단하게 되므로 문제점을 발생 시키고 있다. 따라서 본 연구에서는 이에 대한 분석을 통하여 보수비용 산정기준과 방안을 제시한 후 건축물 하자관련 담당자들에게 합리적인 하자 판단기준을 제안 하고자 한다. 연구결과, 실적공사비를 우선 적용하며 실적공사비에 없는 항목은 표준품셈을 활용하여 산정한다. 지속형 하자 유형인 법규위반 하자의 보수비용 산정은 위반 건물부위만 철거하여 재시공하는 비용을 산정하고, 진행성(확대)하자는 건물 준공의 경과연수에 비례하여 기여율로 산정하며, 반복성 하자는 하자를 최소화시키는 방법의 설비공법을 대안으로 강구하여 산정하고, 가치감소 하자는 내용연수대비 하자보증기간의 비율로 산정하는 방법을 제안하였다. 이중 가치감소하자 보수비용의 산정은 향후 보다 많은 연구가 필요할 것으로 사료된다.

• 대한화장품학회:학술대회논문집
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• 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
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• pp.338-351
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• 2003

UV radiation is the most dangerous stress factor among permanent environmental impacts on human skin. Consequences of UV exposure are aberrant tissue architecture, alterations in skin cells including functional changes. Nowadays new kinds of outdoor leisure-time activities and changing environmental conditions make the question of sun protection more important than ever. It is necessary to recognize that self-confident consumers do not consider to change their way of life, they demand modern solutions on the basis of new scientific developments. In the past one fundamental principle of cosmetics was the use of physical and organic filter systems against damaging UV-rays. Today new research results demonstrate that natural protecting cell mechanisms can be activated. Suitable biological actives strongly support the protection function not from the surface but from the inside of the cell. A soy seed preparation (SSP) was proven to stimulate natural skin protective functions. The major functions are an increased energy level and the prevention of DNA damage. These functions can I be defined as biological UV protection. The tumor suppressor protein p53 plays a key role in the regulation of DNA repair. p53 must be transferred into the phosphorylated form to work as transcription factor for genes which are regulating the cell cycle or organizing DNA repair. A pretreatment with SSP increases the phosphorylation rate of p53 of chronically UV-irradiated human keratinocytes significantly. According to the same test procedure SSP induces a dramatic increase in the expression of the tumor suppressor protein p14$^{ARF}$ that is supporting the p53 activity by blocking the antagonist of p53, the oncoprotein Mdm2. Mdm2, a ubiquitin E3-ligase, downregulates p53 and at the same time it prevents phosphorylation of p53. The positive influence of the tumor suppressor proteins explains the stimulation of DNA repair and prevention of sunburn cell formation by SSP, which was proven in cell culture experiments. In vivo the increased skin tolerance against UV irradiation by SSP could be confirmed too. We have assumed, that an increased repair potential provides full cell functionality.y.