• Journal of Microbiology and Biotechnology
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• 제27권3호
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• pp.633-643
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• 2017

To examine the pro-apoptotic role of the human ortholog (YPEL5) of the Drosophila Yippee protein, the cell viability of Saccharomyces cerevisiae mutant strain with deleted MOH1, the yeast ortholog, was compared with that of the wild-type (WT)-MOH1 strain after exposure to different apoptogenic stimulants, including UV irradiation, methyl methanesulfonate (MMS), camptothecin (CPT), heat shock, and hyperosmotic shock. The $moh1{\Delta}$ mutant exhibited enhanced cell viability compared with the WT-MOH1 strain when treated with lethal UV irradiation, 1.8 mM MMS, $100{\mu}M$ CPT, heat shock at $50^{\circ}C$, or 1.2 M KCl. At the same time, the level of Moh1 protein was commonly up-regulated in the WT-MOH1 strain as was that of Ynk1 protein, which is known as a marker for DNA damage. Although the enhanced UV resistance of the $moh1{\Delta}$ mutant largely disappeared following transformation with the yeast MOH1 gene or one of the human YPEL1-YPEL5 genes, the transformant bearing pYES2-YPEL5 was more sensitive to lethal UV irradiation and its UV sensitivity was similar to that of the WT-MOH1 strain. Under these conditions, the UV irradiation-induced apoptotic events, such as FITC-Annexin V stainability, mitochondrial membrane potential (${\Delta}{\psi}m$) loss, and metacaspase activation, occurred to a much lesser extent in the $moh1{\Delta}$ mutant compared with the WT-MOH1 strain and the mutant strain bearing pYES2-MOH1 or pYES2-YPEL5. These results demonstrate the functional conservation between yeast Moh1 and human YPEL5, and their involvement in mitochondria-dependent apoptosis induced by DNA damage.

• 한국전산구조공학회:학술대회논문집
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• 한국전산구조공학회 1999년도 봄 학술발표회 논문집
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• pp.305-312
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• 1999

This study is intended to propose a systematic and practical life cycle cost(LCC) model for the development of the reliability-based seismic safety and cost-effective performance criteria for design and upgrading of long-span PC bridges. The LCC models consist of five cost functions such as initial cost, repair/replacement cost, human losses, road user cost, and indirect losses of regional economy. The proposed model Is successfully expressed in temrs of Park-Ang damage indices and life cycle damage probability obtained from SMART-DRAIN-2DX which is an existing algorithm for nonlinear time history analysis. The proposed LCC model is successfully applied to a viaduct constructed by PSM, in Seoul. Based on the observations, the proposed systematic procedure for the formulation of LCC model may be useful for the development of the reliability-based seismic safety and cost-effective performance criteria for design and upgrading of long-span PC bridges.

• 한국방재학회 논문집
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• 제5권4호
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• pp.71-78
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• 2005

우리나라 도로교설계기준(2005)에서 규정하고 있는 내진설계의 기본개념은 인명피해를 최소화하고 설계지진은 구조물 수명동안 발생할 확률이 거의 없다는 것이다. 구조물 내진설계의 가장 상위개념이며 합리적인 내진대책은 인명피해를 최소화해야하며 경제성이 있어야 한다. 결과적으로 최우선의 목표를 만족시키기 위해서는 개별적인 구조물 중심이 아닌 도시 전체를 대상으로 한 거시적인 평가방안이 필요하다. 도시지역에 대한 피해상황은 기타지역과 다른 양상을 나타내며, 도시가 거대해질수록 구조물의 파손에 의한 손실보다는 오히려 이에 수반되는 부가적인 손실이 월등히 클 것이다. 그리고 거시적인 지진재해 평가방법은 인구와 구조물이 밀집되고, 정치 경제활동 등의 중심이 되는 오래된 도시일수록 효과가 탁월할 것이다. 본 연구는 지진재해위험을 합리적으로 예측할 수 있는 지진재해위험지수를 개발하고, 서울특별시를 6개 구역으로 분할하여 상대적인 지진재해위험을 평가하였다.

• 생명과학회지
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• 제33권5호
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• pp.414-421
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• 2023

갯사상자는 염생식물의 일종으로 염분이 높은 토양에서 자생하는 식물로 선행연구에 따르면 갯사상자는 항암효과를 가진다고 알려져 있다. 그러나 UVB로 유도된 광노화에 대한 효과는 아직 알려져 있지 않은 실정이다. 본 연구에서는 갯사상자 조추출물이 산화스트레스에 미치는 영향과 UVB 유래 광손상에 미치는 효과와 그 작용기전에 대하여 밝히고자 하였다. 갯사상자 추출물의 항산화 활성은 ROS 생성 억제능을 통해 확인하였으며, 광노화에 대한 효능은 피부노화 관련 인자인 MMP-1, MMP-3 및 MMP-9 발현 저해 효과와 MAPKs 발현기전을 통해 확인하였다. 세포생존율 실험결과를 바탕으로 UVB 조사 기준은 15 mJ/cm² 로 설정하였으며, 갯사상자 추출물의 농도는 10, 50, 그리고 100 ㎍/ml로 설정하였다. 결과적으로 갯사상자 추출물은 농도의존적으로 활성산소종을 억제하는 효과를 가짐을 확인하였고, 피부노화 관련인자인 MMP-1, MMP-3 및 MMP-9 발현을 감소시키는 것을 확인하였다. 노화관련인자인 MMP 발현 억제는 MAPK 전사인자의 발현 억제효과에 의한 것임을 확인할 수 있었다. 이들 결과로부터 갯사상자 추출물이 광노화에 효능을 가진 천연 화장품 소재로서 개발이 가능할 것으로 기대된다.

• Biotechnology and Bioprocess Engineering:BBE
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• 제6권4호
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• pp.231-236
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• 2001

How much do we know about the biology of aging from cell culture studies Most normal somatic cells have a finite potential to divide due to a process termed cellular or replicative senescence. A growing body evidence suggests that senescence evolved to protect higher eu-karyotes, particularly mammals, from developing cancer, We now know that telomere shortening due to the biochemistry of DNA replication, induces replicative senescence in human cells. How-ever in rodent cells, replicative senescence occurs despite very long telomeres. Recent findings suggest that replicative senescence is just the tip of the iceberg of a more general process termed cellular senescence. It appears that cellular senescence is a response to potentially oncogenic in-sults, including oxidative damage. In young orgainsms, growth arrest by cell senescence sup-presses tumor development, but later in life, due to the accumulation of senescent cells which se-cret factors that can disrupt tissues during aging, cellular senescence promotes tumorigenesis. Therefore, antagonistic pleiotropy may explain, if not in whole the apparently paradoxical effects of cellular senescence, though this still remains an open question.

• 대한의생명과학회지
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• 제7권4호
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• pp.181-190
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• 2001

This study was designed to investigate the effects of reactive oxygen species (ROS) on DNA stability in human spermatozoa. To verify human spermatozoa were incubated with xanthine-xanthine oxidase (X 100$\mu$M-XO 50 mlU ~ 400 mIU), $H_2O_2$ (125 $\mu$M ~ 1 mM), sodium nitroprusside (SNP 0.1 $\mu$M ~ 100 $\mu$M) or lymphocyte. Otherwise, spermatozoa were incubated under low $O_2$ (5%) condition. Damage of sperm DNA was analyzed by single cell electrophoresis (Comet assay) and flow cytometry after acridine orange staining. In the presence of ROS, there was increase in DNA damage. The rate of DNA single strand breakage (9.0$\pm$1.0% ~ 46.0$\pm$4.6%) and DNA fragmentation (7.51$\pm$1.0% ~ 29.5$\pm$4.6%) were similar regardless of the kinds of ROS and exposure time. DNA damage in the lower $O_2$ condition (5%) was lower than ambient $O_2$ condition (20%). Taken together, it suggested that sperm DNA might be damaged by ROS. In the presence of ROS, increase in DNA damage and chromatin instability was obvious in spite of short exposure. Although present study reconfirmed that sperm incubation in the low concentration of ROS have the benefit m the induction of capacitation and Ah, the increase in DNA damage by ROS and possible genetic problem should be considered before the human trials.

• Applied Biological Chemistry
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• 제48권2호
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• pp.155-160
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• 2005

본 연구에서는 매우 낮은 음의 산화환원전위를 나타내는 환원전리수가 paraquat에 의한 사람 임파구 DNA의 손상에 미치는 영향을 Comet assay를 사용하여 조사하였다. 환원전리수 처리에 의해서 paraquat에 의해 산화적으로 손상된 DNA가 회복되는 정도를 손상된 DNA로 인한 꼬리부분의 형광광도의 %비율로 나타내었다. Comet assay는 개별 세포의 DNA의 산화적 손상을 측정하는데 널리 사용되고 있다. 사람 임파구에 다양한 농도의 paraquat을 $37^{\circ}C$에서 30분간 처리한 후, 환원전리수를 첨가하여 30분간 반응시켰다. 그 결과 paraquat에 의한 임파구 DNA의 손상은 paraquart 농도증가에 의존적으로 증가하였다. 그러나 환원전리수를 처리한 결과 DNA의 산화적 손상이 paraquat 미처리 대조군 수준으로 거의 다 복구되었다.

• 한국콘크리트학회:학술대회논문집
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• 한국콘크리트학회 2004년도 춘계 학술발표회 제16권1호
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• pp.720-723
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• 2004

This study is intended to propose a systematic approach for determining optimum Life-Cycle Cost (LCC)-effective seismic design for continuous PSC bridges considering lifetime expected seismic risks. In the paper, a set of cost function for LCC analysis of bridges is proposed. The total LCC functions consist of initial cost and direct/indirect damage costs considering repair/replacement costs, human losses and property damage costs, road user costs, and indirect socio-economic losses. The damage costs are expressed in terms of Park-Ang median global damage indices (Park and Ang, 1985) and lifetime damage probabilities. The proposed approach is applied to model bridges of both moderate seismicity regions like Korea and high seismicity regions like Japan. Since, in case of bridges, a number of parameters may have an influence on optimal target reliability, various sensitivity analyses are performed in this study. It may be expected that the proposed approach can be effectively utilized for the development of cost-effective performance criteria for design and upgrading of various types of bridges as well as continuous PC bridges.

• Archives of Pharmacal Research
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• 제29권7호
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• pp.577-581
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• 2006

Oxidative mechanisms are thought to have a major role in cataract formation and diabetic complications. Antioxidant enzymes play an essential role in the antioxidant system of the cells that work to maintain low steady-state concentrations of the reactive oxygen species. When HLE-B3 cells, a human lens cell line were exposed to 50-100 mM glucose for 3 days, decrease of viability, inactivation of antioxidant enzymes, and modulation of cellular redox status were observed. Significant increase of cellular oxidative damage reflected by lipid peroxidation and DNA damage were also found. The glycation-mediated inactivation of antioxidant enzymes may result in the perturbation of cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant condition and may contribute to various pathologies associated with the long term complications of diabetes.

• Biomolecules & Therapeutics
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• 제32권5호
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• pp.640-646
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• 2024

Hair growth cycles are mainly regulated by human dermal papilla cells (hDPCs) and human outer root sheath cells (hORSCs). Protecting hDPCs from excessive oxidative stress and hORSCs from glycogen phosphorylase (PYGL) is crucial to maintaining the hair growth phase, anagen. In this study, we developed a new PYGL inhibitor, hydroxytrimethylpyridinyl methylindolecarboxamide (HTPI) and assessed its potential to prevent hair loss. HTPI reduced oxidative damage, preventing cell death and restored decreased level of anagen marker ALP and its related genes induced by hydrogen peroxide in hDPCs. Moreover, HTPI inhibited glycogen degradation and induced cell survival under glucose starvation in hORSCs. In ex-vivo culture, HTPI significantly enhanced hair growth compared to the control with minoxidil showing comparable results. Overall, these findings suggest that HTPI has significant potential as a therapeutic agent for the prevention and treatment of hair loss.