• 제목/요약/키워드: Delayed Renewal Process

검색결과 3건 처리시간 0.016초

추계학적 확률과정을 이용한 경사제 피복재의 예방적 유지관리를 위한 조건기반모형 (Condition-Based Model for Preventive Maintenance of Armor Units of Rubble-Mound Breakwaters using Stochastic Process)

  • 이철응
    • 한국해안·해양공학회논문집
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    • 제28권4호
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    • pp.191-201
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    • 2016
  • 추계학적 확률과정을 이용하여 경사제 피복재를 예방적으로 유지관리할 수 있는 조건기반모형을 개발하였다. 완전 보수보강 조건에서 가장 경제적으로 보수보강이 수행되어야 하는 최적의 시점을 결정할 수 있는 모형이다. 본 연구에서 개발된 RRP(Renewal Reward Process) 기반 경제성 모형은 이자율을 고려할 수 있을 뿐만 아니라 기존 연구에서 상수로 취급하던 비용을 시간에 따른 확률변수로 고려할 수 있다. 누적피해와 사용한계 그리고 구조물의 중요도를 모두 고려할 수 있는 함수식을 제시하여 ABM(Age-Based Maintenance)을 CBM(Condition-Based Maintenance)으로 쉽게 확장할 수 있게 하였다. 또한 함수식에 포함된 계수들을 수학적으로 산정할 수 있는 방법도 제시하였다. 두 가지 추계학적 확률과정, WP(Wiener Process)와 GP(Gamma Process)를 이용하여 경사제 사석재를 해석하였다. 사용한계, 이자율 그리고 구조물의 중요도에 따라 시간에 따른 기대총비용율을 산정하여 기대총비용율이 최소가 되는 예방적 유지관리의 최적 시점을 쉽게 추정할 수 있었다. 동일한 사용한계에서 이자율이 높을수록 최적시점은 늦어지고 그에 따라 기대총비용율도 낮아졌다. 또한 상대적으로 GP가 WP보다 더 보수적으로 최적시점을 예측하였다. 마지막으로 동일한 조건에서 구조물의 중요도가 높을수록 더 자주 예방적 보수보강을 실시하여야 한다는 것을 알았다.

비 직렬 시스템의 신뢰도 최적화를 위한 시스템 번인 (Optimal System Burn-in for Maximizing Reliability of Non-series Systems)

  • 김경미
    • 대한산업공학회지
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    • 제33권2호
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    • pp.273-281
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    • 2007
  • The decision of how long performing system burn-in must be answered with a probabilistic model of a system lifetime at which infant mortality failures created during assembly processes are quantified. In this paper, we propose such a model which is modified from previous results. Using the system model, we derived system reliability in terms of component and system burn-in times for the two cases of minimal repair at system failure and of component replacement and connection repair at their failure times. The procedure is illustrated with a bridge system and the optimal system burn-in times are obtained for maximizing system reliability. The result suggests that an assumption of minimal repair at system failure may underestimate the optimal burn-in time in practice.

Ten-eleven translocation 1 mediating DNA demethylation regulates the proliferation of chicken primordial germ cells through the activation of Wnt4/β-catenin signaling pathway

  • Yinglin Lu;Ming Li;Heng Cao;Jing Zhou;Fan Li;Debing Yu;Minli Yu
    • Animal Bioscience
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    • 제37권3호
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    • pp.471-480
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    • 2024
  • Objective: The objective of this study was to investigate the regulation relationship of Ten-eleven translocation 1 (Tet1) in DNA demethylation and the proliferation of primordial germ cells (PGCs) in chickens. Methods: siRNA targeting Tet1 was used to transiently knockdown the expression of Tet1 in chicken PGCs, and the genomic DNA methylation status was measured. The proliferation of chicken PGCs was detected by flow cytometry analysis and cell counting kit-8 assay when activation or inhibition of Wnt4/β-catenin signaling pathway. And the level of DNA methylation and hisotne methylation was also tested. Results: Results revealed that knockdown of Tet1 inhibited the proliferation of chicken PGCs and downregulated the mRNA expression of Cyclin D1 and cyclin-dependent kinase 6 (CDK6), as well as pluripotency-associated genes (Nanog, PouV, and Sox2). Flow cytometry analysis confirmed that the population of PGCs in Tet1 knockdown group displayed a significant decrease in the proportion of S and G2 phase cells, which meant that there were less PGCs entered the mitosis process than that of control. Furthermore, Tet1 knockdown delayed the entrance to G1/S phase and this inhibition was rescued by treated with BIO. Consistent with these findings, Wnt/β-catenin signaling was inactivated in Tet1 knockdown PGCs, leading to aberrant proliferation. Further analysis showed that the methylation of the whole genome increased significantly after Tet1 downregulation, while hydroxyl-methylation obviously declined. Meanwhile, the level of H3K27me3 was upregulated and H3K9me2 was downregulated in Tet1 knockdown PGCs, which was achieved by regulating Wnt/β-catenin signaling pathway. Conclusion: These results suggested that the self-renewal of chicken PGCs and the maintenance of their characteristics were regulated by Tet1 mediating DNA demethylation through the activation of Wnt4/β-catenin signaling pathway.