• 대한조선학회논문집
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• 제53권2호
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• pp.135-143
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• 2016

In this study, an embedded system composed of equipment setting, block importing, scenario setting and output reporting is developed in multi-body dynamics program, ADAMS, for conducting dynamic structural analysis of block lifting process. First, equipment used for block lifting process is set in the simulation environment and the shapes and functions of two lifting beams, and six block loaders are provided as the equipment. Second, the modal analysis result of the lifting block is imported from the static structural analysis system, NASTRAN. Third, the lifting scenarios, such as hoisting, waiting, trolley moving, and wire connecting, are set in the system. Finally, output results in the forms of plots, texts and tables, are reported after the dynamic structural analysis. The test examples conducted in a shipyard are applied into the developed system in various condition and scenarios. The loads at the lug points, the stress contours, and the hot spot tables of the developed system are compared with the result of the static analysis system.

• 해양환경안전학회지
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• 제27권2호
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• pp.387-393
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• 2021

본 연구에서는 해양플랫폼의 탑사이드 구조에서 주로 채택하고 있는 파이프 연결 구조의 피로 수명 증가를 위한 방안을 찾기 위하여, 유한요소해석을 수행하였다. 상용해석프로그램인 MSC Patran/Nastran을 적용하였으며, 대표적인 중앙부 구조 형상을 해석모델로 선정하였다. 하중에 따른 응력집중 현상을 구현하기 위하여, 8 절점 솔리드 요소를 이용한 모델링을 구현하였다. 주요하중은 횡방향 하중 2가지와 대각선 파이프에 인장 하중을 고려하였다. 주요 위치에서의 Hot spot 응력을 확인하기 위하여, 0.01 mm dummy 쉘 요소를 적용하였으며, 0.5 t와 1.5 t 위치에서의 주응력을 계산한 후 외삽법에 따라 용접부에 발생하는 응력을 추정하였다. 일부 구간에서는 만족해야 하는 피로 수명 이하로 평가되어, 보강이 필요하였다. 보강은 기존 설계된 파이프의 두께나 지름을 변경하지 않고, 피로수명이 부족한 부위에 응력집중계수를 낮출 수 있도록 브래킷을 추가하였다. 인장 하중에 대해서는 bracket toe에서 응력은 23 % 증가하였고, 기존에 문제가 된 파이프의 내측, 외측에서의 응력은 약 8 % 감소하였다. 휨 하중에 대해서는 bracket toe에서 응력은 3 % 증가하였고, 기존에 문제가 된 파이프의 내측, 외측에서의 응력은 약 48 % 감소하였다. 신규 브래킷 보강으로 인하여, bracket toe의 응력증가가 발생하였지만, S-N 커브 자체가 파이프 조인트에 비해 좋으므로 큰 문제가 되지는 않는다. 본 연구에서 적용한 국부 보강을 통한 피로 수명 개선 방법은 기존 설계안의 변경을 최소화하면서 피로 수명 증가를 효율적으로 할 수 있다는 점에서 관련 산업에서 유용하게 활용될 수 있을 것으로 기대된다.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권5호
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• pp.373-384
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• 2001

Cellular proliferation is an intricately regulated process mediated by the coordinated interactions of critical growth control genes. Two of these factors in mammalian cells are the p53 and mdm-2 genes. A protein product of the mem-2 oncogene has been recently shown to associate with the protein encoded by the tumor suppressor gene p53. The p53 tumor suppressor protein is stabilized in response to DNA damage and other stress signals and causes the cell to undergo growth arrest or apoptosis, thus preventing the establishment of mutations in future cellular generations. Mutation or loss of p53 is a very common event in tumor progression. It occurs in about 50% of all tumors analysed including of colon, lung, breast and liver. The cellular mdm-2 gene, which has potential transforming activity that can be activated by overexpression, is amplified in a significant percentage of human sarcoma and in other mammalian tumors. Proteins encoded by the mdm-2 gene are able to bind to the p53 protein and, when overexpressed, can inhibit p53's transcriptional activation function, thus mdm-2 can act as a negative regulator of p53 function. Experimental study was performed to observe the relationship between p53 gene mutation and mdm-2 protein expression and apply the results to the clinical activity. 36 golden syrian hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek(control side) was treated with mineral oil as the same manner to the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were examined for histology and immunohistochemistry observation, and were completely dissected by microdissection and DNA from both tissue were isolated by proteins K/phenol/chloroform extraction. Segments of the hamster p53 exons 5, 6, 7 and 8 were amplified by PCR using the oligonucleotide primers, and then confirmational change was observed by SSCP respectively. The results were as follows : 1. Dysplasia at 6 weeks, carcinoma in situ at 8 weeks and invasive carcinoma from 10 weeks could be observed in experimental groups. 2. p53 mutations were detected in 10 of the 36(28%) and the exons 6(6 of the 10 : 60%) was the most hot spot area among the highy conserved region(exons 5, 6, 7 & 8). 3. Immunohistochemical study confirmed 22 of the 36(61%) of p53 expression involving 10 of p53 mutations. 4. mdm-2 expression of was showed in 3 of the 36(8%) involving 1 of the 22 of p53 expression and 2 of the 14 of p53 non-expression. From the above results, mutation of p53 gene or expression of p53 protein may have the influence of the DMBA induced carcinoma of hamster buccal pouch but the expression of mdm-2 protein may not have relationship with tumorigenesis.