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- Börvik, Tore, et al.
(författare)
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Experimental and numerical study on the perforation of AA6005-T6 panels
- 2005
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Ingår i: International Journal of Impact Engineering. - : Elsevier BV. - 0734-743X .- 1879-3509. ; 32:1-4, s. 35-64
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Tidskriftsartikel (refereegranskat)abstract
- Extruded aluminium panels find their use in many different structures such as offshore platforms, bridge decks, train and ship components and lightweight protection systems. Impacts or other types of high-speed loading conditions are thus a relevant issue for several of these applications. There are, however, not many investigations published on the perforation of extruded aluminium panels covering experiments in combination with numerical analyses. This paper presents an experimental and numerical study on the perforation of AA6005-T6 aluminium panels impacted by ogival-nosed steel projectiles. The chosen panel has three triangular-shaped cells with a total depth of 130 mm. The wall thickness is 6 mm in the front and rear side plate, and 3 mm in the slanting webs. A rather comprehensive material test programme has been carried out in order to determine the material's response to dynamic loading. The experimental results were used to calibrate slightly modified versions of the Johnson-Cook constitutive relation and fracture criterion. 3D numerical simulations of the perforation process were then performed on a high-performance computer using the MPP version of the explicit finite element code LS-DYNA. In the simulations, the typical dimension of the elements was less than 1 mm. The numerical model is able to capture the main trends in the experiments in an adequate manner, and excellent agreement between numerical and experimental results is obtained.
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| 6. |
- McLean, D., et al.
(författare)
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Cancer mortality in workers exposed to organochlorine compounds in the pulp and paper industry : An international collaborative study
- 2006
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Ingår i: Journal of Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 114:7, s. 1007-1012
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this study was to evaluate cancer mortality in pulp and paper industry workers exposed to chlorinated organic compounds. We assembled a multinational cohort of workers employed between 1920 and 1996 in 11 countries. Exposure to both volatile and nonvolatile organochlorine compounds was estimated at the department level using an exposure matrix. We conducted a standardized mortality ratio (SMR) analysis based on age and calendar-period-specific national mortality rates and a Poisson regression analysis. The study population consisted of 60,468 workers. Workers exposed to volatile organochlorines experienced a deficit of all-cause [SMR = 0.91, 95% confidence interval (CI), 0.89-0.93] and all-cancer (SMR = 0.93, 95% CI, 0.89-0.97) mortality, with no evidence of increased risks for any cancer of a priori interest. There was a weak, but statistically significant, trend of increasing risk of all-cancer mortality with increasing weighted cumulative exposure. A similar deficit in all-cause (SMR = 0.94, 95% CI, 0.91-0.96) and all-cancer (SMR = 0.94, 95% CI, 0.89-1.00) mortality was observed in those exposed to nonvolatile organochlorines. No excess risk was observed in cancers of a priori interest, although mortality from Hodgkin disease was elevated (SMR = 1.76, 95% CI, 1.02-2.82). In this study we found little evidence that exposure to organochlorines at the levels experienced in the pulp and paper industry is associated with an increased risk of cancer, apart from a weak but significant association between all-cancer mortality and weighted cumulative volatile organochlorine exposure.
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| 9. |
- Wibom, Carl, et al.
(författare)
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Glioma Gwas Hits - Markers for Risk or for Prognosis?
- 2014
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Ingår i: Neuro-Oncology. - : Oxford University Press. - 1522-8517 .- 1523-5866. ; 16:Suppl. 2, s. ii109-ii110
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Tidskriftsartikel (refereegranskat)abstract
- One obstacle to developing new treatments for glioma is the generally poor understanding of glioma aetiology. The only generally accepted environmental risk factor or glioma is ionizing radiation. Glioma aetiology has also been shown to contain a genetic component, in part through observations that individuals in families with a history of glioma have an elevated risk of developing glioma themselves. The genetic component in glioma aetiology has been further substantiated through genome wide association studies (GWAS). These studies have identified associations between a number of common genetic variants and an increased glioma risk. However, the studies have all been of case-control design (i.e. including cases at diagnosis), and as such they presumably suffer from a degree of survival bias. Survival bias risks being introduced in a study when rapidly fatal cases are not included. This is an inherent risk of case-control designs, which is particularly pronounced when studying a disease with very poor prognosis, such as glioma. Ultimately, survival bias may result in erroneous conclusions, as it is impossible to separate associations with prognosis from associations with risk of disease. To accurately confirm previously identified glioma risk variants, and ascertain whether they are associated with risk or with prolonged survival, we investigated these variants in a set of pre-diagnostic serum samples (594 cases and 591 matched controls). Analyses of population based, pre-diagnostic samples eliminates the risk of survival bias, and enables distinction between genetic variants associated with glioma risk (i.e. aetiology) and genetic variants associated with prognosis. The serum samples were acquired through The Janus Serum Bank, a Norwegian population based biobank reserved for cancer research. Variant detection was achieved by means of cycling temperature capillary electrophoresis. Our investigation confirmed the association with glioma risk for the investigated variants within five genomic regions; 8q24.21 (CCDC26), 9p21.3 (CDKN2B-AS1), 11q23.3 (PHLDB1), 17p13.1 (TP53), and 20q13.33 (RTEL1). This is indicative of these variants being truly associated with glioma risk, and thus may impact gliomagenesis. However, previously identified risk variants within the 5p15.33 (TERT) and 7p11.2 (EGFR) could not be positively confirmed by this study. The lack of positive confirmation raises the question whether EGFR and TERT genetic variants are linked with prolonged survival, rather than with glioma aetiology.
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