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Sökning: WFRF:(Rack B) > (2013-2014)

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1.
  • Liang, Y., et al. (författare)
  • Mitigation of type-I ELMs with n=2 fields on JET with ITER-like wall
  • 2013
  • Ingår i: Nuclear Fusion. - : IOP Publishing. - 0029-5515 .- 1741-4326. ; 53:7, s. 073036-
  • Tidskriftsartikel (refereegranskat)abstract
    • Mitigation of type-I edge-localized modes (ELMs) was observed with the application of an n = 2 field in H-mode plasmas on the JET tokamak with the ITER-like wall (ILW). Several new findings with the ILW were identified and contrasted to the previous carbon wall (C-wall) results for comparable conditions. Previous results for high collisionality plasmas (nu*(e,ped) similar to 2.0) with the C-wall saw little or no influence of either n = 1 or n = 2 fields on the ELMs. However, recent observations with the ILW show large type-I ELMs with a frequency of similar to 45 Hz were replaced by high-frequency (similar to 200 Hz) small ELMs during the application of the n = 2 field. With the ILW, splitting of the outer strike point was observed for the first time during the strong mitigation of the type-I ELMs. The maximal surface temperature (T-max) on the outer divertor plate reached a stationary state and has only small variations of a few degrees due to the small mitigated ELMs. In moderate collisionality (nu*(e,ped) similar to 0.8) H-mode plasmas, similar to previous results with the C-wall, both an increase in the ELM frequency and density pump-out were observed during the application of the n = 2 field. There are two new observations compared with the C-wall results. Firstly, the effect of ELM mitigation with the n = 2 field was seen to saturate so that the ELM frequency did not further increase above a certain level of n = 2 magnetic perturbations. Secondly splitting of the outer strike point during the ELM crash was seen, resulting in mitigation of the maximal ELM peak heat fluxes on the divertor region.
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2.
  • Purrington, Kristen S., et al. (författare)
  • Genome-wide association study identifies 25 known breast cancer susceptibility loci as risk factors for triple-negative breast cancer
  • 2014
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 35:5, s. 1012-1019
  • Tidskriftsartikel (refereegranskat)abstract
    • In a genome-wide scan, we show that 30 variants in 25 genomic regions are associated with risk of TN breast cancer. Women carrying many of the risk variants may have 4-fold increased risk relative to women with few variants.Triple-negative (TN) breast cancer is an aggressive subtype of breast cancer associated with a unique set of epidemiologic and genetic risk factors. We conducted a two-stage genome-wide association study of TN breast cancer (stage 1: 1529 TN cases, 3399 controls; stage 2: 2148 cases, 1309 controls) to identify loci that influence TN breast cancer risk. Variants in the 19p13.1 and PTHLH loci showed genome-wide significant associations (P < 5 x 10(-) (8)) in stage 1 and 2 combined. Results also suggested a substantial enrichment of significantly associated variants among the single nucleotide polymorphisms (SNPs) analyzed in stage 2. Variants from 25 of 74 known breast cancer susceptibility loci were also associated with risk of TN breast cancer (P < 0.05). Associations with TN breast cancer were confirmed for 10 loci (LGR6, MDM4, CASP8, 2q35, 2p24.1, TERT-rs10069690, ESR1, TOX3, 19p13.1, RALY), and we identified associations with TN breast cancer for 15 additional breast cancer loci (P < 0.05: PEX14, 2q24.1, 2q31.1, ADAM29, EBF1, TCF7L2, 11q13.1, 11q24.3, 12p13.1, PTHLH, NTN4, 12q24, BRCA2, RAD51L1-rs2588809, MKL1). Further, two SNPs independent of previously reported signals in ESR1 [rs12525163 odds ratio (OR) = 1.15, P = 4.9 x 10(-) (4)] and 19p13.1 (rs1864112 OR = 0.84, P = 1.8 x 10(-) (9)) were associated with TN breast cancer. A polygenic risk score (PRS) for TN breast cancer based on known breast cancer risk variants showed a 4-fold difference in risk between the highest and lowest PRS quintiles (OR = 4.03, 95% confidence interval 3.46-4.70, P = 4.8 x 10(-) (69)). This translates to an absolute risk for TN breast cancer ranging from 0.8% to 3.4%, suggesting that genetic variation may be used for TN breast cancer risk prediction.
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