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- Chapman, I. T., et al.
(författare)
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The physics of sawtooth stabilization
- 2007
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Ingår i: Plasma Physics and Controlled Fusion. - 0741-3335 .- 1361-6587. ; 49:12B, s. B385-B394
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Tidskriftsartikel (refereegranskat)abstract
- Long period sawteeth have been observed to result in low-beta triggering of neo-classical tearing modes, which can significantly degrade plasma confinement. Consequently, a detailed physical understanding of sawtooth behaviour is critical, especially for ITER where fusion-born a particles are likely to lead to very long sawtooth periods. Many techniques have been developed to control, and in particular to destabilize the sawteeth. The application of counter-current neutral beam injection (NBI) in JET has resulted in shorter sawtooth periods than in Ohmic plasmas. This result has been explained because, firstly, the counter-passing fast ions give a destabilizing contribution to the n=1 internal kink mode-which is accepted to be related to sawtooth oscillations-and secondly, the flow shear strongly influences the stabilizing trapped particles. A similar experimental result has been observed in counter-NBI heated plasmas in MAST. However, the strong toroidal flows in spherical tokamaks mean that the sawtooth behaviour is determined by the gyroscopic flow stabilization of the kink mode rather than kinetic effects. In NBI heated plasmas in smaller conventional aspect-ratio tokamaks, such as TEXTOR, the flow and kinetic effects compete to give different sawtooth behaviour. Other techniques applied to destabilize sawteeth are the application of electron cyclotron current drive (ECCD) or ion cyclotron resonance heating (ICRH). In JET, it has been observed that localized ICRH is able to destabilize sawteeth which were otherwise stabilized by a co-existing population of energetic trapped ions in the core. This is explained through the dual role of the ICRH in reducing the critical magnetic shear required to trigger a sawtooth crash, and the increase in the local magnetic shear which results from driving current near the q=1 rational surface. Sawtooth control in ITER could be provided by a combination of ECCD and co-passing off-axis negative-NBI fast ions.
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| 2. |
- Talmud, Philippa J., et al.
(författare)
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Gene-centric Association Signals for Lipids and Apolipoproteins Identified via the HumanCVD BeadChip
- 2009
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Ingår i: American Journal of Human Genetics. - : Elsevier BV. - 0002-9297. ; 85:5, s. 628-642
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Tidskriftsartikel (refereegranskat)abstract
- Blood lipids are important cardiovascular disease (CVD) risk factors with both genetic and environmental determinants. The Whitehall II study (n = 5592) was genotyped with the gene-centric HumanCVD BeadChip (Illumina). We identified 195 SNPs in 16 genes/regions associated with 3 major lipid fractions and 2 apolipoprotein components at p < 10(-5), with the associations being broadly concordant with prior genome-wide analysis. SNPs associated with LDL cholesterol and apolipoprotein B were located in LDLR, PCSK9, APOB, CELSR2, HWGCR, CETP, the TOMM40-APOE-C1-C2-C4 cluster, and the APOA5-A4-C3-A1 cluster; SNPs associated with HDL cholesterol and apolipoprotein AI were in CETP, LPL, LIPC, APOA5-A4-C3-A1, and ABCA1; and SNPs associated with triglycerides in GCKR, BAZIB, MLXIPL, LPL, and APOA5-A4-C3-A1. For 48 SNPs in previously unreported loci that were significant at p < 10(-4) in Whitehall II, in silico analysis including the British Women's Heart and Health Study, BRIGHT, ASCOT, and NORDIL studies (total n > 12,500) revealed previously unreported associations of SH2B3 (p < 2.2 x 10(-6)), BMPR2 (p < 2.3 x 10(-7)), BCL3/PVRL2 (flanking APOE; p < 4.4 x 10(-8)), and SMARCA4 (flanking LDLR; p < 2.5 x 10(-7)) with LDL cholesterol. Common alleles in these genes explained 6.1%-14.7% of the variance in the five lipid-related traits, and individuals at opposite tails of the additive allele score exhibited substantial differences in trait levels (e.g., > 1 mmol/L in LDL cholesterol [similar to 1 SD of the trait distribution]). These data suggest that multiple common alleles of small effect can make important contributions to individual differences in blood lipids potentially relevant to the assessment of CVD risk. These genes provide further insights into lipid metabolism and the likely effects of modifying the encoded targets therapeutically.
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