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- Okabayashi, M., et al.
(författare)
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Control of the resistive wall mode with internal coils in the DIII-D tokamak
- 2005
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Ingår i: Nuclear Fusion. - : IOP Publishing. - 1741-4326 .- 0029-5515. ; 45:12, s. 1715-1731
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Tidskriftsartikel (refereegranskat)abstract
- Internal coils, 'I-Coils', were installed inside the vacuum vessel of the DIII-D device to generate non-axisymmetric magnetic fields to act directly on the plasma. These fields are predicted to stabilize the resistive wall mode (RWM) branch of the long-wavelength external kink mode with plasma beta close to the ideal wall limit. Feedback using these I-Coils was found to be more effective as compared to using external coils located outside the vacuum vessel. Locating the coils inside the vessel allows for a faster response and the coil geometry also allows for better coupling to the helical mode structure. Initial results were reported previously (Strait E.J. et al 2004 Phys. Plasmas 11 2505). This paper reports on results from extended feedback stabilization operations, achieving plasma parameters up to the regime of Cβ ≈ 1.0 and open loop growth rates of γopenτw ≳ 25 where the RWM was predicted to be unstable with only the 'rotational viscous stabilization mechanism'. Here Cβ ≈ (β - βno-wall.limit)/(βideal.wall.limit - βno-wall.limit) is a measure of the beta relative to the stability limits without a wall and with a perfectly conducting wall, and τw is the resistive flux penetration time of the wall. These feedback experimental results clarified the processes of dynamic error field correction and direct RWM stabilization, both of which took place simultaneously during RWM feedback stabilization operation. MARS-F modelling provides a critical rotation velocity in reasonable agreement with the experiment and predicts that the growth rate increases rapidly as rotation decreases below the critical. The MARS-F code also predicted that for successful RWM magnetic feedback, the characteristic time of the power supply should be limited to a fraction of the growth time of the targeted RWM. The possibility of further improvements in the presently achievable range of operation of feedback gain values is also discussed.
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- McSherry, Elaine A., et al.
(författare)
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JAM-A expression positively correlates with poor prognosis in breast cancer patients
- 2009
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 125:6, s. 1343-1351
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Tidskriftsartikel (refereegranskat)abstract
- The cell-cell adhesion protein junctional adhesion molecule-A (JAM-A) influences; epithelial cell morphology and migration. As migration is required for tumor cell invasion and metastasis, we sought to elucidate the role of JAM-A in invasive breast cancer. A breast cancer tissue microarray was analyzed for JAM-A protein expression, in parallel with analysis of JAM-A gene expression data from a breast cancer clinical dataset. Our data demonstrate a novel association between JAM-A gene and protein upregulation and poor prognosis in breast cancer. To mechanistically dissect this process, we used lentiviral technology to stably knock down JAM-A gene expression by shRNA in MCF7 breast cancer cells, which express high-endogenous levels of JAM-A. We also antagonized JAM-A function in wild-type MCF7 cells using an inhibitory antibody that blocks JAM-A dimerization. Knockdown or functional antagonism of JAM-A decreased breast cancer cell migration in scratch-wound assays. Reductions in beta 1-integrin protein levels were observed after JAM-A-knockdown in MCF7 cells, suggesting a mechanism for reduced motility after loss of JAM-A. Consistent with this hypothesis, tissue microarray analysis of beta 1-integrin protein expression in invasive breast cancer tissues revealed a trend toward high beta 1-integrin protein levels being indicative of poor prognosis. Twenty-two percent of patients were observed to coexpress high levels of JAM-A and beta 1-integrin protein, and MDA-MB-231 breast cells stably overexpressing JAM-A showed an increase in beta 1-integrin protein expression. Our results are consistent with a previously unreported role for JAM-A overexpression as a possible mechanism contributing to progression in primary breast cancer; and a potential therapeutic target. (C) 2009 UICC
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- Nordin Fredrikson, Gunilla, et al.
(författare)
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Associations between autoantibodies against apolipoprotein B-100 peptides and vascular complications in patients with type 2 diabetes.
- 2009
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 52, s. 1426-1433
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Tidskriftsartikel (refereegranskat)abstract
- AIMS/HYPOTHESIS: Oxidation of LDL in the arterial extracellular matrix is a key event in the development of atherosclerosis and autoantibodies against oxidised LDL antigens reflect disease severity and the risk of developing acute cardiovascular events. Since type 2 diabetes is associated with increased oxidative stress, we tested the hypothesis that autoantibodies against oxidised LDL antigens are biomarkers for vascular complications in diabetes. METHODS: We studied 497 patients with type 2 diabetes without clinical signs of coronary heart disease. Oxidised LDL autoantibodies were determined by ELISA detecting IgG and IgM specific for native and malondialdehyde (MDA)-modified apolipoprotein B-100 peptides p45 and p210. The severity of coronary disease was assessed as the coronary artery calcium score. RESULTS: Patients affected by retinopathy had significantly higher levels of IgG against MDA-p45 and MDA-p210. In contrast, high levels of autoantibodies against the corresponding native peptides were associated with less coronary calcification and a lower risk of progression of coronary disease. CONCLUSIONS/INTERPRETATION: Our observations suggest that LDL oxidation is involved in the pathogenesis of diabetic retinopathy and that autoantibodies against apolipoprotein B peptides may act as biomarkers for both micro- and macrovascular complications in diabetes.
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