| 1. |
- Pospieszczyk, A., et al.
(författare)
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B4C-limiter experiments at TEXTOR
- 2003
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Ingår i: Journal of Nuclear Materials. - 0022-3115 .- 1873-4820. ; 313, s. 223-229
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Tidskriftsartikel (refereegranskat)abstract
- In the TEXTOR tokamak the five top and five bottom poloidal carbon limiter blocks have been replaced by inertially cooled copper blocks coated with a 170 mum VPS-B4C layer. Similar limiter blocks have been inserted through lock systems, extensively diagnosed in situ as well as ex situ. During the thermal load by the plasma, the surface temperature rose and decayed extremely fast which can be explained by a different thermal conductivity and heat capacity of the coating. For heat loads below 8 MW m(-2) no severe cracking or delamination of the B4C-coating were observed. Due to the insulating behaviour of the layer, distinct craters developed on both limiter types, which reached down to the copper surface and are assumed to be caused by electrical arcs. An oscillation of the evolution of the surface temperature has been observed under certain conditions, which is clearly correlated to the use of the coated test limiter. Particle fluxes as well as hydrogen inventory turned out to be very similar to those from a low-Z surface in a carbon surrounding. No significant impact of the plasma on the coating and vice versa was observed.
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| 2. |
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| 3. |
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| 4. |
- Laux, M., et al.
(författare)
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Arcing at B4C-covered limiters exposed to a SOL-plasma
- 2003
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Ingår i: Journal of Nuclear Materials. - 0022-3115 .- 1873-4820. ; 313, s. 62-66
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Tidskriftsartikel (refereegranskat)abstract
- Plasma sprayed B4C-layers considered as wall coatings for the W7X stellarator have been studied during and after exposure to TEXTOR and after arcing experiments in vacuum. Arcing through the B4C layer occurred favoured by high power fluxes and not restricted to less stable phases. But this arcing implies an especially noisy scrape-off layer (SOL). Instead of moving retrograde in the external magnetic field, the arc spot on the B4C-layer sticks to the same location for its whole lifetime. Consequently, the arc erodes the entire B4C layer, finally burning down to the Cu substrate. In the neighbourhood of craters the surface contains Cu originating from those craters. This material, hauled to the surface by the arc, is subject to subsequent erosion, transport, and redeposition by the SOL-plasma. The behaviour of arcs on B4C is Most probably caused by the peculiar temperature dependences of the electrical and heat conductivity of B4C.
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| 5. |
- Carlsson, Lena E, et al.
(författare)
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Platelet receptor and clotting factor polymorphisms as genetic risk factors for thromboembolic complications in heparin-induced thrombocytopenia.
- 2003
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Ingår i: Pharmacogenetics. - 0960-314X .- 1473-561X. ; 13:5, s. 253-8
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Tidskriftsartikel (refereegranskat)abstract
- Heparin-induced thrombocytopenia (HIT) is an immune mediated adverse reaction to heparin treatment often associated with limb- and/or life-threatening thromboembolic complications (TECs). Presently, no prognostic marker has been identified that allows differentiation between mildly (isolated thrombocytopenia) and severely (TECs) affected patients. This study assesses the impact of platelet glycoprotein- and clotting factor polymorphisms in HIT-patients with isolated thrombocytopenia compared to HIT-patients with TECs. Sixty-three HIT-patients with isolated thrombocytopenia and 79 HIT-patients with HIT-related TECs were genotyped for GPIIb-IIIa polymorphisms (HPA-1, HPA-3), GPIa-IIa polymorphisms (HPA-5, GPIaC807T), GPIb-IX-V polymorphisms (HPA-2, Kozak-5, VNTR), and clotting factor polymorphisms (FV-Leiden R506Q, prothrombin PT-G20210A and MTHFR C677T). Women more often presented with TECs than men (P = 0.04). No differences in genotype frequencies could be seen on comparing HIT-patients with and without TECs. Analysing men and women separately, the C allele of the Kozak polymorphism was overrepresented in men who developed TECs (P = 0.034). The enhanced risk of women to develop HIT-associated TECs remains unexplained but it is potentially important in view of recent data on sex-hormone related changes of haemostasis. There was no correlation between platelet glycoprotein- and clotting factor polymorphisms and the risk to develop HIT-associated TECs. An association between the development of TECs and the Kozak-5C allele could be seen among male patients. However, this would need to be assessed in further larger studies. Most likely, the high levels of thrombin generation during acute HIT are so procoagulant that less pronounced risk factors such as polymorphisms are overshadowed.
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| 6. |
- Engstrand, Mats, et al.
(författare)
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Cellular responses to cytomegalovirus in immunosuppressed patients : circulating CD8+ T cells recognizing CMVpp65 are present but display functional impairment
- 2003
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Ingår i: Clinical and Experimental Immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 132:1, s. 96-104
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Tidskriftsartikel (refereegranskat)abstract
- The availability of tetrameric complexes of HLA class I molecules folded with immunodominant peptides makes it possible to utilize flow cytometry for rapid and highly specific visualization of virus specific CD8+ T cells. An alternate technique is to incubate whole blood with specific antigens and to subsequently detect and characterize responding T cells (e.g. by performing intracellular staining of interferon-gamma). By using an HLA-A2 tetramer construct folded with the same immunodominant CMV-peptide as that used for peptide pulsing, we monitored both the presence and functional capacity of CMV-specific CD8+ T cells. In addition T cell activation was assayed by determination of CD38 and CD69 expression. Twelve organ transplant patients and 31 healthy blood donors with latent CMV infection were investigated using CMV pp65 tetramer staining and intracellular staining of interferon-gamma after CMV pp65 peptide pulsing or CMV lysate pulsing. CMV-specific T cells were detected in similar absolute numbers as well as frequencies of T cells in the two groups investigated. However, the CMV-specific CD8+ T cells in immunosuppressed individuals showed a decreased functional response to the CMV-peptide, as evidenced by reduced interferon-gamma production when compared to healthy blood donors (19%; 42%, P < 0·005). In addition, CD38 expression was markedly higher in immunosuppressed patients compared to healthy blood donors (24%; 6%, P < 0·005). In a case report we demonstrate that reactivation of CMV can occur in an immunosuppressed patient with high number of CMV-specific T cells, but without functional capacity. Hence, these findings reflect impaired activation of cytotoxic T cells controlling latent CMV infection in immunosuppressed patients.
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| 7. |
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| 8. |
- Vink, M, et al.
(författare)
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Regulation of Photosystem II core protein phosphorylation at the substrate level : Light induces exposure of the CP43 chlorophyll a protein complex to thylakoid protein kinase(s)
- 2000
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Ingår i: Photosynthesis Research. - 0166-8595 .- 1573-5079. ; 64:2-3, s. 209-219
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Tidskriftsartikel (refereegranskat)abstract
- Light induces conformational changes in the CP43 chl-a-protein antenna complex in isolated PS II core-complexes exposing phosphorylation site(s) to PS II core-associated protein kinase(s), to added solubilized thylakoid protein kinase(s), as well as to tryptic cleavage. The substrate-activation effect is demonstrated by exposure of the PS II cores to light during the kinase assay as well as by preillumination of the PS II cores in which the endogenous kinase(s) has been inactivated by treatment with N-ethylmaleimid. In the latter case, phosphorylation was performed in darkness following addition of the solubilized protein kinase(s). The solubilized protein kinase(s) does not require light activation. The apparent molecular masses of the main protein kinase(s) associated with the PS II cores (about 31-35 kDa and 45 kDa) differ from that of the major protein kinase present in solubilized preparations obtained from spinach thylakoids (64 kDa). The light-induced exposure of CP43 increases with the light intensity in the range of 20-100 mu mol photons m(-2) s(-1) as demonstrated by preillumination of N-ethylmaleimid treated cores followed by addition of the solubilized protein kinase(s) and performing the phosphorylation assay in darkness.
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| 9. |
- Zer, H., et al.
(författare)
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Light affects the accessibility of the thylakoid light harvesting complex II (LHCII) phosphorylation site to the membrane protein kinase(s)
- 2003
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Ingår i: Biochemistry. - : American Chemical Society (ACS). - 0006-2960 .- 1520-4995. ; 42:3, s. 728-738
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Tidskriftsartikel (refereegranskat)abstract
- Redox-controlled, reversible phosphorylation of the thylakoid light harvesting complex II (LHCII) regulates its association with photosystems (PS) I or II and thus, energy distribution between the two photosystems (state transition). Illumination of solubilized LHCII enhances exposure of the phosphorylation site at its N-terminal domain to protein kinase(s) and tryptic cleavage in vitro [Zer et al. (1999) Proc. Natl. Acad. Sci. U.S.A. 96, 8277-8282]. Here we report that short illumination (5-10 min, 15-30, µmol m-2 s-1) enhances the accessibility of LHCII phosphorylation site to kinase(s) activity also in isolated thylakoids. However, prolonged illumination or higher light intensities (30 min, 80-800 µmol m-2 s-1) prevent phosphorylation of LHCII in the isolated membranes as well as in vivo, although redox-dependent protein kinase activity persists in the illuminated thylakoids toward exogenous solubilized LHCII. This phenomenon, ascribed to light-induced inaccessibility of the phosphorylation site to the protein kinase(s), affects in a similar way the accessibility of thylakoid LHCII N-terminal domain to tryptic cleavage. The illumination effect is not redox related, decreases linearly with temperature from 25 to 5°C and may be ascribed to light-induced conformational changes in the complex causing lateral aggregation of dephosphorylated LHCII bound to and/or dissociated from PSII. The later state occurs under conditions allowing turnover of the phospho-LHCII phosphate. The light-induced inaccessibility of LHCII to the membrane-bound protein kinase reverses readily in darkness only if induced under LHCII-phosphate turnover conditions. Thus, phosphorylation prevents irreversible light-induced conformational changes in LHCII allowing lateral migration of the complex and the related state transition process.
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