Simulating Divertor Detachment of Ohmic Discharges in ASDEX Upgrade Using SOLPS: the Role of Carbon

With divertor detachment being a prerequisite for burning plasma operation in ITER, numerical codes such as SOLPS [1] have been developed for predicting and interpreting the divertor performance at all operational regimes in current tokamaks and ITER. In ITER complete detachment from the outer divertor target is not permitted as this might result in an X-point MARFE, imposing an upper limit for the upstream separatrix density, n{sub e}{sup sep}. Despite the knowledge of the basic mechanisms required for achieving detachment, such as radiative power exhaust, volumetric momentum and charge removal [1], a quantitative evaluation of experimentally observed detached regimes proves to be particularly difficult for several tokamaks. In particular the strong asymmetry of the ion flux density between the inner, {Lambda}{sub it}, and the outer target {Lambda}{sub ot} with increasing line averaged density, {bar n}{sub e}, and in particular ''vanishing'' of the ion flux, defined as full/complete detachment, at the inner target cannot be reproduced. It is unclear how this is related to divertor target plates or other plasma facing components containing carbon. As part of a combined effort at various experimental devices this paper contributes to the validation of the SOLPS code against experimental data from ASDEX Upgrade, AUG, at the onset of divertor detachment. In the framework established under the International Tokamak Physics Activity (ITPA) Divertor and SOL working group a series of ohmic discharges have been performed in AUG, which had as similar as possible plasma parameters as companion discharges undertaken in DIII-D [2]. The effect of activating drift terms, the influence of the chemical sputtering yield at the inner target and in addition to [3] the role of impurity influx from the inner heat shield are analyzed

Scrape Off Layer (SOL) transport and filamentary characteristics in high density tokamak regimes

A detailed cross-device investigation on the role of filamentary dynamics in high density regimes has been performed within the EUROfusion framework comparing ASDEX Upgrade (AUG) and TCV tokamaks. Both devices have run density ramp experiments at different levels of plasma current, keeping toroidal field or q95 constant in order to disentangle the role of parallel connection length and the current. During the scan at constant toroidal field, in both devices SOL profiles tend to develop a clear Scrape Off Layer (SOL) density shoulder at lower edge density whenever current is reduced. The different current behavior is substantially reconciled in terms of edge density normalized to Greenwald fraction. During the scan at constant q95 AUG exhibits a similar behaviour whereas in TCV no signature of upstream profile modification has been observed at lower level of currents. The latter behaviour has been ascribed to the lack of target density roll-over. The relation between upstream density profile modification and detachment condition has been investigated. For both devices the relation between blob-size and SOL density e-folding length is found independent of the plasma current, with a clear increase of blob-size with edge density normalized to Greenwald fraction observed. ASDEX Upgrade has also explored the filamentary behaviour in H-Mode. The experiments on AUG focused on the role of neutrals, performing discharges with and without the cryogenic pumps, highlighting how large neutral pressure not only in the divertor but at the midplane is needed in order to develop a H-Mode SOL profile shoulder in AUG

Blocking TLR2 in vivo protects against accumulation of inflammatory cells and neuronal injury in experimental stroke.

Reduced infarct volume in TLR2-knockout mice compared with C57Bl/6 wild-type mice has recently been shown in experimental stroke and confirmed in this study. We now also show a significant decrease of CD11b-positive cell counts and decreased neuronal death in the ischemic hemispheres of TLR2-deficient mice compared with C57Bl/6wt mice 2 days after transient focal cerebral ischemia. To examine the potential benefit of intravascular TLR2 inhibition, C57Bl/6wt mice were treated intraarterially with TLR2-blocking anti-TLR2 antibody (clone T2.5) after 45 minutes of cerebral ischemia and compared with control antibody (isotype) treated wild-type mice. Whereas T2.5-treated mice had no reduction in infarct volumes at 48 hours after reperfusion, they did have decreased numbers of CD11b-positive inflammatory cells and decreased neuronal death compared with isotype-treated control mice. Comparison of the isotype antibody treatment to control (saline) treatment showed no effects on infarct volumes or neuronal survival. However, mice treated with the control isotype antibody had increased numbers of CD11b-positive inflammatory cells compared with saline-treated animals. Thus, antibody treatment itself (i.e., control isotype antibody, but potentially of any antibody) may have adverse effects and limit therapeutic benefit of anti-TLR2-antibody therapy. We conclude that TLR2 mediates leukocyte and microglial infiltration and neuronal death, which can be attenuated by TLR2 inhibition. The TLR2 inhibition in vivo improves neuronal survival and may represent a future stroke therapy.Journal of Cerebral Blood Flow & Metabolism advance online publication, 15 September 2010; doi:10.1038/jcbfm.2010.161

Investigation on the reproducibility of optical constants of TiO2, SiO2, and Al2O3 films, prepared by plasma ion assisted deposition

Titanium dioxide, aluminum oxide, and silicon dioxide layers have been prepared by plasma ion assisted electron beam evaporation employing the Advanced Plasma Source (APS). The refractive indices have been determined by spectrophotometry in order to quantify their reproducibility. Standard deviations in the refractive index turned out to be highest for titanium dioxide, and lowest for silicon dioxide. The refractive index reproducibility of titanium dioxide could be improved by replacing the commonly used BIAS voltage control concept by a novel alternative approach concerning ion beam power, termed J(E). All these findings are discussed in terms of a model that considers the real oxide film as a binary mixture of a solid fraction with a small amount of pores, within the limits provided by the Wiener bounds

Blocking TLR2 in vivo protects against accumulation of inflammatory cells and neuronal injury in experimental stroke

Reduced infarct volume in TLR2-knockout mice compared with C57Bl/6 wild-type mice has recently been shown in experimental stroke and confirmed in this study. We now also show a significant decrease of CD11b-positive cell counts and decreased neuronal death in the ischemic hemispheres of TLR2-deficient mice compared with C57Bl/6wt mice 2 days after transient focal cerebral ischemia. To examine the potential benefit of intravascular TLR2 inhibition, C57Bl/6wt mice were treated intraarterially with TLR2-blocking anti-TLR2 antibody (clone T2.5) after 45 minutes of cerebral ischemia and compared with control antibody (isotype) treated wild-type mice. Whereas T2.5-treated mice had no reduction in infarct volumes at 48 hours after reperfusion, they did have decreased numbers of CD11b-positive inflammatory cells and decreased neuronal death compared with isotype-treated control mice. Comparison of the isotype antibody treatment to control (saline) treatment showed no effects on infarct volumes or neuronal survival. However, mice treated with the control isotype antibody had increased numbers of CD11b-positive inflammatory cells compared with saline-treated animals. Thus, antibody treatment itself (i.e., control isotype antibody, but potentially of any antibody) may have adverse effects and limit therapeutic benefit of anti-TLR2-antibody therapy. We conclude that TLR2 mediates leukocyte and microglial infiltration and neuronal death, which can be attenuated by TLR2 inhibition. The TLR2 inhibition in vivo improves neuronal survival and may represent a future stroke therapy