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Voltage holding capability of a 500 kV, 22 A three-stage electrostatic accelerator, where large- area grids of 0.28 [m.sup.2] and large fiberglass reinforced plastic (FRP) insulators of 1.8 m in diameter are used, was examined. High voltage was independently applied to each acceleration stage, where the voltage holding capabilities of 130 kV were obtained. To identify whether the breakdowns occur in the gaps between the grids or the FRP insulators, high voltages were applied to the accelerator with and without the grids. Breakdown voltages without grids, i.e., the FRP insulator itself reached 170 kV of design value for each stage. These results show that the breakdown voltage of the accelerator was mainly determined by the gaps between the large-area grids. In this paper, the influence of non-uniform electric field and multi-stage grids on the voltage holding capabilities was also discussed. Index Terms--Electrodes, electrostatic accelerator, ion source, vacuum breakdown.

The JT-60 Super Advanced (JT-60SA) tokamak aims to perform the ITER support and to demonstrate steady-state high-beta plasma project with the collaboration between Japan and EU. To attain these objectives, the negative-ion-based NBI (N-NBI) system is required to inject 10 MW for 100 s at the beam energy of 500 keV. On JT-60U, the present N-NBI ion source has injected 3.2 MW for 21 s at 320 keV; however, three key issues should be solved for the JT-60SA N-NBI ion source. One is to improve the voltage holding capability of the large negative ion source, where the available acceleration voltage has been limited to less than ~400 kV due to breakdowns. The accelerator of the JT-60U ion source is composed of large three-stage grids and three fiberglass reinforced plastic (FRP) insulators. Recent R&D tests suggested that the FRP insulators were not the main factor to trigger the breakdowns at the early conditioning stage. The accelerator with a large area of grids and their supporting structure may need a high margin in the design of electric field and a long time for conditioning. The second issue is to reduce the power loading of the acceleration grids. It was found that some beamlets were strongly deflected due to beamlet-beamlet interaction and strike on the grounded grid in the accelerator. Moreover, the electrons generated in the accelerator caused the grid loading and the overheating of the beamline components. The acceleration grids for JT-60SA are to be designed by taking account of the beamlet-beamlet interaction and the applied magnetic field in 3-D simulation. Third is to maintain the D- production for 100 s. Although a constant D- beam power was confirmed on JT-60U for 21 s, an active cooling system is required to keep the temperature of the plasma grid (PG) under optimum condition during 100-s operation. A simple cooling structure is proposed for the active cooled PG, where a key is the temperature gradient on the PG for uniform D- production. In the present schedule, design work, reflecting the latest R&D progress, will continue until ~2011. The modified N-NBI ion source will start on JT-60SA in 2015. Index Terms--Beam optics, injection power, JT-60 Super Advanced (JT-60SA), negative ion beam, negative-ion-based NBI (N-NBI), neutral beam, voltage holding capability.

The power loading of electrons ejected from the negative ion accelerator to the beamline was first measured in the negative-ion-based neutral beam injector on JT-60U. At 0.3 Pa of the operating pressure in the arc chamber, the heat flux and the total power load for the single segment were ~8 W/[cm.sup.2] and 27 kW for the D- ion beam of 300 keV and 3.4 A, respectively. The normalized total power loading on the electron dump was no more than 2.6% of the electric power in the acceleration power supply. About 70% of the total power is originated by the electrons stripped from D- ions due to collisions with residual gas molecules in the accelerator. The calculation of the stripped electron trajectories shows that the electrons stripped in the second acceleration gap are the main origin of the power loading in the beamline. Index Terms--Electrons, JT-60U, negative ion sources, stripping losses.

Voltage holding capability in a 500 keV electrostatic accelerator with large FRP insulators was examined without the beam acceleration. When high voltage was applied, the light with a broad peak at a wavelength of 420 nm was mostly emitted inside the accelerator even though breakdown did not occur. The voltage holding capability has a strong correlation with the light intensity. Stable voltage holding was realized under the conditions in which light emission was well suppressed. Index Terms--Insulators, ion sources, lightning, large-scale systems.

The core fucosylation ([alpha]1,6-fucosylation) of glycoproteins is widely distributed in mammalian tissues, and is altered under pathological conditions. To investigate physiological functions of the core fucose, we generated [alpha]1,6-fucosyltransferase (Fut8)-null mice and found that disruption of Fut8 induces severe growth retardation and death during postnatal development. Histopathological analysis revealed that [Fut8.sup.-/-] mice showed emphysema-like changes in the lung, verified by a physiological compliance analysis. Biochemical studies indicated that lungs from [Fut.sup.8-/-] mice exhibit a marked overexpression of matrix metalloproteinases (MMPs), such as MMP-12 and MMP-13, highly associated with lung-destructive phenotypes, and a down-regulation of extracellular matrix (ECM) proteins such as elastin, as well as retarded alveolar epithelia cell differentiation. These changes should be consistent with a deficiency in TGF-[beta]1 signaling, a pleiotropic factor that controls ECM homeostasis by down-regulating MMP expression and inducing ECM protein components. In fact, [Fut8.sup.-/-] mice have a marked dysregulation of TGF-[beta]1 receptor activation and signaling, as assessed by TGF-[beta]1 binding assays and Smad2 phosphorylation analysis. We also show that these TGF-[beta]1 receptor defects found in [Fut8.sup.-/-] cells can be rescued by reintroducing Fut8 into [Fut8.sup.-l-] cells. Furthermore, exogenous TGF-[beta]1 potentially rescued emphysema-like phenotype and concomitantly reduced MMP expression in [Fut8.sup.-/-] lung. We propose that the lack of core fucosylation of TGF-[beta]1 receptors is crucial for a developmental and progressive/ destructive emphysema, suggesting that perturbation of this function could underlie certain cases of human emphysema. fucosylation | glycobiology | matrix metalloproteinase