First Direct Observation of Runaway-Electron-Driven Whistler Waves in Tokamaks.

DIII-D experiments at low density (n_{e}∼10^{19} m^{-3}) have directly measured whistler waves in the 100-200 MHz range excited by multi-MeV runaway electrons. Whistler activity is correlated with runaway intensity (hard x-ray emission level), occurs in novel discrete frequency bands, and exhibits nonlinear limit-cycle-like behavior. The measured frequencies scale with the magnetic field strength and electron density as expected from the whistler dispersion relation. The modes are stabilized with increasing magnetic field, which is consistent with wave-particle resonance mechanisms. The mode amplitudes show intermittent time variations correlated with changes in the electron cyclotron emission that follow predator-prey cycles. These can be interpreted as wave-induced pitch angle scattering of moderate energy runaways. The tokamak runaway-whistler mechanisms have parallels to whistler phenomena in ionospheric plasmas. The observations also open new directions for the modeling and active control of runaway electrons in tokamaks.

Spatiotemporal Evolution of Runaway Electron Momentum Distributions in Tokamaks.

Novel spatial, temporal, and energetically resolved measurements of bremsstrahlung hard-x-ray (HXR) emission from runaway electron (RE) populations in tokamaks reveal nonmonotonic RE distribution functions whose properties depend on the interplay of electric field acceleration with collisional and synchrotron damping. Measurements are consistent with theoretical predictions of momentum-space attractors that accumulate runaway electrons. RE distribution functions are measured to shift to a higher energy when the synchrotron force is reduced by decreasing the toroidal magnetic field strength. Increasing the collisional damping by increasing the electron density (at a fixed magnetic and electric field) reduces the energy of the nonmonotonic feature and reduces the HXR growth rate at all energies. Higher-energy HXR growth rates extrapolate to zero at the expected threshold electric field for RE sustainment, while low-energy REs are anomalously lost. The compilation of HXR emission from different sight lines into the plasma yields energy and pitch-angle-resolved RE distributions and demonstrates increasing pitch-angle and radial gradients with energy.

Kinetic effects of energetic particles on resistive MHD stability.

We show that the kinetic effects of energetic particles can play a crucial role in the stability of the m/n=2/1 tearing mode in tokamaks (e.g., JET, JT-60U, and DIII-D), where the fraction of energetic particle beta(frac) is high. Using model equilibria based on DIII-D experimental reconstructions, the nonideal MHD linear stability of cases unstable to the 2/1 mode is investigated including a deltaf particle-in-cell model for the energetic particles coupled to the nonlinear 3D resistive MHD code NIMROD [C. C. Kim et al., Phys. Plasmas 15, 072507 (2008)10.1063/1.2949704]. It is observed that energetic particles have significant damping and stabilizing effects at experimentally relevant beta, beta(frac), and S, and excite a real frequency of the 2/1 mode. Extrapolation of the results is discussed for implications to JET and ITER, where the effects are projected to be significant.

rHox: a homeobox gene expressed in osteoblastic cells.

Homeodomain proteins are characterized by a conserved domain with a helix-turn-helix motif. These proteins act as regulatory factors in tissue differentiation and proliferation. However, their role in the regulation of osteoblast differentiation is unknown. In this study we have identified and characterized a homeobox gene in osteoblast-like cells. This gene, termed rHox, was isolated from a cDNA library derived from rat osteoblast-like cells. The nucleotide sequence of the 1,375 base pair (bp) cDNA contains a noncoding leader sequence of 329 bp, a 735 bp open reading frame, and 312 bp of 3' noncoding sequence. Sequence comparison demonstrates that rHox is identical to the mouse Pmx gene (also called MHox) at the amino acid level and 90% homologous at the nucleotide level. Both Southwestern blotting and gel shift analyses indicate that rHox has potential to bind both the collagen I alpha 1 and the osteocalcin promoters. Transfection experiments using an rHox expression vector showed a strong repression of target promoter activity, regardless of whether the target promoters contained homeodomain binding response elements. These data suggest that rHox is a potent negative regulator of gene expression, although the specific role of rHox in bone gene regulation remains to be determined.

Downregulation of parathyroid hormone receptors in renal membranes from aged rats.

The mechanism of the inhibition or blunting of parathyroid hormone (PTH)-stimulated Na(+)-Ca2+ exchange activity in renal cortical cells from aged rats was examined. The number of PTH binding sites in basolateral membranes prepared from adult (6 mo) and old (24 mo) rats was quantitated by the binding of the synthetic analogue 125I-labeled [Nle8,18, Tyr34]bPTH-(1-34) amide to the membrane. The maximum number of specific PTH binding sites, Bmax, was 92.7 +/- 9.3 and 36.7 +/- 6.1 fmol/mg protein, respectively, in membranes prepared from adult and old rats. The affinity of the receptor to PTH was unaffected with age. The level of PTH binding components (68 and 70 kDa) estimated by a ligand affinity blot technique using biotinylated bPTH-(1-34) as the ligand was similarly reduced in membranes isolated from senescent rats. To test the hypothesis that change in the number of PTH binding sites and level of PTH binding components represented an adaptive response to a high serum PTH level, rats were parathyroidectomized (PTX) and the changes were reexamined. Decreases in the number of PTH binding sites and PTH binding components were either partially or completely negated by the surgery. These findings suggest that the blunting of both the PTH-stimulated Na(+)-Ca2+ exchange and adenylate cyclase activities in the kidneys of aged rats was due, in part, to be loss of PTH receptors in basolateral membranes and that this defect could be partially reversed by removal of the parathyroid gland.

Characterization of soluble and particulate parathyroid hormone receptors using a biotinylated bioactive hormone analog.

A bioactive biotin-containing derivative of the synthetic bovine parathyroid hormone analog [Nle8,Nle18,Tyr34]bovine parathyroid hormone-(1-34) (bPTH-(1-34] amide was prepared by reacting the peptide with N-biotinyl-epsilon-aminocaproic acid N-hydroxysuccinimide ester. The derivative was incubated with particulate renal plasma membranes or with detergent [3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate) extracts of renal cortical membranes, and two membrane components were identified. Labeling of these components was competitively inhibited by underivatized bPTH-(1-34) or bPTH-(3-34) but not by insulin, adrenocorticotropin, or oxidized rat PTH-(1-34). PTH-binding components that were immobilized on nitrocellulose could be detected by incubating the membrane with biotinyl-bPTH-(1-34). Binding components of apparent molecular mass 68, 70, and 150 kDa were specifically labeled in plasma membranes derived from canine, human, and porcine renal cortex, rat liver, and human fibroblasts. The 68-kDa binding protein was found to be consistently more acidic than the 70-kDa binding protein in human, porcine, and canine renal membranes analyzed by two-dimensional electrophoresis. The 68-70-kDa receptor doublet could be specifically isolated by streptavidin-agarose chromatography of solubilized membrane extracts that had first been incubated with biotinyl-BPTH-(1-34). Biotinyl-bPTH-(1-34) should be useful as a tool for further characterization and purification of the PTH receptor.