Scaling of spontaneous rotation with temperature and plasma current in tokamaks

Using theoretical arguments, a simple scaling law for the size of the intrinsic rotation observed in tokamaks in the absence of momentum injection is found: the velocity generated in the core of a tokamak must be proportional to the ion temperature difference in the core divided by the plasma current, independent of the size of the device. The constant of proportionality is of the order of $10\,\mathrm{km \cdot s^{-1} \cdot MA \cdot keV^{-1}}$. When the intrinsic rotation profile is hollow, i.e. it is counter-current in the core of the tokamak and co-current in the edge, the scaling law presented in this Letter fits the data remarkably well for several tokamaks of vastly different size and heated by different mechanisms.Comment: 5 pages, 3 figure

Ejecta Knot Flickering, Mass Ablation, and Fragmentation in Cassiopeia A

Ejecta knot flickering, ablation tails, and fragmentation are expected signatures associated with the gradual dissolution of high-velocity supernova (SN) ejecta caused by their passage through an inhomogeneous circumstellar medium or interstellar medium (ISM). Such phenomena mark the initial stages of the gradual merger of SN ejecta with and the enrichment of the surrounding ISM. Here we report on an investigation of this process through changes in the optical flux and morphology of several high-velocity ejecta knots located in the outskirts of the young core-collapse SN remnant Cassiopeia A using Hubble Space Telescope images. Examination of WFPC2 F675W and combined ACS F625W + F775W images taken between 1999 June and 2004 December of several dozen debris fragments in the remnant's northeast ejecta stream and along the remnant's eastern limb reveal substantial emission variations ("flickering") over timescales as short as nine months. Such widespread and rapid variability indicates knot scale lengths similar or equal to 10(15) cm and a highly inhomogeneous surrounding medium. We also identify a small percentage of ejecta knots located all around the remnant's outer periphery which show trailing emissions typically 0 ''.2-0 ''.7 in length aligned along the knot's direction of motion suggestive of knot ablation tails. We discuss the nature of these trailing emissions as they pertain to ablation cooling, knot disruption, and fragmentation, and draw comparisons to the emission "strings" seen in eta Car. Finally, we identify several tight clusters of small ejecta knots which resemble models of shock-induced fragmentation of larger SN ejecta knots caused by a high-velocity interaction with a lower density ambient medium

Role of AMPA Receptor Cycling in Synaptic Transmission and Plasticity

AbstractCompounds known to disrupt exocytosis or endocytosis were introduced into CA1 pyramidal cells while monitoring excitatory postsynaptic currents (EPSCs). Disrupting exocytosis or the interaction of GluR2 with NSF caused a gradual reduction in the AMPAR EPSC, while inhibition of endocytosis caused a gradual increase in the AMPAR EPSC. These manipulations had no effect on the NMDAR EPSC but prevented the subsequent induction of LTD. These results suggest that AMPARs, but not NMDARs, cycle into and out of the synaptic membrane at a rapid rate and that certain forms of synaptic plasticity may utilize this dynamic process

[S IV] in the NGC 5253 Supernebula: Ionized Gas Kinematics at High Resolution

The nearby dwarf starburst galaxy NGC 5253 hosts a deeply embedded radio-infrared supernebula excited by thousands of O stars. We have observed this source in the 10.5{\mu}m line of S+3 at 3.8 kms-1 spectral and 1.4" spatial resolution, using the high resolution spectrometer TEXES on the IRTF. The line profile cannot be fit well by a single Gaussian. The best simple fit describes the gas with two Gaussians, one near the galactic velocity with FWHM 33.6 km s-1 and another of similiar strength and FWHM 94 km s-1 centered \sim20 km s-1 to the blue. This suggests a model for the supernebula in which gas flows towards us out of the molecular cloud, as in a "blister" or "champagne flow" or in the HII regions modelled by Zhu (2006).Comment: Accepted for publication in the Astrophysical Journal 4 June 201

Deuterium Balmer/Stark spectroscopy and impurity profiles: first results from mirror-link divertor spectroscopy system on the JET ITER-like wall

For the ITER-like wall, the JET mirror link divertor spectroscopy system was redesigned to fully cover the tungsten horizontal strike plate with faster time resolution and improved near-UV performance. Since the ITER-like wall project involves a change in JET from a carbon dominated machine to a beryllium and tungsten dominated machine with residual carbon, the aim of the system is to provide the recycling flux, equivalent, to the impinging deuterium ion flux, the impurity fluxes (C, Be, O) and tungsten sputtering fluxes and hence give information on the tungsten divertor source. In order to do this self-consistently, the system also needs to provide plasma characterization through the deuterium Balmer spectra measurements of electron density and temperature during high density. L-Mode results at the density limit from Stark broadening/line ratio analysis will be presented and compared to Langmuir probe profiles and 2D-tomography of low-n Balmer emission [1]. Comparison with other diagnostics will be vital for modelling attempts with the EDGE2D-EIRENE code[2] as the best possible data sets need to be provided to study detachment behaviour.Comment: 18 pages, 11 figure

Subcellular localization of MC4R with ADCY3 at neuronal primary cilia underlies a common pathway for genetic predisposition to obesity.

Most monogenic cases of obesity in humans have been linked to mutations in genes encoding members of the leptin-melanocortin pathway. Specifically, mutations in MC4R, the melanocortin-4 receptor gene, account for 3-5% of all severe obesity cases in humans1-3. Recently, ADCY3 (adenylyl cyclase 3) gene mutations have been implicated in obesity4,5. ADCY3 localizes to the primary cilia of neurons 6 , organelles that function as hubs for select signaling pathways. Mutations that disrupt the functions of primary cilia cause ciliopathies, rare recessive pleiotropic diseases in which obesity is a cardinal manifestation 7 . We demonstrate that MC4R colocalizes with ADCY3 at the primary cilia of a subset of hypothalamic neurons, that obesity-associated MC4R mutations impair ciliary localization and that inhibition of adenylyl cyclase signaling at the primary cilia of these neurons increases body weight. These data suggest that impaired signaling from the primary cilia of MC4R neurons is a common pathway underlying genetic causes of obesity in humans