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

Discrimination between FRET and non-FRET quenching in a photochromic CdSe quantum dot/dithienylethene dye system

A photochromic Förster resonance energy transfer (FRET) system was employed to disentangle the fluorescence quenching mechanisms in quantum dot/photochromic dye hybrids. In the off-state of the dye the main quenching mechanism is FRET whereas the moderate quenching in the on-state is due to non-FRET pathways opened up upon assembly

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

Effect of toroidal field ripple on plasma rotation in JET

Dedicated experiments on TF ripple effects on the performance of tokamak plasmas have been carried out at JET. The TF ripple was found to have a profound effect on the plasma rotation. The central Mach number, M, defined as the ratio of the rotation velocity and the thermal velocity, was found to drop as a function of TF ripple amplitude (3) from an average value of M = 0.40-0.55 for operations at the standard JET ripple of 6 = 0.08% to M = 0.25-0.40 for 6 = 0.5% and M = 0.1-0.3 for delta = 1%. TF ripple effects should be considered when estimating the plasma rotation in ITER. With standard co-current injection of neutral beam injection (NBI), plasmas were found to rotate in the co-current direction. However, for higher TF ripple amplitudes (delta similar to 1%) an area of counter rotation developed at the edge of the plasma, while the core kept its co-rotation. The edge counter rotation was found to depend, besides on the TF ripple amplitude, on the edge temperature. The observed reduction of toroidal plasma rotation with increasing TF ripple could partly be explained by TF ripple induced losses of energetic ions, injected by NBI. However, the calculated torque due to these losses was insufficient to explain the observed counter rotation and its scaling with edge parameters. It is suggested that additional TF ripple induced losses of thermal ions contribute to this effect

Occurrence of testicular microlithiasis in androgen insensitive hypogonadal mice

<b>Background</b>: Testicular microliths are calcifications found within the seminiferous tubules. In humans, testicular microlithiasis (TM) has an unknown etiology but may be significantly associated with testicular germ cell tumors. Factors inducing microlith development may also, therefore, act as susceptibility factors for malignant testicular conditions. Studies to identify the mechanisms of microlith development have been hampered by the lack of suitable animal models for TM.<BR/> <b>Methods</b>: This was an observational study of the testicular phenotype of different mouse models. The mouse models were: cryptorchid mice, mice lacking androgen receptors (ARs) on the Sertoli cells (SCARKO), mice with a ubiquitous loss of androgen ARs (ARKO), hypogonadal (hpg) mice which lack circulating gonadotrophins, and hpg mice crossed with SCARKO (hpg.SCARKO) and ARKO (hpg.ARKO) mice.<BR/> <b>Results</b>: Microscopic TM was seen in 94% of hpg.ARKO mice (n=16) and the mean number of microliths per testis was 81 +/- 54. Occasional small microliths were seen in 36% (n=11) of hpg testes (mean 2 +/- 0.5 per testis) and 30% (n=10) of hpg.SCARKO testes (mean 8 +/- 6 per testis). No microliths were seen in cryptorchid, ARKO or SCARKO mice. There was no significant effect of FSH or androgen on TM in hpg.ARKO mice.<BR/> <b>Conclusions</b>: We have identified a mouse model of TM and show that lack of endocrine stimulation is a cause of TM. Importantly, this model will provide a means with which to identify the mechanisms of TM development and the underlying changes in protein and gene expression

Reaction-Based Probes for Imaging Mobile Zinc in Live Cells and Tissues

Chelatable, or mobile, forms of zinc play critical signaling roles in numerous biological processes. Elucidating the action of mobile Zn(II) in complex biological environments requires sensitive tools for visualizing, tracking, and manipulating Zn(II) ions. A large toolbox of synthetic photoinduced electron transfer (PET)-based fluorescent Zn(II) sensors are available, but the applicability of many of these probes is limited by poor zinc sensitivity and low dynamic ranges owing to proton interference. We present here a general approach for acetylating PET-based probes containing a variety of fluorophores and zinc-binding units. The new sensors provide substantially improved zinc sensitivity and allow for incubation of live cells and tissue slices with nM probe concentrations, a significant improvement compared to the μM concentrations that are typically required for a measurable fluorescence signal. Acetylation effectively reduces or completely quenches background fluorescence in the metal-free sensor. Binding of Zn(II) selectively and quickly mediates hydrolytic cleavage of the acetyl groups, providing a large fluorescence response. An acetylated blue coumarin-based sensor was used to carry out detailed analyses of metal binding and metal-promoted acetyl hydrolysis. Acetylated benzoresorufin-based red-emitting probes with different zinc-binding sites are effective for sensing Zn(II) ions in live cells when applied at low concentrations (∼50–100 nM). We used green diacetylated Zinpyr1 (DA-ZP1) to image endogenous mobile Zn(II) in the molecular layer of mouse dorsal cochlear nucleus (DCN), confirming that acetylation is a suitable approach for preparing sensors that are highly specific and sensitive to mobile zinc in biological systems.National Institutes of Health (U.S.) (NIH grant GM065519)National Institutes of Health (U.S.) (NIH grant R01-DC007905)National Institutes of Health (U.S.) (NIH Fellowship (F32- EB019243))National Institutes of Health (U.S.) (NIH Fellowship (T32-DC011499))National Institutes of Health (U.S.) (NIH Fellowship (F32-DC013734)