Analysis of fast turbulent reconnection with self-consistent determination of turbulence timescale

We present results of Reynolds-averaged turbulence model simulation on the problem of magnetic reconnection. In the model, in addition to the mean density, momentum, magnetic field, and energy equations, the evolution equations of the turbulent cross-helicity $W$, turbulent energy $K$ and its dissipation rate $\varepsilon$ are simultaneously solved to calculate the rate of magnetic reconnection for a Harris-type current sheet. In contrast to previous works based on algebraic modeling, the turbulence timescale is self-determined by the nonlinear evolutions of $K$ and $\varepsilon$, their ratio being a timescale. We compare the reconnection rate produced by our mean-field model to the resistive non-turbulent MHD rate. To test whether different regimes of reconnection are produced, we vary the initial strength of turbulent energy and study the effect on the amount of magnetic flux reconnected in time.Comment: 10 pages, 7 figure

Note on Triangle Anomalies and Assignment of Singlet in 331-like Model

It is pointed out that in the $331-$like model which uses both fundamental and complex conjugate representations for an assignment of the representations to the left-handed quarks and the scalar representation to their corresponding right-handed counterparts, the nature of the scalar should be taken into account in order to make the fermion triangle anomalies in the theory anomaly-free, i.e. renormalizable in a sense with no anomalies, even after the spontaneous symmetry breaking.Comment: 8 page no figures, acknowledgments adde

An Upsilon Point in a Spin Model

We present analytic evidence for the occurrence of an upsilon point, an infinite checkerboard structure of modulated phases, in the ground state of a spin model. The structure of the upsilon point is studied by calculating interface--interface interactions using an expansion in inverse spin anisotropy.Comment: 18 pages ReVTeX file, including 6 figures encoded with uufile

Alteration of Striatal Dopaminergic Neurotransmission in a Mouse Model of DYT11 Myoclonus-Dystonia

Background: DYT11 myoclonus-dystonia (M-D) syndrome is a neurological movement disorder characterized by myoclonic jerks and dystonic postures or movement that can be alleviated by alcohol. It is caused by mutations in SGCE encoding e-sarcoglycan (e-SG); the mouse homolog of this gene is Sgce. Paternally-inherited Sgce heterozygous knockout (Sgce KO) mice exhibit myoclonus, motor impairment and anxiety- and depression-like behaviors, modeling several clinical symptoms observed in DYT11 M-D patients. The behavioral deficits are accompanied by abnormally high levels of dopamine and its metabolites in the striatum of Sgce KO mice. Neuroimaging studies of DYT11 M-D patients show reduced dopamine D2 receptor (D2R) availability, although the possibility of increased endogenous dopamine, and consequently, competitive D2R occupancy cannot be ruled out. Methodology/Principal Findings: The protein levels of striatal D2R, dopamine transporter (DAT), and dopamine D1 receptor (D1R) in Sgce KO mice were analyzed by Western blot. The striatal dopamine release after amphetamine injection in Sgce KO mice were analyzed by microdialysis in vivo. The striatal D2R was significantly decreased in Sgce KO mice without altering DAT and D1R. Sgce KO mice also exhibited a significant increase of dopamine release after amphetamine injection in comparison to wild-type (WT) littermates. Conclusion/Significance: The results suggest e-SG may have a role in the regulation of D2R expression. The loss of e-S

Motor Deficits and Decreased Striatal Dopamine Receptor 2 Binding Activity in the Striatum-Specific Dyt1 Conditional Knockout Mice

DYT1 early-onset generalized dystonia is a hyperkinetic movement disorder caused by mutations in DYT1 (TOR1A), which codes for torsinA. Recently, significant progress has been made in studying pathophysiology of DYT1 dystonia using targeted mouse models. Dyt1 ΔGAG heterozygous knock-in (KI) and Dyt1 knock-down (KD) mice exhibit motor deficits and alterations of striatal dopamine metabolisms, while Dyt1 knockout (KO) and Dyt1 ΔGAG homozygous KI mice show abnormal nuclear envelopes and neonatal lethality. However, it has not been clear whether motor deficits and striatal abnormality are caused by Dyt1 mutation in the striatum itself or the end results of abnormal signals from other brain regions. To identify the brain region that contributes to these phenotypes, we made a striatum-specific Dyt1 conditional knockout (Dyt1 sKO) mouse. Dyt1 sKO mice exhibited motor deficits and reduced striatal dopamine receptor 2 (D2R) binding activity, whereas they did not exhibit significant alteration of striatal monoamine contents. Furthermore, we also found normal nuclear envelope structure in striatal medium spiny neurons (MSNs) of an adult Dyt1 sKO mouse and cerebral cortical neurons in cerebral cortex-specific Dyt1 conditional knockout (Dyt1 cKO) mice. The results suggest that the loss of striatal torsinA alone is sufficient to produce motor deficits, and that this effect may be mediated, at least in part, through changes in D2R function in the basal ganglia circuit

NMR studies of Successive Phase Transitions in Na0.5CoO2 and K0.5CoO2

59Co- and 23Na-NMR measurements have been carried out on polycrystalline and c-axis aligned samples of Na0.5CoO2, which exhibits successive transitions at temperatures T = 87 K (= Tc1) and T = 53 K (= Tc2). 59Co-NMR has also been carried out on c-axis aligned crystallites of K0.5CoO2 with similar successive transitions at Tc1 ~ 60 K and Tc2 ~ 20 K. For Na0.5CoO2, two sets of three NMR lines of 23Na nuclei explained by considering the quadrupolar frequencies nuQ ~1.32 and 1.40 MHz have been observed above Tc1, as is expected from the crystalline structure. Rather complicated but characteristic variation of the 23Na-NMR spectra has been observed with varying T through the transition temperatures, and the internal fields at two crystallographically distinct Na sites are discussed on the basis of the magnetic structures reported previously. The internal fields at two distinct Co sites observed below Tc1 and the 591/T1-T curves of Na0.5CoO2 and K0.5CoO2 are also discussed in a comparative way.Comment: 7 pages, 10 figures, submitted to J. Phys. Soc. Jpn, correction is made in right colum of p6 (35th line) as K0.5CoO2-->Na0.5CoO

Yoshizawa's cross-helicity effect and its quenching

A central quantity in mean-field magnetohydrodynamics is the mean electromotive force EMF, which in general depends on the mean magnetic field. It may however have a part independent of the mean magnetic field. Here we study an example of a rotating conducting body of turbulent fluid with non-zero cross-helicity, in which a contribution to the EMF proportional to the angular velocity occurs (Yoshizawa 1990). If the forcing is helical, it also leads to an alpha effect, and large-scale magnetic fields can be generated. For not too rapid rotation, the field configuration is such that Yoshizawa's contribution to the EMF is considerably reduced compared to the case without alpha effect. In that case, large-scale flows are also found to be generated.Comment: 10 pages, 8 figures, compatible with published versio

Electron-Phonon mechanism for Superconductivity in Na0.35_{0.35}CoO2_2: Valence-Band Suhl-Kondo effect Driven by Shear Phonons

To study the possible mechanism of superconductivity in Na$_{0.35}$CoO$_2$, we examine the interaction between all the relevant optical phonons (breathing and shear phonons) and $t_{2g}(a_{1g}+e_g')$-electrons of Co-ions, and study the transition temperature for a s-wave superconductivity. The obtained $T_{\rm c}$ is very low when the $e_g'$-valence-bands are far below the Fermi level. However, $T_{\rm c}$ is strongly enhanced when the top of the $e_g'$-valence-bands is close to the Fermi level (say -50meV), thanks to interband hopping of Cooper pairs caused by shear phonons. This ``valence-band Suhl-Kondo mechanism'' due to shear phonons is significant to understand the superconductivity in Na$_{0.35}$CoO$_2$. By the same mechanism, the kink structure of the band-dispersion observed by ARPES, which indicates the strong mass-enhancement ($m^\ast/m\sim3$) due to optical phonons, is also explained.Comment: 5 pages, 4 figures; v2:Added references, published in J. Phys. Soc. Jp