Dissipation of Quasiclassical Turbulence in Superfluid

We compare the decay of turbulence in superfluid ^{4}He produced by a moving grid to the decay of turbulence created by either impulsive spin-down to rest or by intense ion injection. In all cases, the vortex line density L decays at late time t as L∝t^{-3/2}. At temperatures above 0.8 K, all methods result in the same rate of decay. Below 0.8 K, the spin-down turbulence maintains initial rotation and decays slower than grid turbulence and ion-jet turbulence. This may be due to a decoupling of the large-scale superfluid flow from the normal component at low temperatures, which changes its effective boundary condition from no-slip to slip.

Visualizing Pure Quantum Turbulence in Superfluid 3He: Andreev Reflection and its Spectral Properties.

Superfluid 3He-B in the zero-temperature limit offers a unique means of studying quantum turbulence by the Andreev reflection of quasiparticle excitations by the vortex flow fields. We validate the experimental visualization of turbulence in 3He-B by showing the relation between the vortex-line density and the Andreev reflectance of the vortex tangle in the first simulations of the Andreev reflectance by a realistic 3D vortex tangle, and comparing the results with the first experimental measurements able to probe quantum turbulence on length scales smaller than the intervortex separation.

Excimers He2* as tracers of quantum turbulence in 4He in the t = 0 limit.

We have studied the interaction of metastable 4He2* excimer molecules with quantized vortices in superfluid 4He in the zero temperature limit. The vortices were generated by either rotation or ion injection. The trapping diameter of the molecules on quantized vortices was found to be 96±6 nm at a pressure of 0.1 bar and 27±5 nm at 5.0 bar. We have also demonstrated that a moving tangle of vortices can carry the molecules through the superfluid helium.

Magnetic phase transition in a nanonetwork of solid 3He in aerogel.

When immersed in liquid 3He, the nanometer strands of aerogel are coated with a thin layer of solid 3He, forming a network of irregular nanotubes. Owing to its high purity and weak interactions, this system is ideal for studying fundamental processes. We report the first experiments on solid 3He in aerogel at ultralow temperatures, cooled by direct adiabatic demagnetization. Simultaneous nuclear magnetic susceptibility and heat capacity measurements indicate a magnetic phase transition.

Fluctuations and Correlations of Pure Quantum Turbulence in Superfluid 3He-B.

We describe the first measurements of line-density fluctuations and spatial correlations of quantum turbulence in superfluid 3He-B. All of the measurements are performed in the low-temperature regime, where the normal-fluid density is negligible. The quantum turbulence is generated by a vibrating grid. The vortex-line density is found to have large length-scale correlations, indicating large-scale collective motion of vortices. Furthermore, we find that the power spectrum of fluctuations versus frequency obeys a -5/3 power law which verifies recent speculations that this behavior is a generic feature of fully developed quantum turbulence, reminiscent of the Kolmogorov spectrum for velocity fluctuations in classical turbulence.

Contrasting mechanical anisotropies of the superfluid 3He phases in aerogel.

There has been much recent interest in how impurity scattering may affect the phases of the p-wave superfluid 3He. Impurities may be added to the otherwise absolutely pure superfluid by immersing it in aerogel. Some predictions suggest that impurity scattering may destroy orientational order and force all of the superfluid phases to have an isotropic superfluid density. In contrast to this, we present experimental data showing that the response of the A-like phase to superfluid flow is highly anisotropic, revealing a texture that is easily modified by flow.

Decay of pure quantum turbulence in superfluid 3He-B.

We describe measurements of the decay of pure superfluid turbulence in superfluid 3He-B, in the low temperature regime where the normal fluid density is negligible. We follow the decay of the turbulence generated by a vibrating grid as detected by vibrating wire resonators. Despite the absence of any classical normal fluid dissipation processes, the decay is consistent with turbulence having the classical Kolmogorov energy spectrum and is remarkably similar to that measured in superfluid 4He at relatively high temperatures. Further, our results strongly suggest that the decay is governed by the superfluid circulation quantum rather than kinematic viscosity.

Emission of discrete vortex rings by a vibrating grid in superfluid 3He-B: a precursor to quantum turbulence.

We report a transition in the vorticity generated by a grid moving in the B phase of superfluid 3He at T<

Quantum turbulence in superfluid 3He illuminated by a beam of quasiparticle excitations.

We have measured directly the Andreev scattering of a controllable beam of quasiparticle excitations by a localized tangle of quantum vortices in superfluid 3He-B at low temperatures. We present a microscopic description of the Andreev scattering from a vortex line allowing us to estimate the vortex separation scale in a dilute tangle of vortices, providing a better comparison of the observed decay time of the turbulence with recent numerical simulations. The experiments also suggest that below 200 microK we reach the low temperature limit for turbulent dynamics.

Interfacial energy of the superfluid 3He a-B phase interface in the zero-temperature limit.

We have measured the surface energy of the interface between the A and B phases of superfluid 3He in the low temperature limit at zero pressure. Using a shaped magnetic field, we control the passage of the phase boundary through a small aperture. We obtain the interphase surface energy from the over- or undermagnetization required to force the interface through the aperture in both directions, yielding values of the surface tension and the interfacial contact angle. This is the first measurement of the interfacial energy in high magnetic fields and in the zero-temperature limit.

Thermal conductivity of liquid 3He in aerogel: a gapless superfluid.

We have measured the thermal conductivity of liquid 3He in 98% aerogel at ultralow temperatures. Aerogel introduces disorder on a scale comparable to the superfluid coherence length. At low pressures the liquid in the aerogel shows normal-state behavior with conductivity linear in temperature. At pressures above approximately 6 bars the onset of superfluidity suppresses the conductivity and the thermal conductivity again tends towards linear behavior in the very low temperature limit, providing strong evidence that here the liquid 3He in the aerogel is behaving as a gapless superfluid.

Phase diagram of the A and B phases of superfluid 3He in aerogel.

We report the first measurements of the A-B phase transition of superfluid 3He confined within 98% silica aerogel in high magnetic fields and low temperatures. A disk of aerogel is attached to a vibrating wire resonator. The resonant frequency yields a measure of the superfluid fraction rho(s)/rho of the 3He within the aerogel. The inferred rho(s)/rho value increases substantially at the A-to- B transition of the confined superfluid, allowing us to map the A-B phase diagram as a function of field and temperature. At 4.8 bars, the B-T transition curve looks very similar to that in bulk with a simple reduction factor of order 0.45 for both transition field and temperature.

Generation and detection of quantum turbulence in superfluid 3He-B.

We describe the first direct observations of turbulence in superfluid 3He-B. The turbulence is generated by a vibrating-wire resonator driven at velocities exceeding the pair-breaking critical velocity. It is detected by the resulting decrease in the thermal damping on a neighboring "detector" vibrating-wire resonator. The superfluid flow field associated with the turbulence Andreev reflects thermal quasiparticle excitations, effectively screening the detector wire, resulting in a decrease in the thermal damping.

Binding of a protein to an AU-rich domain of tumour necrosis factor alpha mRNA as a 35 kDa complex and its regulation in primary rat astrocytes.

Newcastle disease virus (NDV) induces tumour necrosis factor alpha (TNF alpha) gene transcription and increases the mRNA stability. NDV stabilizes TNF alpha mRNA by preventing poly(A) shortening in a protein kinase C-dependent manner. TNF alpha 3'-untranslated region (UTR) contains an AU-rich domain (ARD) with seven AUUUA pentamers, a motif implicated in poly(A) removal and mRNA degradation. In this report, protein binding to TNF alpha ARD and the effects of NDV and kinases on ARD-binding activity were investigated in primary rat astrocytes. Both nuclear and cytoplasmic extracts contained proteins binding to centrally located 27 nt AUUUAUUAUUUAUUUAUUAUUUAUUUA, within TNF alpha ARD. Portions of ARD with a single AUUUA did not show ARD-binding activity. The ARD-protein complexes migrated as two bands on electrophoretic mobility-shift assay. The slower moving complexes appeared either as a broader band or doublets. The UV cross-linked ARD-protein complexes, however, migrated as a single 35 kDa band on SDS/PAGE. In cytoplasmic extracts treated with alkaline phosphatase there was a decrease in the faster moving complex and an increase in the slower moving complex, whereas NDV infection produced the reverse effect. In addition, the faster moving complex was decreased when cytoplasmic extracts from NDV-infected cells were treated with protein phosphatase 1 or 2A. Neither NDV infection nor phosphatase treatment affected the mobility pattern of nuclear extracts. The data indicate that a protein of molecular mass less than 35 kDa binds to a segment of TNF alpha ARD containing primarily UUAUUUAUU motifs, and the ARD-binding activity in cytoplasmic compartment is post-transcriptionally modified.

Regulatory mechanisms of MuRantes and CRG-2 chemokine gene induction in central nervous system glial cells by virus.

In this report we characterize the induction mechanisms of two chemokine genes, MuRantes and crg-2, the murine homologs of human RANTES and IP-10, respectively, in primary rat astrocytes and microglia by the neurotropic paramyxovirus, Newcastle Disease Virus (NDV). The time course for NDV induction of both MuRantes and crg-2 genes in astrocytes and microglia was similar, with peak mRNA expression at 10-12 h. Unlike crg-2, MuRantes mRNA was not induced by IFN-gamma. MuRantes and crg-2 are transcriptionally induced by noninfectious, UV-irradiated NDV in astrocytes and microglia, unlike TNFalpha gene transcription, which is induced only by live NDV. These data indicate that signals generated through virus-receptor interaction on the target cell surface suffice to initiate MuRantes and crg-2 gene transcription in the absence of viral replication. In astrocytes, MuRantes mRNA accumulation in response to NDV was completely blocked by tyrosine kinase inhibitors, and partially by PKC and PKA inhibitors, whereas crg-2 mRNA accumulation was significantly inhibited by PKC inhibitors, but minimally or not affected by inhibitors of tyrosine kinase or PKA activity. These kinase inhibitors also affected MuRantes and crg-2 gene transcription in similar patterns to those observed for mRNA levels, but did not reduce the mRNA stability. Therefore, the signals required for mRNA accumulation appear to operate at the level of transcription. Efficient transcription of MuRantes and crg-2 genes may require different sets of transcriptional proteins and enhancers that are regulated by different signaling pathways activated by NDV.

Tyrosine kinase activation by Newcastle disease virus is required for TNF-alpha gene induction in astrocytes.

Astrocytes, when appropriately stimulated, produce a variety of cytokines including TNF-alpha. Production of TNF-alpha by astrocytes stimulated with Newcastle disease virus (NDV) is achieved by transcriptional activation and mRNA stabilization. A PKC-dependent pathway is responsible for a 10-fold increase in TNF-alpha mRNA stability by reducing poly(A) tail removal. The present study examined signal pathways induced by NDV in primary rat astrocytes that are responsible for TNF-alpha gene transcription as well as the possible source of kinase activity required for mRNA stabilization. Transcription of TNF-alpha gene in astrocytes stimulated by NDV or LPS and IFN-gamma was inhibited completely by the tyrosine kinase inhibitor herbimycin, and partially by a PKC inhibitor H7, as determined by nuclear run-on assay. HA-1004, a cyclic nucleotide-dependent kinase inhibitor, showed no effect. These results indicated that tyrosine kinase signaling pathways seemed to precede the activation of PKC in induction of TNF-alpha gene. Increase in tyrosine kinase activity in NDV-infected astrocytes was demonstrated by a two- to threefold increase in tyrosine phosphorylation of Pl-PLC gamma 1. Because astrocytes contain minimal Pl-PLC beta, and NDV-induced TNF-alpha mRNA was affected by pertussis toxin only modestly, Pl-PLC gamma 1 is likely the enzyme responsible for DAG generation and the PKC-dependent mRNA stabilization in response to NDV.

Definition of a lipopolysaccharide-responsive element in the 5'-flanking regions of MuRantes and crg-2.

Macrophages are stimulated by lipopolysaccharide (LPS) of gram-negative organisms. The changes in LPS-stimulated macrophages include transcriptional activation of multiple immediate-early genes, which may contribute to the natural immunity to microorganisms. We have defined by deletion and mutational analysis LPS-responsive elements (LREs) in two chemokine genes, MuRantes and crg-2, which are activated in an immediate-early manner. LRE consists of two motifs, TCAYR, which is an AP-1 half site with two flanking bases, and (A/T) (G/C)NTTYC(A/T)NTTY, which resembles in part the interferon-stimulated responsive element (ISRE). The orientation of these two motifs relative to each other in MuRantes differed from that in crg-2. These two motifs are separated by 10 and 6 nonconsensus nucleotides in the MuRantes and crg-2 LREs, respectively. Stimulation of macrophage-like RAW 264.7 cells with alpha/beta interferon did not activate MuRantes, indicating that the ISRE-like motif in MuRantes does not have ISRE activity. Upon stimulation of RAW 264.7 cells with LPS, proteins capable of binding to LRE accumulate in the nuclei as measured by electrophoretic mobility shift assay. These LRE-binding proteins include c-Jun and CREB.

Proton magnetic resonance spectroscopy of human brain: applications to normal white matter, chronic infarction, and MRI white matter signal hyperintensities.

A modified ISIS method, for image-selected localized proton magnetic resonance spectroscopy (1H MRS), was used to determine the ratios and T2 relaxation times of proton metabolites in normal subjects and in patients with chronic infarction and MRI white matter signal hyperintensities (WMSH). First, in patients with cerebral infarctions, increased concentrations of lactate were found in the majority of patients, and N-acetyl aspartate (NAA) was reduced to a significantly greater extent than choline (Cho) or creatine (Cre). For TE = 270 ms, the raw ratios of Cho/NAA, Cre/NAA, and Lac/NAA were significantly (P less than 0.05) increased from 0.23 +/- 0.02 (mean +/- SE), 0.20 +/- 0.01, and 0.05 +/- 0.01, respectively in the normal group to 0.39 +/- 0.08, 0.37 +/- 0.05, and 0.48 +/- 0.15 in the stroke group. Also, the T2 relaxation time of creatine was significantly (P = 0.007) increased from 136 ms in normal white matter to 171 ms in cerebral infarcts. Second, in patients with WMSH, no significant change of the proton metabolite concentrations could be detected with the exception of the choline which was significantly (P = 0.003) altered. The Cho/NAA ratio, after T2 and excitation profile correction, increased from 0.47 +/- 0.02 in the normal group to 0.64 +/- 0.05 in the WMSH group. Third, in normal white matter, the concentration of N-acetyl aspartate, choline, and lactate was estimated to 11.5, 2.0, and 0.6 mM, respectively, by assuming a total creatine concentration of 10 mM.