Room-temperature ferromagnetism and the scaling relation between magnetization and average granule size in nanocrystalline Zn/ZnO core-shell structures prepared by sputtering.

Ferromagnetism is found in nanocrystalline Zn/ZnO core-shell structures prepared by sputtering pure Zn with subsequent oxidation. The saturation magnetization (M(S)) of the passivated ZnO shells increases with decrease in average particle size (d). The Curie temperature of the samples is above 400 degrees C. It is found that the ferromagnetism has a close relationship with point defects in ZnO shells. The maximum magnetization is estimated to be 28 emu cm(-3) (i.e. 0.14 mu(B) per unit cell) at 300 K, which is over three orders of magnitude larger than that of undoped ZnO nanoparticles or nanorods (10(-3)-10(-2) emu cm(-3)). More importantly, there is a scaling relation of M(s) alpha 1/d(n) (n = 5.20 +/- 0.20) for samples with d

Superconductivity in 4 angstrom single-walled carbon nanotubes.

Investigation of the magnetic and transport properties of single-walled small-diameter carbon nanotubes embedded in a zeolite matrix revealed that at temperatures below 20 kelvin, 4 angstrom tubes exhibit superconducting behavior manifest as an anisotropic Meissner effect, with a superconducting gap and fluctuation supercurrent. The measured superconducting characteristics display smooth temperature variations owing to one-dimensional fluctuations, with a mean-field superconducting transition temperature of 15 kelvin. Statistical mechanic calculations based on the Ginzburg-Landau free-energy functional yield predictions that are in excellent agreement with the experiments.

Intrathecal magnesium sulfate attenuates algogenic behavior and spinal amino acids release after kainic acid receptor activation in rats.

Activation of N-methyl-D-asparate (NMDA) receptor and non-NMDA classes of glutamate receptors play a key role in spinal nociceptive processing. Using with a lumbar intrathecal (IT) catheter and a loop dialysis catheter in lightly anesthetized (1% isoflurane) rats, the effect of IT pre-treatment with magnesium sulfate (100, 300 or 500 microg) on IT kainic acid (KA: 1 microg; non-NMDA receptor agonist) evoked amino acids (AAs) release and corresponding behavior was examined. IT KA produced significant increases (mean+/-SD of % baseline concentration) in dialysate concentrations of aspartate (424+/-88%), glutamate (241+/-35%) and taurine (398+/-58%). IT pre-treatment with MgSO(4) resulted in a dose-dependent suppression of the evoked algogenic behavior and aspartate release. These data suggest that activation of spinal KA receptors provides a powerful stimulus for secondary spinal excitatory AAs release and corresponding appearance of pain behavior. The regulation of this release by magnesium suggests the possible role of this divalent cation in regulating this excitatory effect of non-NMDA receptor activation.