Antiferromagnetism in a Family of S = 1 Square Lattice Coordination Polymers NiX2(pyz)2 (X = Cl, Br, I, NCS; pyz = Pyrazine).

The crystal structures of NiX2(pyz)2 (X = Cl (1), Br (2), I (3), and NCS (4)) were determined by synchrotron X-ray powder diffraction. All four compounds consist of two-dimensional (2D) square arrays self-assembled from octahedral NiN4X2 units that are bridged by pyz ligands. The 2D layered motifs displayed by 1-4 are relevant to bifluoride-bridged [Ni(HF2)(pyz)2]EF6 (E = P, Sb), which also possess the same 2D layers. In contrast, terminal X ligands occupy axial positions in 1-4 and cause a staggered packing of adjacent layers. Long-range antiferromagnetic (AFM) order occurs below 1.5 (Cl), 1.9 (Br and NCS), and 2.5 K (I) as determined by heat capacity and muon-spin relaxation. The single-ion anisotropy and g factor of 2, 3, and 4 were measured by electron-spin resonance with no evidence for zero-field splitting (ZFS) being observed. The magnetism of 1-4 spans the spectrum from quasi-two-dimensional (2D) to three-dimensional (3D) antiferromagnetism. Nearly identical results and thermodynamic features were obtained for 2 and 4 as shown by pulsed-field magnetization, magnetic susceptibility, as well as their Néel temperatures. Magnetization curves for 2 and 4 calculated by quantum Monte Carlo simulation also show excellent agreement with the pulsed-field data. Compound 3 is characterized as a 3D AFM with the interlayer interaction (J⊥) being slightly stronger than the intralayer interaction along Ni-pyz-Ni segments (J(pyz)) within the two-dimensional [Ni(pyz)2](2+) square planes. Regardless of X, J(pyz) is similar for the four compounds and is roughly 1 K.

Quenching the haldane gap in spin-1 Heisenberg antiferromagnets.

We consider a quasi-one-dimensional system of spin-1 Heisenberg antiferromagnetic chains in two-dimensional and three-dimensional hypercubic lattices with interchain coupling J and uniaxial single-ion anisotropy D. Using large-scale numerical simulations, we map out the J-D phase diagram and investigate the low-lying excitations of the Haldane phase in the J≪1 limit. We also provide direct evidence that the Haldane phase remains a nontrivial symmetry-protected topological state for small but finite J.

Columnar antiferromagnetic order and spin supersolid phase on the extended Shastry-Sutherland lattice.

We use large scale quantum Monte Carlo simulations to study an extended version of the canonical Shastry-Sutherland model--including additional interactions and exchange anisotropy--over a wide range of interaction parameters and an applied magnetic field. The model is appropriate for describing the low energy properties of some members of the rare earth tetraborides. Working in the limit of large Ising-like exchange anisotropy, we demonstrate the stabilization of columnar antiferromagnetic order in the ground state at zero field and an extended magnetization plateau at 1/2 the saturation magnetization in the presence of an applied longitudinal magnetic field--qualitatively similar to experimentally observed low-temperature phases in ErB(4). Our results show that for an optimal range of exchange parameters, a spin supersolid ground state is realized over a finite range of an applied field between the columnar antiferromagnetic phase and the magnetization plateau. The full momentum dependence of the longitudinal and transverse components of the static structure factor is calculated in the spin supersolid phase to demonstrate the simultaneous existence of diagonal and off-diagonal long-range order. Our results provide crucial guidance in designing further experiments to search for the interesting spin supersolid phase in ErB(4).

Complex bursting in pancreatic islets: a potential glycolytic mechanism.

The electrical activity of insulin-secreting pancreatic islets of Langerhans is characterized by bursts of action potentials. Most often this bursting is periodic, but in some cases it is modulated by an underlying slower rhythm. We suggest that the modulatory rhythm for this complex bursting pattern is due to oscillations in glycolysis, while the bursting itself is generated by some other slow process. To demonstrate this hypothesis, we couple a minimal model of glycolytic oscillations to a minimal model for activity-dependent bursting in islets. We show that the combined model can reproduce several complex bursting patterns from mouse islets published in the literature, and we illustrate how these complex oscillations are produced through the use of a fast/slow analysis.