Ordered valence bond states in symmetric two-dimensional spin-orbital systems

We consider a superexchange Hamiltonian, $H=-\sum_{}(2{\bf S}_i\cdot {\bf S}_j-\frac 12)(2{\bf T}_i\cdot {\bf T}_j-\frac 12)$, which describes systems with orbital degeneracy and strong electron-phonon coupling in the limit of large on-site repulsion. In an SU(4) Schwinger boson representation, a reduced spin-orbital interaction is derived {\it exactly}, and a mean field theory has been developed by introducing a symmetric valence bond pairing order parameter. In one dimension, a spin-orbital liquid state with a finite gap is obtained. On a two-dimensional square lattice a novel type of spin-orbital ferromagnetically ordered state appears, while spin and orbital are antiferromagnetic. Moreover, an important relation has been found, relating the spin and orbital correlation functions to the combined spin-orbital ones.Comment: four pages in Revtex, no figures, accepted for publication in Physical Review Letter

Itinerant chiral ferromagnetism in a trapped Rashba spin-orbit coupled Fermi gas

How ferromagnetic phases emerge in itinerant systems is an outstanding problem in quantum magnetism. Here we consider a repulsive two-component Fermi gas confined in a two dimensional isotropic harmonic potential and subject to a large Rashba spin-orbit (SO) coupling, whose single-particle dispersion can be tailored by adjusting the SO coupling strength. We show that the interplay among SO coupling, correlation effects and mean-field repulsion leads to a competition between ferromagnetic and non-magnetic phases. At intermediate interaction strengths, ferromagnetic phase emerges which can be well described by the mean-field Hartree-Fock theory; whereas at strong interaction strengths, a strongly correlated non-magnetic phase is favored due to the beyond-mean-field quantum correlation effects. Furthermore, the ferromagnetic phase of this system possesses a chiral current density induced by the Rashba spin-orbit coupling, whose experimental signature is investigated.Comment: Main text: 5 pages, 6 figures; Supplement: 4 pages, 2 figure

The Cross-Talk Between Neurons and Microglia Through Interleukin-4 After Ischemic Injury

After ischemic stroke, the loss of blood supply to the affected region of the brain leads to a series of pathological events known as ischemic cascades, that include excitotoxicity and microglia/macrophage over-activation resulting in damaging inflammatory responses. Studies from our research group suggest that the viable neurons in the ischemic penumbra (location receiving less profound damage, as compare to ischemic core) produce and release a potent anti-inflammatory cytokine, interleukin(IL) -4. We propose that this neuronal response to sublethal ischemia is designed to guide surrounding microglia/macrophages to a reparative and anti-inflammatory (M2) phenotype. The research included in this study is designed to establish the mechanisms that underlie neuronal production and secretion of IL-4 under ischemic injury. To investigate this process we used primary rat cortical neurons in culture and a well-validated in vitro ischemic injury model that is based on transient oxygen- and glucose- deprivation, (OGD). In this model, only longer durations of OGD result in neuronal death. We discover that short-duration, sublethal OGD, as determined by LDH release assay, more LDH release correspond to greater damage) induces neuronal IL-4 production at the gene (RT-qPCR) and protein (ELISA) level. Furthermore, we show that mild excitotoxic stress produced by N-methyl-D-aspartate (NMDA) receptor (NMDAR) activation (process that normally occurs in the cerebral ischemia) triggers IL-4 production and release by neurons in the primary neuron culture. We also implicated calcineurin and nuclear factor of activated T cell (NFAT) as potential players in the transcriptional regulation of the IL-4 synthesis in neurons. Finally, using neuron conditioned medium transfer to microglia, we find that neuronal IL-4 is capable of polarizing microglia toward a restorative, anti-inflammatory, and phagocytic phenotype. For the first time, this study demonstrates that the ischemia-evoked NMDAR activation, through calcineurin/NFAT pathway induces IL-4 production by neurons, and that this neuron-secreted IL-4 is capable of regulating microglia phenotype change. This cross-talk between neurons and microglia could represent a therapeutic target for cerebral ischemia