Unveiling a nematic quantum critical point in multi-orbital systems

Electronic nematicity, proposed to exist in a number of transition metal materials, can have different microscopic origins. In particular, the anisotropic resistivity and meta-magnetic jumps observed in Sr3Ru2O7 are consistent with an earlier proposal that the isotropic-nematic transition is generically first order and accompanied by meta-magnetism when tuned by a magnetic field. However, additional striking experimental features such as a non-Fermi liquid resistivity and critical thermodynamic behavior imply the presence of an unidentified quantum critical point (QCP). Here we show that orbital degrees of freedom play an essential role in revealing a nematic QCP, even though it is overshadowed by a nearby meta-nematic transition at low temperature. We further present a finite temperature phase diagram including the entropy landscape and discuss our findings in light of the phenomena observed in Sr3Ru2O7.Comment: 11 pages, 4 figure

Study of the electronic nematic phase of Sr3Ru2O7 with precise control of the applied magnetic field vector

This work was supported by the EPSRC.We report a study of the magnetoresistivity of high purity Sr3Ru2O7, in the vicinity of its electronic nematic phase. By employing a triple-axis (9/1/1 T) vector magnet, we were able to precisely tune both the magnitude and direction of the in-plane component of the magnetic field (H-parallel to). We report the dependence of the resistively determined anisotropy on H-parallel to in the phase, as well as across the wider temperature-field region. Our measurements reveal a high-temperature anisotropy which mimics the behavior of fluctuations from the underlying quantum critical point, and suggest the existence of a more complicated phase diagram. DOI: 10.1103/PhysRevB.87.161106Publisher PDFPeer reviewe

The injury response of oligodendrocyte precursor cells is induced by platelets, macrophages and inflammation-associated cytokines

Oligodendrocyte precursor cells recognized with the NG2 antibody respond rapidly to CNS injuries with hypertrophy and upregulation of the NG2 chondroitin sulfate proteoglycan within 24 h. These cells participate in glial scar formation, remaining around the injury site for several weeks. After injury, reactive oligodendrocyte precursor cells increase their production of several chondroitin sulfate proteoglycans, including NG2: this cell type thus represents a component of the inhibitory environment that prevents regeneration of axons in the injured CNS. This study analyzes factors that activate oligodendrocyte precursor cells. Both microglia and astrocytes become reactive around motor neurons following peripheral nerve lesions. We show that oligodendrocyte precursor cells do not hypertrophy or increase NG2 levels after these lesions. Those lesions that cause an oligodendrocyte precursor cell reaction generally open the bloodbrain barrier. We therefore opened the blood-brain barrier with microinjections of vascular endothelial growth factor or lipopolysaccharide to the rat and mouse brain, and examined oligodendrocyte precursor cell reactivity after 24 h. Both treatments led to increases in NG2 and hypertrophy of oligodendrocyte precursor cells. Of directly injected blood components serum and thrombin were without effect, while platelets and macrophages activated oligodendrocyte precursor cells. We tested the effects of a range of injury-related cytokines, of which tumor necrosis factor alpha; interleukin-1; transforming growth factor beta; interferon gamma had effects on oligodendrocyte precursor cells. Oligodendrocyte precursor cell chemokines, and mitogens did not increase NG2 levels. (c) 2006 Published by Elsevier Ltd on behalf of IBRO