Nematic transition and highly two-dimensional superconductivity in BaTi2_2Bi2_2O revealed by 209^{209}Bi-nuclear magnetic resonance/nuclear quadrupole resonance measurements

In this Rapid Communication, a set of $^{209}$Bi-nuclear magnetic resonance (NMR)/nuclear quadrupole resonance (NQR) measurements has been performed to investigate the physical properties of superconducting (SC) BaTi$_2$Bi$_2$O from a microscopic point of view. The NMR and NQR spectra at 5~K can be reproduced with a non-zero in-plane anisotropic parameter $\eta$, indicating the breaking of the in-plane four-fold symmetry at the Bi site without any magnetic order, i.e., `the electronic nematic state'. In the SC state, the nuclear spin-lattice relaxation rate divided by temperature, $1/T_1T$, does not change even below $T_{\rm c}$, while a clear SC transition was observed with a diamagnetic signal. This observation can be attributed to the strong two-dimensionality in BaTi$_2$Bi$_2$O. Comparing the NMR/NQR results among BaTi$_2$$Pn$$_2$O ($Pn$ = As, Sb, and Bi), it was found that the normal and SC properties of BaTi$_2$Bi$_2$O were considerably different from those of BaTi$_2$Sb$_2$O and BaTi$_2$As$_2$O, which might explain the two-dome structure of $T_{\rm c}$ in this system.Comment: 5 pages, 6 figure

Structure of Shock Waves in Bubbly Liquid

In this paper, steady and unsteady shock waves in a bubbly liquid are treated numerically. A new system of model equations describing the bubbly flow is applied and the detailed flow structure behind a shock front is investigated in detail. It is proved that the velocity difference between the liquid and the gas phases induced by a stationary shock wave is of order α1/2, wher α is the void fraction of the gas-phase. Radial oscillation of bubbles tends to produce a oscillatory profile of the translational velocity of the bubbles near the wave fronts. Numerical simulation shows that oscillatory behaviour of the mixture pressure is significantly suppressed by the translational motion of bubbles and that the whole shock structure is remarkably affected by the velocity difference between the phases especially in the case of weak shocks. It is confirmed that the stationary shock wave is realized as an asymptotic solution for a shock tube problem with uniform conditions in the low pressure and high pressure chambers

A novel Rac1-GSPT1 signaling pathway controls astrogliosis following central nervous system injury

Astrogliosis (i.e. glial scar), which is comprised primarily of proliferated astrocytes at the lesion site and migrated astrocytes from neighboring regions, is one of the key reactions in determining outcomes after CNS injury. In an effort to identify potential molecules/pathways that regulate astrogliosis, we sought to determine whether Rac/Rac-mediated signaling in astrocytes represents a novel candidate for therapeutic intervention following CNS injury. For these studies, we generated mice with Rac1 deletion under the control of the GFAP (glial fibrillary acidic protein) promoter (GFAP-Cre;Rac1(flox/flox)). GFAP-Cre;Rac1(flox/flox) (Rac1-KO) mice exhibited better recovery after spinal cord injury and exhibited reduced astrogliosis at the lesion site relative to control. Reduced astrogliosis was also observed in Rac1-KO mice following microbeam irradiation-induced injury. Moreover, knockdown (KD) or KO of Rac1 in astrocytes (LN229 cells, primary astrocytes, or primary astrocytes from Rac1-KO mice) led to delayed cell cycle progression and reduced cell migration. Rac1-KD or Rac1-KO astrocytes additionally had decreased levels of GSPT1 (G(1) to S phase transition 1) expression and reduced responses of IL-1β and GSPT1 to LPS treatment, indicating that IL-1β and GSPT1 are downstream molecules of Rac1 associated with inflammatory condition. Furthermore, GSPT1-KD astrocytes had cell cycle delay, with no effect on cell migration. The cell cycle delay induced by Rac1-KD was rescued by overexpression of GSPT1. Based on these results, we propose that Rac1-GSPT1 represents a novel signaling axis in astrocytes that accelerates proliferation in response to inflammation, which is one important factor in the development of astrogliosis/glial scar following CNS injury