Ferromagnetic Quantum Criticality in the Quasi-One-Dimensional Heavy Fermion Metal YbNi4P2

We present a new Kondo-lattice system, YbNi4P2, which is a clean heavy-fermion metal with a severely reduced ferromagnetic ordering temperature at T_C=0.17K, evidenced by distinct anomalies in susceptibility, specific-heat, and resistivity measurements. The ferromagnetic nature of the transition, with only a small ordered moment of ~0.05mu_B, is established by a diverging susceptibility at T_C with huge absolute values in the ferromagnetically ordered state, severely reduced by small magnetic fields. Furthermore, YbNi4P2 is a stoichiometric system with a quasi-one-dimensional crystal and electronic structure and strong correlation effects which dominate the low temperature properties. This is reflected by a stronger-than-logarithmically diverging Sommerfeld coefficient and a linear-in-T resistivity above T_C which cannot be explained by any current theoretical predictions. These exciting characteristics are unique among all correlated electron systems and make this an interesting material for further in-depth investigations.Comment: 14 pages, 6 figure

Magnetic and structural properties of the iron silicide superconductor LaFeSiH

The magnetic and structural properties of the recently discovered pnictogen/chalcogen-free superconductor LaFeSiH ($T_c\simeq10$~K) have been investigated by $^{57}$Fe synchrotron M{\"o}ssbauer source (SMS) spectroscopy, x-ray and neutron powder diffraction and $^{29}$Si nuclear magnetic resonance spectroscopy (NMR). No sign of long range magnetic order or local moments has been detected in any of the measurements and LaFeSiH remains tetragonal down to 2 K. The activated temperature dependence of both the NMR Knight shift and the relaxation rate $1/T_1$ is analogous to that observed in strongly overdoped Fe-based superconductors. These results, together with the temperature-independent NMR linewidth, show that LaFeSiH is an homogeneous metal, far from any magnetic or nematic instability, and with similar Fermi surface properties as strongly overdoped iron pnictides. This raises the prospect of enhancing the $T_c$ of LaFeSiH by reducing its carrier concentration through appropriate chemical substitutions. Additional SMS spectroscopy measurements under hydrostatic pressure up to 18.8~GPa found no measurable hyperfine field

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

Nonlocal Kondo coupling and selective doping from cerium <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>f</mml:mi></mml:math> electrons in iron-based superconductors

In this paper, we consider an unconventional doping effect of strongly correlated cerium 4 f electrons in layered intermetallic systems. The conduction electron part of the model is taken to reproduce the hole and electron pockets of iron-based superconductors (FeSCs), and the cerium contribution is studied through an effective tight-binding Hamiltonian arising from the slave-boson mean-field theory of the periodic Anderson model. We show how the consideration of the nonlocal Kondo coupling naturally present in real materials can lead to a pocket-selective doping effect from cerium f electrons. The model is designed for paramagnetic materials of the ZrCuSiAs-type structure such as CeFeSiH, CeFePO, or the high-pressure phase of CeFeAsO. In certain conditions, the model shows a Lifshitz transition which can be induced by either doping or change in the hybridization strength between iron and cerium orbitals. We present some signatures of both pocket-selective doping and Lifshitz transition by means of the density of states at the Fermi level, the static spin susceptibility, the optical conductivity, and Raman spectroscopy

Strain-induced crystallization in sustainably crosslinked epoxidized natural rubber

International audienc

Interleukin-1 enhances the ATP-evoked release of arachidonic acid from mouse astrocytes.

During neuropathological states associated with inflammation, the levels of cytokines such as interleukin-1beta (IL-1beta) are increased. Several studies have suggested that the neuronal damage observed in pathogenesis implicating IL-1beta are caused by an alteration in the neurochemical interactions between neurons and astrocytes. We report here that treating striatal astrocytes in primary culture with IL-1beta for 22-24 hr enhances the ATP-evoked release of arachidonic acid (AA) with no effect on the ATP-induced accumulation of inositol phosphates. The molecular mechanism responsible for this effect involves the expression of P2Y2 receptors (a subtype of purinoceptor activated by ATP) and cytosolic phospholipase A2 (cPLA2, an enzyme that mediates AA release). Indeed, P2Y2 antisense oligonucleotides reduce the ATP-evoked release of AA only from IL-1beta-treated astrocytes. Further, both the amount of cPLA2 (as assessed by Western blotting) and the release of AA resulting from direct activation of cPLA2 increased fourfold in cells treated with IL-1beta. We also report evidence indicating that the coupling of newly expressed P2Y2 receptors to cPLA2 is dependent on PKC activity. These results suggest that during inflammatory conditions, IL-1beta reveals a functional P2Y2 signaling pathway in astrocytes that results in a dramatic increase in the levels of free AA. This pathway may thus contribute to the neuronal loss associated with cerebral ischemia or traumatic brain injury

Interleukin-1 enhances the ATP-evoked release of arachidonic acid from mouse astrocytes.

During neuropathological states associated with inflammation, the levels of cytokines such as interleukin-1beta (IL-1beta) are increased. Several studies have suggested that the neuronal damage observed in pathogenesis implicating IL-1beta are caused by an alteration in the neurochemical interactions between neurons and astrocytes. We report here that treating striatal astrocytes in primary culture with IL-1beta for 22-24 hr enhances the ATP-evoked release of arachidonic acid (AA) with no effect on the ATP-induced accumulation of inositol phosphates. The molecular mechanism responsible for this effect involves the expression of P2Y2 receptors (a subtype of purinoceptor activated by ATP) and cytosolic phospholipase A2 (cPLA2, an enzyme that mediates AA release). Indeed, P2Y2 antisense oligonucleotides reduce the ATP-evoked release of AA only from IL-1beta-treated astrocytes. Further, both the amount of cPLA2 (as assessed by Western blotting) and the release of AA resulting from direct activation of cPLA2 increased fourfold in cells treated with IL-1beta. We also report evidence indicating that the coupling of newly expressed P2Y2 receptors to cPLA2 is dependent on PKC activity. These results suggest that during inflammatory conditions, IL-1beta reveals a functional P2Y2 signaling pathway in astrocytes that results in a dramatic increase in the levels of free AA. This pathway may thus contribute to the neuronal loss associated with cerebral ischemia or traumatic brain injury