7 research outputs found

    Critical change in the Fermi surface of iron arsenic superconductors at the onset of superconductivity

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    The phase diagram of a correlated material is the result of a complex interplay between several degrees of freedom, providing a map of the material's behavior. One can understand (and ultimately control) the material's ground state by associating features and regions of the phase diagram, with specific physical events or underlying quantum mechanical properties. The phase diagram of the newly discovered iron arsenic high temperature superconductors is particularly rich and interesting. In the AE(Fe1-xTx)2As2 class (AE being Ca, Sr, Ba, T being transition metals), the simultaneous structural/magnetic phase transition that occurs at elevated temperature in the undoped material, splits and is suppressed by carrier doping, the suppression being complete around optimal doping. A dome of superconductivity exists with apparent equal ease in the orthorhombic / antiferromagnetic (AFM) state as well as in the tetragonal state with no long range magnetic order. The question then is what determines the critical doping at which superconductivity emerges, if the AFM order is fully suppressed only at higher doping values. Here we report evidence from angle resolved photoemission spectroscopy (ARPES) that critical changes in the Fermi surface (FS) occur at the doping level that marks the onset of superconductivity. The presence of the AFM order leads to a reconstruction of the electronic structure, most significantly the appearance of the small hole pockets at the Fermi level. These hole pockets vanish, i. e. undergo a Lifshitz transition, at the onset of superconductivity. Superconductivity and magnetism are competing states in the iron arsenic superconductors. In the presence of the hole pockets superconductivity is fully suppressed, while in their absence the two states can coexist.Comment: Updated version accepted in Nature Physic

    Disentangling Cooper-pair formation above Tc from the pseudogap state in the cuprates

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    The discovery of the pseudogap in the cuprates created significant excitement amongst physicists as it was believed to be a signature of pairing, in some cases well above the room temperature. In this "pre-formed pairs" scenario, the formation of pairs without quantum phase rigidity occurs below T*. These pairs condense and develop phase coherence only below Tc. In contrast, several recent experiments reported that the pseudogap and superconducting states are characterized by two different energy scales, pointing to a scenario, where the two compete. However a number of transport, magnetic, thermodynamic and tunneling spectroscopy experiments consistently detect a signature of phase-fluctuating superconductivity above leaving open the question of whether the pseudogap is caused by pair formation or not. Here we report the discovery of a spectroscopic signature of pair formation and demonstrate that in a region of the phase diagram commonly referred to as the "pseudogap", two distinct states coexist: one that persists to an intermediate temperature Tpair and a second that extends up to T*. The first state is characterized by a doping independent scaling behavior and is due to pairing above Tc, but significantly below T*. The second state is the "proper" pseudogap - characterized by a "checker board" pattern in STM images, the absence of pair formation, and is likely linked to Mott physics of pristine CuO2 planes. Tpair has a universal value around 130-150K even for materials with very different Tc, likely setting limit on highest, attainable Tc in cuprates. The observed universal scaling behavior with respect to Tpair indicates a breakdown of the classical picture of phase fluctuations in the cuprates.Comment: 9 pages, 4 figure

    A p97/Valosin-Containing Protein Inhibitor Drug CB-5083 Has a Potent but Reversible Off-Target Effect on Phosphodiesterase-6.

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    CB-5083 is an inhibitor of p97/valosin-containing protein (VCP), for which phase I trials for cancer were terminated because of adverse effects on vision, such as photophobia and dyschromatopsia. Lower dose CB-5083 could combat inclusion body myopathy with early-onset Paget disease and frontotemporal dementia or multisystem proteinopathy caused by gain-of-function mutations in VCP. We hypothesized that the visual impairment in the cancer trial was due to CB-5083's inhibition of phosphodiesterase (PDE)-6, which mediates signal transduction in photoreceptors. To test our hypothesis, we used in vivo and ex vivo electroretinography (ERG) in mice and a PDE6 activity assay of bovine rod outer segment (ROS) extracts. Additionally, histology and optical coherence tomography were used to assess CB-5083's long-term ocular toxicity. A single administration of CB-5083 led to robust ERG signal deterioration, specifically in photoresponse kinetics. Similar recordings with known PDE inhibitors sildenafil, tadalafil, vardenafil, and zaprinast showed that only vardenafil had as strong an effect on the ERG signal in vivo as did CB-5083. In the biochemical assay, CB-5083 inhibited PDE6 activity with a potency higher than sildenafil but lower than that of vardenafil. Ex vivo ERG revealed a PDE6 inhibition constant of 80 nM for CB-5083, which is 7-fold smaller than that for sildenafil. Finally, we showed that the inhibitory effect of CB-5083 on visual function is reversible, and its chronic administration does not cause permanent retinal anomalies in aged VCP-disease model mice. Our results warrant re-evaluation of CB-5083 as a clinical therapeutic agent. We recommend preclinical ERG recordings as a routine drug safety screen. SIGNIFICANCE STATEMENT: This report supports the use of a valosin-containing protein (VCP) inhibitor drug, CB-5083, for the treatment of neuromuscular VCP disease despite CB-5083's initial clinical failure for cancer treatment due to side effects on vision. The data show that CB-5083 displays a dose-dependent but reversible inhibitory action on phosphodiesterase-6, an essential enzyme in retinal photoreceptor function, but no long-term consequences on retinal function or structure
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