Coherent organization of electronic correlations as a mechanism to enhance and stabilize high-T C cuprate superconductivity.

Strong diffusive or incoherent electronic correlations are the signature of the strange-metal normal state of the cuprate superconductors, with these correlations considered to be undressed or removed in the superconducting state. A critical question is if these correlations are responsible for the high-temperature superconductivity. Here, utilizing a development in the analysis of angle-resolved photoemission data, we show that the strange-metal correlations don't simply disappear in the superconducting state, but are instead converted into a strongly renormalized coherent state, with stronger normal state correlations leading to stronger superconducting state renormalization. This conversion begins well above T C at the onset of superconducting fluctuations and it greatly increases the number of states that can pair. Therefore, there is positive feedback--the superconductive pairing creates the conversion that in turn strengthens the pairing. Although such positive feedback should enhance a conventional pairing mechanism, it could potentially also sustain an electronic pairing mechanism.

Novel Electron-Phonon Relaxation Pathway in Graphite Revealed by Time-Resolved Raman Scattering and Angle-Resolved Photoemission Spectroscopy.

Time dynamics of photoexcited electron-hole pairs is important for a number of technologies, in particular solar cells. We combined ultrafast pump-probe Raman scattering and photoemission to directly follow electron-hole excitations as well as the G-phonon in graphite after an excitation by an intense laser pulse. This phonon is known to couple relatively strongly to electrons. Cross-correlating effective electronic and phonon temperatures places new constraints on model-based fits. The accepted two-temperature model predicts that G-phonon population should start to increase as soon as excited electron-hole pairs are created and that the rate of increase should not depend strongly on the pump fluence. Instead we found that the increase of the G-phonon population occurs with a delay of ~65 fs. This time-delay is also evidenced by the absence of the so-called self-pumping for G phonons. It decreases with increased pump fluence. We show that these observations imply a new relaxation pathway: Instead of hot carriers transferring energy to G-phonons directly, the energy is first transferred to optical phonons near the zone boundary K-points, which then decay into G-phonons via phonon-phonon scattering. Our work demonstrates that phonon-phonon interactions must be included in any calculations of hot carrier relaxation in optical absorbers even when only short timescales are considered.

Hallmarks of the Mott-metal crossover in the hole-doped pseudospin-1/2 Mott insulator Sr2IrO4.

The physics of doped Mott insulators remains controversial after decades of active research, hindered by the interplay among competing orders and fluctuations. It is thus highly desired to distinguish the intrinsic characters of the Mott-metal crossover from those of other origins. Here we investigate the evolution of electronic structure and dynamics of the hole-doped pseudospin-1/2 Mott insulator Sr2IrO4. The effective hole doping is achieved by replacing Ir with Rh atoms, with the chemical potential immediately jumping to or near the top of the lower Hubbard band. The doped iridates exhibit multiple iconic low-energy features previously observed in doped cuprates-pseudogaps, Fermi arcs and marginal-Fermi-liquid-like electronic scattering rates. We suggest these signatures are most likely an integral part of the material's proximity to the Mott state, rather than from many of the most claimed mechanisms, including preformed electron pairing, quantum criticality or density-wave formation.

Lentiviral-mediated delivery of Bcl-2 or GDNF protects against excitotoxicity in the rat hippocampus.

Nutrient deprivation during ischemia leads to severe insult to neurons causing widespread excitotoxic damage in specific brain regions such as the hippocampus. One possible strategy for preventing neurodegeneration is to express therapeutic proteins in the brain to protect against excitotoxicity. We investigated the utility of equine infectious anemia virus (EIAV)-based vectors as genetic tools for delivery of therapeutic proteins in an in vivo excitotoxicity model. The efficacy of these vectors at preventing cellular loss in target brain areas following excitotoxic insult was also assessed. EIAV vectors generated to overexpress the human antiapoptotic Bcl-2 or growth factor glial-derived neurotrophic factor (GDNF) genes protected against glutamate-induced toxicity in cultured hippocampal neurons. In an in vivo excitotoxicity model, adult Wistar rats received a unilateral dose of the glutamate receptor agonist N-methyl-D-aspartate to the hippocampus that induced a large lesion in the CA1 region. Neuronal loss could not be protected by prior transduction of a control vector expressing beta-galactosidase. In contrast, EIAV-mediated expression of Bcl-2 and GDNF significantly reduced lesion size thus protecting the hippocampus from excitotoxic damage. These results demonstrate that EIAV vectors can be effectively used to deliver putative neuroprotective genes to target brain areas and prevent cellular loss in the event of a neurological insult. Therefore these lentiviral vectors provide potential therapeutic tools for use in cases of acute neurotrauma such as cerebral ischemia.