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High-temperature cuprate superconductivity remains a defining problem in condensed-matter physics. Among myriad approaches to addressing this problem has been the study of alternative transition metal oxides with similar structures and 3d electron count that are suggested as proxies for cuprate physics. None of these analogues has been superconducting, and few are even metallic. Here, we report that the low-valent, quasi-two-dimensional trilayer compound Pr4Ni3O8 avoids a charge-stripe-ordered phase previously reported for La4Ni3O8, leading to a metallic ground state. X-ray absorption spectroscopy shows that metallic Pr4Ni3O8 exhibits a low-spin configuration with significant orbital polarization and pronounced character in the unoccupied states above the Fermi energy, a hallmark of the cuprate superconductors. Density functional theory calculations corroborate this finding, and reveal that the orbital dominates the near-Ef occupied states as well. Belonging to a regime of 3d electron count found for hole-doped cuprates, Pr4Ni3O8 thus represents one of the closest analogues to cuprates yet reported and a singularly promising candidate for high-Tc superconductivity if electron doping could be achieved. A careful study of the low-valent, quasi-two-dimensional trilayer metallic nickelate Pr4Ni3O8 is presented, revealing this system to be a close analogue of cuprate systems, and offering tantalizing hope that it may superconduct if appropriate electron doping can be achieved.

An argument by contradiction shows that the pseudogap state in the high-temperature superconducting cuprates is due to the superconducting pairing rather than being an independent or even competing state.

A brief overview is given of the problem of high temperature superconductivity in the cuprates, with emphasis on theoretical ideas.

We use the gradient of the energy-integrated angle resolved photoemission (ARPES) intensity in order to define precisely the Fermi surface (FS) in BSCCO superconductors. We show that, independent of the photon energy, the FS is a hole barrel centered at ({pi},{pi}), Then, the superconducting gap along the FS is precisely determined from ARPES measurements on over-doped and underdoped samples of Bi2212. As the doping decreases, the maximum gap increases, but the slope of the gap near the nodes decreases. Though consistent with d-wave symmetry, the gap with underdoping cannot be fit by the simple cos(k{sub x})-cos(k{sub y}) form. A comparison of our ARPES results with available penetration depth data indicates that the renormalization of the linear T suppression of the superfluid density at low temperatures due to quasiparticle excitations around the d-wave nodes is large and doping dependent.

We review the spin dynamics of the normal state of the cuprates with special emphasis on neutron data in both the YBa{sub 2}Cu{sub 3}O{sub 7-{delta}} and La{sub 2-x}Sr{sub x}CuO{sub 4} systems. When realistic models of the Fermi surface shapes are incorporated, along with a moderate degree of spin fluctuations, we find good semi-quantiative agreement with experiment for both cuprates. Building on the success of this Fermi-liquid-based scheme, we explore the implications for d-wave pairing from a number of vantage points. We conclude that our present experimental and theoretical understanding is inadequate to confirm or refute the d-wave scenario.

Using linkage analysis, we previously showed that the growth hormone receptor (GHR) was involved in Laron dwarfism, an autosomal recessive GH resistant disorder. Interestingly, the extracellular domain of the GHR is found in the serum in the form of a hormone binding protein (GHBP), which binds GH with approximately the same affinity as the native receptor and which is undetectable, in terms of binding activity, in the serum of patients with Laron syndrome. We have analyzed the GHR gene in two unrelated Asian families in which patients displayed the classical features of Laron phenotype except for the presence of serum GH binding activity. To evaluate the involvement of the GHR in ihis new phenotype, we first performed linkage studies: in one family, the GHR markers cosegregated with the disease phenotype whereas the other family was not informative. Analysis of the coding region of the GHR gene revealed, in both families, a missense defect (Asp152→His) within the exoplasmic domain of the receptor. Expression of Ihe corresponding mutated cDNA into eukaryotic cells led to the synthesis of a receptor that displayed normal binding kinetics. We expect that this mutation is deleterious since it is linked to the disease phenotype and involves a highly conserved amino acid. In addition, previous studies have shown that the complex between GH and the extracellular domain of its receptor (GHBP) consists of one molecule of GH per two molecules of GHBP (1 and II) and that hormone-induced receptor dimerization is relevant to the signal transduction mechanism. Interestingly, since the mutation described is located at the GHBPI / GHBPII interface, it is very probable that it plays a critical role in growth signal transduction.

Previous work has shown that the lethal effects of glucocorticoids on the human lymphoblastoid cell line, CEM-C7, are antagonized by the simultaneous presence of 1-beta-D-arabinofuranosylcytosine (Ara-C). A possible cell cycle mechanism prompted further studies using flow microfluorimetry. We now report that (1) Ara-C (10-100 nM) blocks cells in S-phase and (2) the block is reversible after the drug is removed. A second treatment protocol, in which glucocorticoid is added to cells recovering from the effects of 24 h exposure to Ara-C, results in a clear synergism between the 2 drugs. This synergism is observed over a range of concentrations (5-100 nM), but is most significant at low doses, where inhibition of cell growth by Ara-C occurs but cell killing is minimal. Prior treatment with Ara-C increases the number of cells killed in the presence of steroid during the period 12-24 h after removal of the S-phase block. Combinations of Ara-C and steroid can thus be either synergistic or antagonistic, depending on the drug scheduling.