Universal scaling relation in high-temperature superconductors

Scaling laws express a systematic and universal simplicity among complex systems in nature. For example, such laws are of enormous significance in biology. Scaling relations are also important in the physical sciences. The seminal 1986 discovery of high transition-temperature (high-T_c) superconductivity in cuprate materials has sparked an intensive investigation of these and related complex oxides, yet the mechanism for superconductivity is still not agreed upon. In addition, no universal scaling law involving such fundamental properties as T_c and the superfluid density \rho_s, a quantity indicative of the number of charge carriers in the superconducting state, has been discovered. Here we demonstrate that the scaling relation \rho_s \propto \sigma_{dc} T_c, where the conductivity \sigma_{dc} characterizes the unidirectional, constant flow of electric charge carriers just above T_c, universally holds for a wide variety of materials and doping levels. This surprising unifying observation is likely to have important consequences for theories of high-T_c superconductivity.Comment: 11 pages, 2 figures, 2 table

Chemical potential oscillations from a single nodal pocket in the underdoped high-Tc superconductor YBa2Cu3O6+x

The mystery of the normal state in the underdoped cuprates has deepened with the use of newer and complementary experimental probes. While photoemission studies have revealed solely `Fermi arcs' centered on nodal points in the Brillouin zone at which holes aggregate upon doping, more recent quantum oscillation experiments have been interpreted in terms of an ambipolar Fermi surface, that includes sections containing electron carriers located at the antinodal region. To address the question of whether an ambipolar Fermi surface truly exists, here we utilize measurements of the second harmonic quantum oscillations, which reveal that the amplitude of these oscillations arises mainly from oscillations in the chemical potential, providing crucial information on the nature of the Fermi surface in underdoped YBa2Cu3O6+x. In particular, the detailed relationship between the second harmonic amplitude and the fundamental amplitude of the quantum oscillations leads us to the conclusion that there exists only a single underlying quasi-two dimensional Fermi surface pocket giving rise to the multiple frequency components observed via the effects of warping, bilayer splitting and magnetic breakdown. A range of studies suggest that the pocket is most likely associated with states near the nodal region of the Brillouin zone of underdoped YBa2Cu3O6+x at high magnetic fields.Comment: 7 pages, 4 figure

The connection between superconducting phase correlations and spin excitations in YBa2_2Cu3_3O6.6_{6.6}: A magnetic field study

One of the most striking universal properties of the high-transition-temperature (high-$T_c$) superconductors is that they are all derived from the hole-doping of their insulating antiferromagnetic (AF) parent compounds. From the outset, the intimate relationship between magnetism and superconductivity in these copper-oxides has intrigued researchers. Evidence for this link comes from neutron scattering experiments that show the unambiguous presence of short-range AF correlations (excitations) in cuprate superconductors. Even so, the role of such excitations in the pairing mechanism and superconductivity is still a subject of controversy. For YBa$_2$Cu$_3$O$_{6+x}$, where $x$ controls the hole-doping level, the most prominent feature in the magnetic excitations spectra is the ``resonance''. Here we show that for underdoped YBa$_2$Cu$_3$O$_{6.6}$, where $x$ and $T_c$ are below the optimal values, modest magnetic fields suppress the resonance significantly, much more so for fields approximately perpendicular rather than parallel to the CuO$_2$ planes. Our results indicate that the resonance measures pairing and phase coherence, suggesting that magnetism plays an important role in the superconductivity of cuprates. The persistence of a field effect above $T_c$ favors mechanisms with preformed pairs in the normal state of underdoped cuprates.Comment: 12 pages, 4 figures, Nature (in press

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Expression and pharmacological inhibition of TrkB and EGFR in glioblastoma

A member of the Trk family of neurotrophin receptors, tropomyosin receptor kinase B (TrkB, encoded by the NTRK2 gene) is an increasingly important target in various cancer types, including glioblastoma (GBM). EGFR is among the most frequently altered oncogenes in GBM, and EGFR inhibition has been tested as an experimental therapy. Functional interactions between EGFR and TrkB have been demonstrated. In the present study, we investigated the role of TrkB and EGFR, and their interactions, in GBM. Analyses of NTRK2 and EGFR gene expression from The Cancer Genome Atlas (TCGA) datasets showed an increase in NTRK2 expression in the proneural subtype of GBM, and a strong correlation between NTRK2 and EGFR expression in glioma CpG island methylator phenotype (G-CIMP+) samples. We showed that when TrkB and EGFR inhibitors were combined, the inhibitory effect on A172 human GBM cells was more pronounced than when either inhibitor was given alone. When U87MG GBM cells were xenografted into the flank of nude mice, tumor growth was delayed by treatment with TrkB and EGFR inhibitors, given alone or combined, only at specific time points. Intracranial GBM growth in mice was not significantly affected by drug treatments. Our findings indicate that correlations between NTRK2 and EGFR expression occur in specific GBM subgroups. Also, our results using cultured cells suggest for the first time the potential of combining TrkB and EGFR inhibition for the treatment of GBM