Universal turbulence on branes in holography

At a meson melting transition in holographic QCD, a weak turbulence of mesons was found with critical embeddings of probe D-branes in gravity duals. The turbulent mesons have a power-law energy distribution $\varepsilon_n \propto (\omega_n)^\alpha$ where $\omega_n$ is the mass of the $n$-th excited resonance of the meson tower. In this paper, we find that the turbulence power $\alpha$ is universal, irrespective of how the transition is driven, by numerically calculating the power in various static brane setups at criticality. We also find that the power $\alpha$ depends only on the cone dimensions of the probe D-branes.Comment: 28 pages, 16 figures, v2: a reference adde

Magnetic instability in AdS/CFT : Schwinger effect and Euler-Heisenberg Lagrangian of Supersymmetric QCD

To reveal the Schwinger effect for quarks, i.e., pair creation process of quarks and antiquarks, we derive the vacuum decay rate at strong coupling using AdS/CFT correspondence. Magnetic fields, in addition to the electric field responsible for the pair creation, causes prominent effects on the rate, and is important also in experiments such as RHIC/LHC heavy ion collisions. In this paper, through the gravity dual we obtain the full Euler-Heisenberg Lagrangian of N=2 supersymmetric QCD and study the Schwinger mechanism with not only a constant electric field but also a constant magnetic field as external fields. We determine the quark mass and temperature dependence of the Lagrangian. In sharp contrast with the zero magnetic field case, we find that the imaginary part, and thus the vacuum decay rate, diverges in the massless zero-temperature limit. This may be related to a strong instability of the QCD vacuum in strong magnetic fields. The real part of the Lagrangian serves as a generating function for non-linear electro-magnetic responses, and is found such that the Cotton-Mouton effect vanishes. Interestingly, our results of the Schwinger / Cotton-Mouton effects coincide precisely with those of N=2 supersymmetric QED.Comment: 21 pages. v2:references added, footnotes adde

Electromagnetic instability in holographic QCD

Using the AdS/CFT correspondence, we calculate the vacuum decay rate for the Schwinger effect in confining large $N_{c}$ gauge theories. The instability is induced by the quark antiquark pair creation triggered by strong electromagnetic fields. The decay rate is obtained as the imaginary part of the Euler-Heisenberg effective Lagrangian evaluated from the D-brane action with a constant electromagnetic field in holographic QCD models such as the Sakai-Sugimoto model and the deformed Sakai-Sugimoto model. The decay rate is found to increase with the magnetic field parallel to the electric field, while it decreases with the magnetic field perpendicular to the electric field. We discuss generic features of a critical electric field as a function of the magnetic field and the QCD string tension in the Sakai-Sugimoto model.Comment: 19 pages, v2: a reference adde

Somatic mutations affect key pathways in lung adenocarcinoma

Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well- classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers - including NF1, APC, RB1 and ATM - and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.National Human Genome Research InstituteWe thank A. Lash, M.F. Zakowski, M.G. Kris and V. Rusch for intellectual contributions, and many members of the Baylor Human Genome Sequencing Center, the Broad Institute of Harvard and MIT, and the Genome Center at Washington University for support. This work was funded by grants from the National Human Genome Research Institute to E.S.L., R.A.G. and R.K.W.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62885/1/nature07423.pd