On the relativistic origin of the kink effect in the chain of Pb isotopes

We investigate the origin of the kink effect (KE) in the relativistic mean field theory by transforming the single-particle Dirac equation into a Schrodinger-like equation. It is found that relativistic self-consistent effects as well as contributions from the rho meson determine the actual structure of the KE. However, the spin-orbit force generated by the rho meson has no significant influence on the KE.Comment: 11 pages, RevTeX, 3 postscript figs., Phys. Lett.

Relativistic Coulomb Sum Rules for (e,e′)(e,e^\prime)

A Coulomb sum rule is derived for the response of nuclei to $(e,e^\prime)$ scattering with large three-momentum transfers. Unlike the nonrelativistic formulation, the relativistic Coulomb sum is restricted to spacelike four-momenta for the most direct connection with experiments; an immediate consequence is that excitations involving antinucleons, e.g., $N{\bar N}$ pair production, are approximately eliminated from the sum rule. Relativistic recoil and Fermi motion of target nucleons are correctly incorporated. The sum rule decomposes into one- and two-body parts, with correlation information in the second. The one-body part requires information on the nucleon momentum distribution function, which is incorporated by a moment expansion method. The sum rule given through the second moment (RCSR-II) is tested in the Fermi gas model, and is shown to be sufficiently accurate for applications to data.Comment: 32 pages (LaTeX), 4 postscript figures available from the author

Oncogenic Signaling Pathways in The Cancer Genome Atlas

Genetic alterations in signaling pathways that control cell-cycle progression, apoptosis, and cell growth are common hallmarks of cancer, but the extent, mechanisms, and co-occurrence of alterations in these pathways differ between individual tumors and tumor types. Using mutations, copy-number changes, mRNA expression, gene fusions and DNA methylation in 9,125 tumors profiled by The Cancer Genome Atlas (TCGA), we analyzed the mechanisms and patterns of somatic alterations in ten canonical pathways: cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGFb signaling, p53 and beta-catenin/Wnt. We charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity. Eighty-nine percent of tumors had at least one driver alteration in these one alteration potentially targetable by currently available drugs. Thirty percent of tumors had multiple targetable alterations, indicating opportunities for combination therapy