Search for a Structure in the B_{s}^{0}π^{±} Invariant Mass Spectrum with the ATLAS Experiment.

A search for the narrow structure, X(5568), reported by the D0 Collaboration in the decay sequence X→B_{s}^{0}π^{±}, B_{s}^{0}→J/ψϕ, is presented. The analysis is based on a data sample recorded with the ATLAS detector at the LHC corresponding to 4.9  fb^{-1} of pp collisions at 7 TeV and 19.

SOX17 Regulates Conversion of Human Fibroblasts Into Endothelial Cells and Erythroblasts by Dedifferentiation Into CD34 Progenitor Cells.

Background: The mechanisms underlying the dedifferentiation and lineage conversion of adult human fibroblasts into functional endothelial cells have not yet been fully defined. Furthermore, it is not known whether fibroblast dedifferentiation recapitulates the generation of multipotent progenitors during embryonic development, which give rise to endothelial and hematopoietic cell lineages. Here we established the role of the developmental transcription factor SOX17 in regulating the bilineage conversion of fibroblasts by the generation of intermediate progenitors.

Determination of the Ratio of b-Quark Fragmentation Fractions f(s)/f(d) in pp Collisions at √s=7 TeV with the ATLAS Detector.

With an integrated luminosity of 2.47  fb(-1) recorded by the ATLAS experiment at the LHC, the exclusive decays B(s)(0)→J/ψϕ and B(d)(0)→J/ψK(*0) of B mesons produced in pp collisions at √s=7  TeV are used to determine the ratio of fragmentation fractions f(s)/f(d). From the observed B(s)(0)→J/ψϕ and B(d)(0)→J/ψK(*0) yields, the quantity (f(s)/f(d))[B(B(s)(0)→J/ψϕ)/B(B(d)(0)→J/ψK(*0))] is measured to be 0.

Survivin-induced abnormal ploidy contributes to cystic kidney and aneurysm formation.

Background: Cystic kidneys and vascular aneurysms are clinical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology (ciliopathy). Survivin overexpression is associated with cancer, but the clinical pathology associated with survivin downregulation or knockout has never been studied before. The present studies aim to examine whether and how cilia function (Pkd1 or Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin downregulation.