44 research outputs found
The Minimal Phantom Sector of the Standard Model: Higgs Phenomenology and Dirac Leptogenesis
We propose the minimal, lepton-number conserving, SU(3)xSU(2)xU(1)
gauge-singlet, or phantom, extension of the Standard Model. The extension is
natural in the sense that all couplings are of O(1) or forbidden due to a
phantom sector global U(1)_D symmetry, and basically imitates the standard
Majorana see-saw mechanism. Spontaneous breaking of the U(1)_D symmetry
triggers consistent electroweak gauge symmetry breaking only if it occurs at a
scale compatible with small Dirac neutrino masses and baryogenesis through
Dirac leptogenesis. Dirac leptogenesis proceeds through the usual
out-of-equilibrium decay scenario, leading to left and right-handed neutrino
asymmetries that do not fully equilibrate after they are produced. The model
contains two physical Higgs bosons and a massless Goldstone boson. The
existence of the Goldstone boson suppresses the Higgs to bb branching ratio and
instead the Higgs bosons will mainly decay to invisible Goldstone and/or to
visible vector boson pairs. In a representative scenario, we estimate that with
30 fb^-1 integrated luminosity, the LHC could discover this invisibly decaying
Higgs, with mass ~120 GeV. At the same time a significantly heavier, partner
Higgs boson with mass ~210 GeV could be found through its vector boson decays.
Electroweak constraints as well as astrophysical and cosmological implications
are analysed and discussed.Comment: 21 pages, 4 figures. Corrected typos and added references. To appear
in JHE
A simple approach to describe hadron production rates in annihilation
We show that, based on the idea of string fragmentation, the production rates
of light flavored mesons and baryons originating from fragmentation can be
described by the spin, the binding energy of the particle, and a strangeness
suppression factor. Apart from a normalization factor, data at
different center-of-mass energies can be described simultaneously. Applying to
the heavy flavor production, we find that our predictions are in good agreement
with data.Comment: latex(stwol.sty), 4 pages, 2 figure
Singularities In Scalar-Tensor Cosmologies
In this article, we examine the possibility that there exist special
scalar-tensor theories of gravity with completely nonsingular FRW solutions.
Our investigation in fact shows that while most probes living in such a
Universe never see the singularity, gravity waves always do. This is because
they couple to both the metric and the scalar field, in a way which effectively
forces them to move along null geodesics of the Einstein conformal frame. Since
the metric of the Einstein conformal frame is always singular for
configurations where matter satisfies the energy conditions, the gravity wave
world lines are past inextendable beyond the Einstein frame singularity, and
hence the geometry is still incomplete, and thus singular. We conclude that the
singularity cannot be entirely removed, but only be made invisible to most, but
not all, probes in the theory.Comment: 23 pages, latex, no figure
Unconventional Cosmology
I review two cosmological paradigms which are alternative to the current
inflationary scenario. The first alternative is the "matter bounce", a
non-singular bouncing cosmology with a matter-dominated phase of contraction.
The second is an "emergent" scenario, which can be implemented in the context
of "string gas cosmology". I will compare these scenarios with the inflationary
one and demonstrate that all three lead to an approximately scale-invariant
spectrum of cosmological perturbations.Comment: 45 pages, 10 figures; invited lectures at the 6th Aegean Summer
School "Quantum Gravity and Quantum Cosmology", Chora, Naxos, Greece, Sept.
12 - 17 2012, to be publ. in the proceedings; these lecture notes form an
updated version of arXiv:1003.1745 and arXiv:1103.227
EXTL3 mutations cause skeletal dysplasia, immune deficiency, and developmental delay.
We studied three patients with severe skeletal dysplasia, T cell immunodeficiency, and developmental delay. Whole-exome sequencing revealed homozygous missense mutations affecting exostosin-like 3 (EXTL3), a glycosyltransferase involved in heparan sulfate (HS) biosynthesis. Patient-derived fibroblasts showed abnormal HS composition and altered fibroblast growth factor 2 signaling, which was rescued by overexpression of wild-type EXTL3 cDNA. Interleukin-2-mediated STAT5 phosphorylation in patients' lymphocytes was markedly reduced. Interbreeding of the extl3-mutant zebrafish (box) with Tg(rag2:green fluorescent protein) transgenic zebrafish revealed defective thymopoiesis, which was rescued by injection of wild-type human EXTL3 RNA. Targeted differentiation of patient-derived induced pluripotent stem cells showed a reduced expansion of lymphohematopoietic progenitor cells and defects of thymic epithelial progenitor cell differentiation. These data identify EXTL3 mutations as a novel cause of severe immune deficiency with skeletal dysplasia and developmental delay and underline a crucial role of HS in thymopoiesis and skeletal and brain development
Transcription factor induction of vascular blood stem cell niches in vivo
The hematopoietic niche is a supportive microenvironment composed of distinct cell types, including specialized vascular endothelial cells that directly interact with hematopoietic stem and progenitor cells (HSPCs). The molecular factors that specify niche endothelial cells and orchestrate HSPC homeostasis remain largely unknown. Using multi-dimensional gene expression and chromatin accessibility analyses in zebrafish, we define a conserved gene expression signature and cis-regulatory landscape that are unique to sinusoidal endothelial cells in the HSPC niche. Using enhancer mutagenesis and transcription factor overexpression, we elucidate a transcriptional code that involves members of the Ets, Sox, and nuclear hormone receptor families and is sufficient to induce ectopic niche endothelial cells that associate with mesenchymal stromal cells and support the recruitment, maintenance, and division of HSPCs in vivo. These studies set forth an approach for generating synthetic HSPC niches, in vitro or in vivo, and for effective therapies to modulate the endogenous niche