Phenomenology of a light scalar: the dilaton

We make use of the language of non-linear realizations to analyze electro-weak symmetry breaking scenarios in which a light dilaton emerges from the breaking of a nearly conformal strong dynamics, and compare the phenomenology of the dilaton to that of the well motivated light composite Higgs scenario. We argue that -- in addition to departures in the decay/production rates into massless gauge bosons mediated by the conformal anomaly -- characterizing features of the light dilaton scenario (as well as other scenarios admitting a light CP-even scalar not directly related to the breaking of the electro-weak symmetry) are off-shell events at high invariant mass involving two longitudinally polarized vector bosons and a dilaton, and tree-level flavor violating processes. Accommodating both electro-weak precision measurements and flavor constraints appears especially challenging in the ambiguous scenario in which the Higgs and the dilaton fields strongly mix. We show that warped higgsless models of electro-weak symmetry breaking are explicit and tractable realizations of this limiting case. The relation between the naive radion profile often adopted in the study of holographic realizations of the light dilaton scenario and the actual dynamical dilaton field is clarified in the Appendix.Comment: 21 page

On a problem of Pillai with k-generalized Fibonacci numbers and powers of 2

For an integer $k\geq 2$, let $\{F^{(k)}_{n} \}_{n\geq 0}$ be the $k$--generalized Fibonacci sequence which starts with $0, \ldots, 0, 1$ ($k$ terms) and each term afterwards is the sum of the $k$ preceding terms. In this paper, we find all integers $c$ having at least two presentations as a difference between a $k$--generalized Fibonacci number and a powers of 2 for any fixed $k \geqslant 4$. This paper extends previous work from [9] for the case $k=2$ and [6] for the case $k=3$

Chaos in Robertson-Walker Cosmology

Chaos in Robertson-Walker cosmological models where gravity is coupled to one or more scalar fields has been studied by a few authors, mostly using numerical simulations. In this paper we begin a systematic study of the analytical aspect. We consider one conformally coupled scalar field and, using the fact that the model is integrable when the field is massless, we show in detail how homoclinic chaos arises for nonzero masses using a perturbative method.Comment: 16 pages, Tex, no figures. Minor changes have been added. To appear in Journal of Mathematical Physic

Precision measurement of the rotational energy-level structure of the three-electron molecule He2+_2^+

The term values of all rotational levels of the $^4$He{_2}^+\,X^+\,^2\Sigma_u^+\,(\nu^+=0) ground vibronic state with rotational quantum number $N^+\le 19$ have been determined with an accuracy of 8 x 10$^{-4}$ cm$^{-1}$ ($\sim{25}$ MHz) by MQDT-assisted Rydberg spectroscopy of metastable He$_2^*$. Comparison of these term values with term values recently calculated ab initio by Tung et al. [J. Chem. Phys. 136, 104309 (2012)] reveal discrepancies that rapidly increase with increasing rotational quantum number and reach values of 0.07 cm$^{-1}$ ($\sim{2.1}$ GHz) at $N^+=19$.Comment: 11 pages, 6 figure

Transport proteins determine drug sensitivity and resistance in a protozoan parasite, Trypanosoma brucei

Drug resistance in pathogenic protozoa is very often caused by changes to the ‘transportome’ of the parasites. In Trypanosoma brucei, several transporters have been implicated in uptake of the main classes of drugs, diamidines and melaminophenyl arsenicals. The resistance mechanism had been thought to be due to loss of a transporter known to carry both types of agents: the aminopurine transporter P2, encoded by the gene TbAT1. However, although loss of P2 activity is well-documented as the cause of resistance to the veterinary diamidine diminazene aceturate (Berenil®), cross-resistance between the human-use arsenical melarsoprol and the diamidine pentamidine (MPXR) is the result of loss of a separate High Affinity Pentamidine Transporter (HAPT1). A genome-wide RNAi library screen for resistance to pentamidine, published in 2012, gave the key to the genetic identity of HAPT1 by linking the phenomenon to a locus that contains the closely related T. brucei aquaglyceroporin genes TbAQP2 and TbAQP3. Further analysis determined that knockdown of only one pore, TbAQP2, produced the MPXR phenotype. TbAQP2 is an unconventional aquaglyceroporin with unique residues in the “selectivity region” of the pore, and it was found that in several MPXR lab strains the WT gene was either absent or replaced by a chimeric protein, recombined with parts of TbAQP3. Importantly, wild-type AQP2 was also absent in field isolates of T. b. gambiense, correlating with the outcome of melarsoprol treatment. Expression of a wild-type copy of TbAQP2 in even the most resistant strain completely reversed MPXR and re-introduced HAPT1 function and transport kinetics. Expression of TbAQP2 in Leishmania mexicana introduced a pentamidine transport activity indistinguishable from HAPT1. Although TbAQP2 has been shown to function as a classical aquaglyceroporin it is now clear that it is also a high affinity drug transporter, HAPT1. We discuss here a possible structural rationale for this remarkable ability