Implications of the dark axion portal for SHiP and FASER and the advantages of monophoton signals

We investigate the implications of the dark axion portal interaction, the axion-photon-dark photon vertex, for the future experiments SHiP and FASER. We also study the phenomenology of the combined vector portal (kinetic mixing of the photon and dark photon) and dark axion portal. The muon $g-2$ discrepancy is unfortunately not solved even with the two portals, but the low-energy beam dump experiments with monophoton detection capability can open new opportunities in light dark sector searches using the combined portals.Comment: 11 pages, 8 figures. v2 added an additional reference. v3 version published in Phys. Rev. D. Added discussion of MATHUSLA, REDTOP and NA6

Implications of the dark axion portal for the muon g-2, B-factories, fixed target neutrino experiments and beam dumps

The dark axion portal is a recently introduced portal between the standard model and the dark sector. It connects both the dark photon and the axion (or axion-like particle) to the photon simultaneously through an anomaly triangle. While the vector portal and the axion portal have been popular venues to search for the dark photon and axion, respectively, the new portal provides new detection channels if they coexist. The dark axion portal is not a result of the simple combination of the two portals, and its value is not determined by the other portal values; it should be tested independently. In this paper, we discuss implications of the new portal for the leptonic g-2, B-factories, fixed target neutrino experiments, and beam dumps. We provide the model-independent constraints on the axion-photon-dark photon coupling and discuss the sensitivities of the recently activated Belle-II experiment, which will play an important role in testing the new portal.Comment: 14 pages, 12 figures. v2 - Additional discussion and references added. v3 - Version accepted for publication by PRD. v4 - Correction to equation following Eq. (15

Susceptibility of a spinon Fermi surface coupled to a U(1) gauge field

We study the theory of a U(1) gauge field coupled to a spinon Fermi surface. Recently this model has been proposed as a possible description of the organic compound $\kappa-(BEDT-TTF)_2 Cu_2 (CN)_3$. We calculate the susceptibility of this system and in particular examine the effect of pairing of the underlying spin liquid. We show that this proposed theory is consistent with the observed susceptibility measurements.Comment: 5 pages, 4 figure

U(1) Gauge Theory of the Hubbard Model : Spin Liquid States and Possible Application to k-(BEDT-TTF)_2 Cu_2 (CN)_3

We formulate a U(1) gauge theory of the Hubbard model in the slave-rotor representation. From this formalism it is argued that spin liquid phases may exist near the Mott transition in the Hubbard model on triangular and honeycomb lattices at half filling. The organic compound k-(BEDT-TTF)_2 Cu_2 (CN)_3 is a good candidate for the spin liquid state on a triangular lattice. We predict a highly unusual temperature dependence for the thermal conductivity of this material.Comment: 5 pages, 2 figures; paper shortened and the phase diagram of anisotropic triangular lattice correcte

Vortex description of the fractionalized phase in exciton bose condensate

As a sequel to the previous work [Phys. Rev. B 72, 235104 (2005)] we present a vortex description of the fractionalized phase in exciton bose condensate. Magnetic flux line and monopole of the 3+1D emergent U(1) gauge theory are identified in the exciton picture. A bundle of vortex/anti-vortex pairs of all flavors of excitons corresponds to the magnetic flux line and a point at which the vortices and anti-vortices recombine is identified as magnetic monopole. This completes the magnetic sector of the low energy excitation in the fractionalized phase.Comment: 8 pages, 6 figures; clarification made in introductio

Senataxin: A Putative RNA: DNA Helicase Mutated in ALS4—Emerging Mechanisms of Genome Stability in Motor Neurons

Amyotrophic lateral sclerosis type 4 (ALS4) is a rare, autosomal dominant childhood- or adolescent-onset motor neuron disease caused by genetic defects in senataxin (SETX), a putative RNA–DNA helicase. Studies on the yeast SETX ortholog Sen1 revealed its role in small RNA termination pathways. It has been postulated that ALS4-associated neuronal pathologies could stem from defects in RNA metabolism and altered gene expression. Importantly, SETX prevents the accumulation of R-loops, which are potentially pathogenic RNA–DNA hybrids that stem from perturbations in transcription. SETX also interacts with the tumor suppressor BRCA1 that helps promote DNA double-strand break repair by homologous recombination. As such, SETX could contribute toward the removal of harmful R-loops and DSBs in postmitotic neurons. This chapter will visit the plausible mechanistic role of SETX in R-loop removal and DNA break repair that could prevent the activation of apoptotic cell death in neurons and pathological manifestation of ALS4

Parity in the Spanish healthcare system: an analysis of the policies of the Aznar and Zapatero governments of 1996-2008

Disparity within the Spanish healthcare system has been prevalent since the inception of the democracy after the fall of Franco. This disparity has particularly affected the poorer regions of Spain, which did not have the resources or infrastructure of the wealthier regions, such as the Basque Country and Catalonia. This thesis sought to analyze the policies of the national-level governments of the Popular Party's Jose Maria Aznar (1996-2000 and 2000-2004) and social democratic leader Jose Luis Rodriguez Zapatero (2004-present). After research on the policies of the governments and collection of data on healthcare expenditure per capita at each time point (the status of the healthcare system in 1996 before the first Aznar government and at the end of each government's term) in all regions of Spain, it was found that the PSOE government of Zapatero was more successful in promoting parity than the PP governments of Aznar

Immune and bacterial toxin genes expression in different giant tiger prawn, Penaeus monodon post-larvae stages following AHPND-causing strain of Vibrio parahaemolyticus challenge

Acute Hepatopancreatic Necrosis Disease (AHPND), a disease caused by Vibrio parahaemolyticus (V-PAHPND), kills Penaeid shrimps worldwide, resulting in severe economic losses during aquaculture. To further understand how Penaeus monodon post-larvae (PL) respond towards infection of this pathogenic bacterium, the expression of several important immune and bacterial toxin genes in three stages of P. monodon PL (PL15, PL30 and PL45) upon V-PAHPND challenge, were determined. A 20-hrs challenge test with 2.7 x 10(7) cfu ml(-1) of V-PADPND resulted 81, 65 and 1.7% mortality respectively for PL30, PL15 and PL45, indicating that PL30 was most vulnerable to V-PADPNEP The immune response of shrimp PL at this stage was robust, with Toll-like receptor (TLR), prophenoloxidase (proPO), lysozyme (lyso) and penaeidin (PEN) augmented approximately 10.7, 4.7, 6.5 and 3.2-fold, respectively. The expression initiated at one hour post-infection (h.p.i), peaked at 16 h.p.i and 20 h.p.i, and decreased at 18 h.p.i, indicating the crucial involvement of these immune related genes in the defence and recovery of the first-line defence mechanisms during V-PADPND infection. This work also revealed that toxR gene represents a good indicator gene for Vibrio detection whereas PIR A, for V-PADPND pathogenicity determination of P. monodon. Overall, these findings provided novel insights into the immune response and V-PADPND No susceptibility of different P. monodon PL stages during infection, with outcomes potentially useful in enhancing the application of health therapy and biosecured aquaculture practices to minimize the damaging risk of AHPND towards sustainable production of P. monodon