The Effective Lagrangian in the Randall-Sundrum Model and Electroweak Physics

We consider the two-brane Randall-Sundrum (RS) model with bulk gauge fields. We carefully match the bulk theory to a 4D low-energy effective Lagrangian. In addition to the four-fermion operators induced by KK exchange we find that large negative S and T parameters are induced in the effective theory. This is a tree-level effect and is a consequence of the shapes of the W and Z wave functions in the bulk. Such effects are generic in extra dimensional theories where the standard model (SM) gauge bosons have non-uniform wave functions along the extra dimension. The corrections to precision electroweak observables in the RS model are mostly dominated by S. We fit the parameters of the RS model to the experimental data and find somewhat stronger bounds than previously obtained; however, the standard model bound on the Higgs mass from precision measurements can only be slightly relaxed in this theory.Comment: 16 pages, LaTeX, 1 figure included, uses JHEP.cls, extended introduction, added reference

RS1, Custodial Isospin and Precision Tests

We study precision electroweak constraints within a RS1 model with gauge fields and fermions in the bulk. The electroweak gauge symmetry is enhanced to SU(2)_L \times SU(2)_R \times U(1)_{B-L}, thereby providing a custodial isospin symmetry sufficient to suppress excessive contributions to the T parameter. We then construct complete models, complying with all electroweak constraints, for solving the hierarchy problem, without supersymmetry or large hierarchies in the fundamental couplings. Using the AdS/CFT correspondence our models can be interpreted as dual to a strongly coupled conformal Higgs sector with global custodial symmetry, gauge and fermionic matter being fundamental fields external to the CFT. This scenario has interesting collider signals, distinct from other RS models in the literature.Comment: 32 pages, 6 figures, latex2e, minor changes, references adde

Search for CP violation in D0 and D+ decays

A high statistics sample of photoproduced charm particles from the FOCUS (E831) experiment at Fermilab has been used to search for CP violation in the Cabibbo suppressed decay modes D+ to K-K+pi+, D0 to K-K+ and D0 to pi-pi+. We have measured the following CP asymmetry parameters: A_CP(K-K+pi+) = +0.006 +/- 0.011 +/- 0.005, A_CP(K-K+) = -0.001 +/- 0.022 +/- 0.015 and A_CP(pi-pi+) = +0.048 +/- 0.039 +/- 0.025 where the first error is statistical and the second error is systematic. These asymmetries are consistent with zero with smaller errors than previous measurements.Comment: 12 pages, 4 figure

High-time Resolution Astrophysics and Pulsars

The discovery of pulsars in 1968 heralded an era where the temporal characteristics of detectors had to be reassessed. Up to this point detector integration times would normally be measured in minutes rather seconds and definitely not on sub-second time scales. At the start of the 21st century pulsar observations are still pushing the limits of detector telescope capabilities. Flux variations on times scales less than 1 nsec have been observed during giant radio pulses. Pulsar studies over the next 10 to 20 years will require instruments with time resolutions down to microseconds and below, high-quantum quantum efficiency, reasonable energy resolution and sensitive to circular and linear polarisation of stochastic signals. This chapter is review of temporally resolved optical observations of pulsars. It concludes with estimates of the observability of pulsars with both existing telescopes and into the ELT era.Comment: Review; 21 pages, 5 figures, 86 references. Book chapter to appear in: D.Phelan, O.Ryan & A.Shearer, eds.: High Time Resolution Astrophysics (Astrophysics and Space Science Library, Springer, 2007). The original publication will be available at http://www.springerlink.co

Prevalence of Frailty in European Emergency Departments (FEED): an international flash mob study

Introduction Current emergency care systems are not optimized to respond to multiple and complex problems associated with frailty. Services may require reconfiguration to effectively deliver comprehensive frailty care, yet its prevalence and variation are poorly understood. This study primarily determined the prevalence of frailty among older people attending emergency care. Methods This cross-sectional study used a flash mob approach to collect observational European emergency care data over a 24-h period (04 July 2023). Sites were identified through the European Task Force for Geriatric Emergency Medicine collaboration and social media. Data were collected for all individuals aged 65 + who attended emergency care, and for all adults aged 18 + at a subset of sites. Variables included demographics, Clinical Frailty Scale (CFS), vital signs, and disposition. European and national frailty prevalence was determined with proportions with each CFS level and with dichotomized CFS 5 + (mild or more severe frailty). Results Sixty-two sites in fourteen European countries recruited five thousand seven hundred eighty-five individuals. 40% of 3479 older people had at least mild frailty, with countries ranging from 26 to 51%. They had median age 77 (IQR, 13) years and 53% were female. Across 22 sites observing all adult attenders, older people living with frailty comprised 14%. Conclusion 40% of older people using European emergency care had CFS 5 + . Frailty prevalence varied widely among European care systems. These differences likely reflected entrance selection and provide windows of opportunity for system configuration and workforce planning

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Transcription of a 'photosynthetic' T4-type phage during infection of a marine cyanobacterium

The transcription of S-PM2 phage following infection of Synechococcus sp. WH7803, a marine cyanobacterium, was analysed by quantitative real-time PCR. Unlike the distantly related coliphage T4, there were only two (early and late) instead of three (early, middle and late) classes of transcripts during the developmental cycle of the phage. This difference is consistent with the absence from the S-PM2 genome of T4-like middle mode promoter sequences and the transcription factors associated with their recognition. Phage S-PM2 carries the 'photosynthetic' genes psbA and psbD that encode homologues of the host photosystem II proteins D1 and D2. Transcripts of the phage psbA gene appeared soon after infection and remained at high levels until lysis. Throughout the course of infection, the photosynthetic capacity of the cells remained constant. A considerable transient increase in the abundance of the host psbA transcripts occurred shortly after infection, suggesting that the host responds to the trauma of phage infection in a similar way as it does to a variety of other environmental stresses. The very substantial transcription of the phage psbA gene during the latter phase of phage infection suggests that S-PM2 has acquired this cellular gene to ensure that D1 levels and thus photosynthesis are fully maintained until the infected cell finally lyses. Unexpectedly, transcripts of a phage-encoded S-layer protein gene were among the earliest and most abundant detected, suggesting that this partial homologue of a host protein plays an important role in the S-PM2 infection process