Electroweak Fits and Constraints on the Higgs Mass

The current status of the quantities entering into the global electroweak fits is reviewed, highlighting changes since Summer 2003. These data include the precision electroweak properties of the Z and W bosons, the top-quark mass and the value of the electromagnetic coupling constant, at the scale of the Z boson mass. Using these Z and W (high Q^2) data, the value of the Higss mass is extracted, within the context of the Standard Model (SM). The consistency of the data, and the overall agreement with the SM, are discussed.Comment: 8 pages, 5 postscript figure

Are there anomalous Z fermion couplings ?

The couplings of the fermions to the Z boson are of great importance in establishing the validity of the Standard Model and in looking for physics beyond it. The couplings of the b-quark to the Z boson have been the subject of much experimental study and theoretical interpretation. The apparent excess in the value of \Rbbz, the ratio of the partial width of the Z boson to \bbbar to its total hadronic width, above the Standard Model expectation reported a few years ago has now become much less significant. However, the measurements of the pole forward-backward asymmetry \Afbzb for b-quarks at the Z pole and of the {\it polarisation parameter} \Ab, obtained using a polarised electron beam, have improved considerably in accuracy. The latest data are examined and values of the vector and axial-vector b-quark and c-quark couplings to the Z are extracted. The left and right handed couplings are also extracted. It is found that whereas the c-quark couplings are compatible with the Standard Model, those of the b-quark data are only compatible with the Standard Model at about the 1% level. In addition, the individual lepton couplings are extracted and the hypothesis of {\it lepton universality} is examined. The sensitivity of the limits from electroweak fits to the Higgs boson mass to these data is examined.Comment: 16 pages, 6 figures. Figure captions correcte

Precise bounds on the Higgs boson mass

We study the renormalization group evolution of the Higgs quartic coupling $\lambda_{H}$ and the Higgs mass $m_{H}$ in the Standard Model. The one loop equation for $\lambda_{H}$ is non linear and it is of the Riccati type which we numerically and analytically solve in the energy range $[m_{t},E_{GU}]$ where $m_{t}$ is the mass of the top quark and $E_{GU}=10^{14}$ GeV. We find that depending on the value of $\lambda_{H}(m_{t})$ the solution for $\lambda_{H}(E)$ may have singularities or zeros and become negative in the former energy range so the ultra violet cut off of the standard model should be below the energy where the zero or singularity of $\lambda_{H}$ occurs. We find that for $0.369\leq\lambda_{H}(m_{t})\leq0.613$ the Standard Model is valid in the whole range $[m_{t},E_{GU}]$. We consider two cases of the Higgs mass relation to the parameters of the standard model: (a) the effective potential method and (b) the tree level mass relations. The limits for $\lambda_{H}(m_{t})$ correspond to the following Higgs mass relation $150\leq m_{H}\lessapprox 193$ GeV. We also plot the dependence of the ultra violet cut off on the value of the Higgs mass. We analyze the evolution of the vacuum expectation value of the Higgs field and show that it depends on the value of the Higgs mass. The pattern of the energy behavior of the VEV is different for the cases (a) and (b). The behavior of $\lambda_{H}(E)$, $m_{H}(E)$ and $v(E)$ indicates the existence of a phase transition in the standard model. For the effective potential this phase transition occurs at the mass range $m_{H}\approx 180$ GeV and for the tree level mass relations at $m_{H}\approx 168$ GeV.Comment: 14 pages, 7 figures. Expanded the discussion of the Higgs mass relation between the parameters of the Standard Model. Included the method of the Higgs effective potentia

Precision Electroweak Tests of the Standard Model

The present status of precision electroweak data is reviewed. These data include measurements of e+e- -> f+fbar, taken at the Z resonance at LEP, which are used to determine the mass and width of the Z boson. In addition, measurements have also been made of the forward-backward asymmetries for leptons and heavy quarks, and also the final state polarisation of the tau-lepton. At SLAC, where the electron beam was polarised, measurements were made of the left-right polarised asymmetry, A_LR, and the left-right forward-backward asymmetries for b and c quarks. The mass, MW, and width, GW, of the W boson have been measured at the Tevatron and at LEP, and the mass of the top quark, Mt, has been measured at the Tevatron. These data, plus other electroweak data, are used in global electroweak fits in which various Standard Model parameters are determined. A comparison is made between the results of the direct measurements of MW and Mt with the indirect results coming from electroweak radiative corrections. Using all precision electroweak data fits are also made to determine limits on the mass of the Higgs boson. The influence on these limits of specific measurements, particularly those which are somewhat inconsistent with the Standard Model, is explored. The data are also analysed in terms of the quasi model-independent epsilon variables. Finally, the impact on the electroweak fits of the improvements in the determination of the W-boson and top-quark masses, expected from the Tevatron Run 2, is examined.Comment: 80 pages, 36 Figures, Late

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Genetic epidemiology of motor neuron disease-associated variants in the Scottish population

Genetic understanding of motor neuron disease (MND) has evolved greatly in the past 10 years, including the recent identification of association between MND and variants in TBK1 and NEK1. Our aim was to determine the frequency of pathogenic variants in known MND genes and to assess whether variants in TBK1 and NEK1 contribute to the burden of MND in the Scottish population. SOD1, TARDBP, OPTN, TBK1, and NEK1 were sequenced in 441 cases and 400 controls. In addition to 44 cases known to carry a C9orf72 hexanucleotide repeat expansion, we identified 31 cases and 2 controls that carried a loss-of-function or pathogenic variant. Loss-of-function variants were found in TBK1 in 3 cases and no controls and, separately, in NEK1 in 3 cases and no controls. This study provides an accurate description of the genetic epidemiology of MND in Scotland and provides support for the contribution of both TBK1 and NEK1 to MND susceptibility in the Scottish population

In pursuit of visual attention: SSVEP frequency-tagging moving targets.

Previous research has shown that visual attention does not always exactly follow gaze direction, leading to the concepts of overt and covert attention. However, it is not yet clear how such covert shifts of visual attention to peripheral regions impact the processing of the targets we directly foveate as they move in our visual field. The current study utilised the co-registration of eye-position and EEG recordings while participants tracked moving targets that were embedded with a 30 Hz frequency tag in a Steady State Visually Evoked Potentials (SSVEP) paradigm. When the task required attention to be divided between the moving target (overt attention) and a peripheral region where a second target might appear (covert attention), the SSVEPs elicited by the tracked target at the 30 Hz frequency band were significantly, but transiently, lower than when participants did not have to covertly monitor for a second target. Our findings suggest that neural responses of overt attention are only briefly reduced when attention is divided between covert and overt areas. This neural evidence is in line with theoretical accounts describing attention as a pool of finite resources, such as the perceptual load theory. Altogether, these results have practical implications for many real-world situations where covert shifts of attention may discretely reduce visual processing of objects even when they are directly being tracked with the eyes

NEK1 variants confer susceptibility to amyotrophic lateral sclerosis

To identify genetic factors contributing to amyotrophic lateral sclerosis (ALS), we conducted whole-exome analyses of 1,022 index familial ALS (FALS) cases and 7,315 controls. In a new screening strategy, we performed gene-burden analyses trained with established ALS genes and identified a significant association between loss-of-function (LOF) NEK1 variants and FALS risk. Independently, autozygosity mapping for an isolated community in the Netherlands identified a NEK1 p.Arg261His variant as a candidate risk factor. Replication analyses of sporadic ALS (SALS) cases and independent control cohorts confirmed significant disease association for both p.Arg261His (10,589 samples analyzed) and NEK1 LOF variants (3,362 samples analyzed). In total, we observed NEK1 risk variants in nearly 3% of ALS cases. NEK1 has been linked to several cellular functions, including cilia formation, DNA-damage response, microtubule stability, neuronal morphology and axonal polarity. Our results provide new and important insights into ALS etiopathogenesis and genetic etiology

The Prevalence of Sexually Transmitted Infections in Papua New Guinea: A Systematic Review and Meta-Analysis

Patellofemoral osteoarthritis (PF OA) is more prevalent than previously thought and contributes to patient's suffering from knee OA. Synthesis of prevalence data can provide estimates of the burden of PF OA

TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions

Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9orf72) have recently been linked to frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis, and may be the most common genetic cause of both neurodegenerative diseases. Genetic variants at TMEM106B influence risk for the most common neuropathological subtype of FTLD, characterized by inclusions of TAR DNA-binding protein of 43 kDa (FTLD-TDP). Previous reports have shown that TMEM106B is a genetic modifier of FTLD-TDP caused by progranulin (GRN) mutations, with the major (risk) allele of rs1990622 associating with earlier age at onset of disease. Here, we report that rs1990622 genotype affects age at death in a single-site discovery cohort of FTLD patients with C9orf72 expansions (n = 14), with the major allele correlated with later age at death (p = 0.024). We replicate this modifier effect in a 30-site international neuropathological cohort of FTLD-TDP patients with C9orf72 expansions (n = 75), again finding that the major allele associates with later age at death (p = 0.016), as well as later age at onset (p = 0.019). In contrast, TMEM106B genotype does not affect age at onset or death in 241 FTLD-TDP cases negative for GRN mutations or C9orf72 expansions. Thus, TMEM106B is a genetic modifier of FTLD with C9orf72 expansions. Intriguingly, the genotype that confers increased risk for developing FTLD-TDP (major, or T, allele of rs1990622) is associated with later age at onset and death in C9orf72 expansion carriers, providing an example of sign epistasis in human neurodegenerative disease