The global electroweak fit at NNLO and prospects for the LHC and ILC

For a long time, global fits of the electroweak sector of the Standard Model (SM) have been used to exploit measurements of electroweak precision observables at lepton colliders (LEP, SLC), together with measurements at hadron colliders (Tevatron, LHC), and accurate theoretical predictions at multi-loop level, to constrain free parameters of the SM, such as the Higgs and top masses. Today, all fundamental SM parameters entering these fits are experimentally determined, including information on the Higgs couplings, and the global fits are used as powerful tools to assess the validity of the theory and to constrain scenarios for new physics. Future measurements at the Large Hadron Collider (LHC) and the International Linear Collider (ILC) promise to improve the experimental precision of key observables used in the fits. This paper presents updated electroweak fit results using newest NNLO theoretical predictions, and prospects for the LHC and ILC. The impact of experimental and theoretical uncertainties is analysed in detail. We compare constraints from the electroweak fit on the Higgs couplings with direct LHC measurements, and examine present and future prospects of these constraints using a model with modified couplings of the Higgs boson to fermions and bosons.Comment: 26 pages, 9 figure

HistFitter software framework for statistical data analysis

We present a software framework for statistical data analysis, called HistFitter, that has been used extensively by the ATLAS Collaboration to analyze big datasets originating from proton-proton collisions at the Large Hadron Collider at CERN. Since 2012 HistFitter has been the standard statistical tool in searches for supersymmetric particles performed by ATLAS. HistFitter is a programmable and flexible framework to build, book-keep, fit, interpret and present results of data models of nearly arbitrary complexity. Starting from an object-oriented configuration, defined by users, the framework builds probability density functions that are automatically fitted to data and interpreted with statistical tests. A key innovation of HistFitter is its design, which is rooted in core analysis strategies of particle physics. The concepts of control, signal and validation regions are woven into its very fabric. These are progressively treated with statistically rigorous built-in methods. Being capable of working with multiple data models at once, HistFitter introduces an additional level of abstraction that allows for easy bookkeeping, manipulation and testing of large collections of signal hypotheses. Finally, HistFitter provides a collection of tools to present results with publication-quality style through a simple command-line interface.Comment: 35 pages (excluding appendix) and 10 figures. Code publicly available at: http://cern.ch/histfitte

Association of ABCB1, 5-HT3B receptor and CYP2D6 genetic polymorphisms with ondansetron and metoclopramide antiemetic response in Indonesian cancer patients treated with highly emetogenic chemotherapy.

Our study shows that in Indonesian cancer patients treated with highly cytostatic emetogenic, carriership of the CTG haplotype of the ABCB1 gene is related to an increased risk of delayed chemotherapy-induced nausea and vomiting

Approximate Homomorphisms of Ternary Semigroups

A mapping $f:(G_1,[ ]_1)\to (G_2,[ ]_2)$ between ternary semigroups will be called a ternary homomorphism if $f([xyz]_1)=[f(x)f(y)f(z)]_2$. In this paper, we prove the generalized Hyers--Ulam--Rassias stability of mappings of commutative semigroups into Banach spaces. In addition, we establish the superstability of ternary homomorphisms into Banach algebras endowed with multiplicative norms.Comment: 10 page

Effect of beta-adrenergic stimulation on whole-body and abdominal subcutaneous adipose tissue lipolysis in lean and obese men

AIMS/HYPOTHESIS: Obesity is characterised by increased triacylglycerol storage in adipose tissue. There is in vitro evidence for a blunted beta-adrenergically mediated lipolytic response in abdominal subcutaneous adipose tissue (SAT) of obese individuals and evidence for this at the whole-body level in vivo. We hypothesised that the beta-adrenergically mediated effect on lipolysis in abdominal SAT is also impaired in vivo in obese humans. METHODS: We investigated whole-body and abdominal SAT glycerol metabolism in vivo during 3 h and 6 h [2H5]glycerol infusions. Arterio-venous concentration differences were measured in 13 lean and ten obese men after an overnight fast and during intravenous infusion of the non-selective beta-adrenergic agonist isoprenaline [20 ng (kg fat free mass)(-1) min(-1)]. RESULTS: Lean and obese participants showed comparable fasting glycerol uptake by SAT (9.7+/-3.4 vs 9.3+/-2.5% of total release, p=0.92). Furthermore, obese participants showed an increased whole-body beta-adrenergically mediated lipolytic response versus lean participants. However, their fasting lipolysis was blunted [glycerol rate of appearance: 7.3+/-0.6 vs 13.1+/-0.9 micromol (kg fat mass)(-1) min(-1), p<0.01], as was the beta-adrenergically mediated lipolytic response per unit SAT [Delta total glycerol release: 140+/-71 vs 394+/-112 nmol (100 g tissue)(-1) min(-1), p<0.05] compared with lean participants. Net triacylglycerol flux tended to increase in obese compared with lean participants during beta-adrenergic stimulation [Delta net triacylglycerol flux: 75+/-32 vs 16+/-11 nmol (100 g tissue)(-1) min(-1), p=0.06]. CONCLUSIONS/INTERPRETATION: We demonstrated in vivo that beta-adrenergically mediated lipolytic response is impaired systematically and in abdominal SAT of obese versus lean men. This may be important in the development or maintenance of increased triacylglycerol stores and obesity

Changes in subcellular doxorubicin distribution and cellular accumulation alone can largely account for doxorubicin resistance in SW-1573 lung cancer and MCF-7 breast cancer multidrug resistant tumour cells.

Doxorubicin accumulation defects in multidrug resistant tumour cells are generally small in comparison to the resistance factors. Therefore additional mechanisms must be operative. In this paper we show by a quantitative approach that doxorubicin resistance in several P-glycoprotein-positive non-small cell lung cancer and breast cancer multidrug resistant cell lines can be explained by a summation of accumulation defect and alterations in the efficacy of the drug once present in the cell. This alteration of efficacy was partly due to changes in intracellular drug localisation, characterised by decreased nuclear/cytoplasmic doxorubicin fluorescence ratios (N/C-ratios). N/C-ratios were 2.8-3.6 in sensitive cells, 0.1-0.4 in cells with high (> 70-fold) levels of doxorubicin resistance and 1.2 and 1.9 in cells with low or intermediate (7.5 and 24-fold, respectively) levels of doxorubicin resistance. The change of drug efficacy was reflected by an increase in the total amount of doxorubicin present in the cell at equitoxic (IC50) concentrations. N/C ratios in highly resistant P-glycoprotein-containing cells could be increased with the resistance modifier verapamil to values of 1.3-2.7, a process that was paralleled by a decrease of the cellular doxorubicin amounts present at IC50. At the low to moderate residual levels of resistance, obtained with different concentrations of verapamil, a linear relationship between IC50 and cellular doxorubicin amounts determined at IC50 was found. This shows that at this stage of residual resistance, extra reversal by verapamil should be explained by further increase of drug efficacy rather than by increase of cellular drug accumulation. A similar relationship was found for P-glycoprotein-negative MDR cells with low levels of resistance. Since in these cells N/C ratios could not be altered, verapamil-induced decrease of IC50 must be due to increased drug efficacy by action on as yet unidentified targets. Although the IC50 of sensitive human cells cannot be reached with resistance modifiers, when using these relationships it can be shown by extrapolation that cellular and nuclear doxorubicin amounts at IC50 at complete reversal of resistance were the same as in sensitive cells. It is concluded that doxorubicin resistance factors for multidrug resistant cells can for a large part, and in the case of P-glycoprotein-containing cells probably fully, be accounted for by decreased amounts of drug at nuclear targets, which in turn is characterised by two processes only: decreased cellular accumulation and a shift in the ratio nuclear drug/cytoplasmic drug

Probing for Invisible Higgs Decays with Global Fits

We demonstrate by performing a global fit on Higgs signal strength data that large invisible branching ratios Br_{inv} for a Standard Model (SM) Higgs particle are currently consistent with the experimental hints of a scalar resonance at the mass scale m_h ~ 124 GeV. For this mass scale, we find Br_{inv} < 0.64 (95 % CL) from a global fit to individual channel signal strengths supplied by ATLAS, CMS and the Tevatron collaborations. Novel tests that can be used to improve the prospects of experimentally discovering the existence of a Br_{inv} with future data are proposed. These tests are based on the combination of all visible channel Higgs signal strengths, and allow us to examine the required reduction in experimental and theoretical errors in this data that would allow a more significantly bounded invisible branching ratio to be experimentally supported. We examine in some detail how our conclusions and method are affected when a scalar resonance at this mass scale has couplings deviating from the SM ones.Comment: 32pp, 15 figures v2: JHEP version, ref added & comment added after Eq.

Early multidrug resistance, defined by changes in intracellular doxorubicin distribution, independent of P-glycoprotein.

Resistance to multiple antitumour drugs, mostly antibiotics or alkaloids, has been associated with a cellular plasma membrane P-glycoprotein (Pgp), causing energy-dependent transport of drugs out of cells. However, in many common chemotherapy resistant human cancers there is no overexpression of Pgp, which could explain drug resistance. In order to characterise early steps in multidrug resistance we have derived a series of P-glycoprotein-positive (Pgp/+) and P-glycoprotein-negative (Pgp/-) multidrug resistant cell lines, from a human non-small cell lung cancer cell line, SW-1573, by stepwise selection with increasing concentrations of doxorubicin. These cells were exposed to doxorubicin and its fluorescence in nucleus (N) and cytoplasm (C) was quantified with laserscan microscopy and image analysis. The fluorescence N/C ratio in parent cells was 3.8 and decreased both in Pgp/+ and Pgp/- cells with increasing selection pressure to 1.2-2.6 for cells with a resistance factor of 7-17. N/C ratios could be restored partly with verapamil only in Pgp/+ cells. N/C ratio measurements may define a general Pgp-independent type of defense of mammalian cells against certain anticancer agents which may precede Pgp expression in early doxorubicin resistance