Radiative corrections to W gamma gamma production at the LHC

Radiative W production at hadron colliders is an important testing ground for the Standard Model. We consider W gamma gamma production which is sensitive to the quartic WW gamma gamma coupling. Furthermore the Standard Model amplitude for this process contains a radiation zero. We present a calculation of the NLO QCD corrections for W gamma gamma production at the LHC.Comment: 6 pages, talk given at RADCOR 2009 - 9th International Symposium on Radiative Corrections (Applications of Quantum Field Theory to Phenomenology) October 25-30 2009, Ascona, Switzerlan

Full NLO massive gauge boson pair production at the LHC

Electroweak gauge boson pair production is a very important process at the LHC as it probes the non-abelian structure of electroweak interactions and is a background process for many searches. We present full next-to-leading order predictions for the production cross sections and distributions of on-shell massive gauge boson pair production in the Standard Model, including both QCD and electroweak corrections. The hierarchy between the ZZ, WW and WZ channels, observed in the transverse momentum distributions, will be analyzed. We will also present a comparison with experimental data for the total cross sections including a study of the theoretical uncertainties.Comment: 4 pages, 4 figures. Proceeding of the inaugural conference "Windows on the Universe" (August 11-17, Quy Nhon, Vietnam) including updated results compared to arXiv:1307.433

NLO corrections to WWZ and ZZZ production at the ILC

We calculate the full one-loop electroweak corrections to tri-boson production (ZZZ and WWZ) at the ILC. This is important to understand the Standard Model (SM) gauge quartic couplings which can be a window on the mechanism of spontaneous symmetry breaking. We find that even after subtracting the leading QED corrections, the electroweak corrections can still be large especially as the energy increases.Comment: 7 pages, proceedings of the 3rd CPP Workshop, September 23-25, 2010, KEK Tsukuba Japa

Gluon-Induced Weak Boson Fusion

The gluon-gluon induced terms for Higgs production through weak boson fusion (WBF) are computed. Formally, these are of NNLO in the strong coupling constant. This is the lowest order at which non-zero color exchange occurs between the scattering quarks, leading to a color field and thus additional hadronic activity between the outgoing jets. Using a minimal set of cuts, the numerical impact of these terms is at the percent level with respect to the NLO rate for weak boson fusion. Applying the so-called WBF cuts leads to an even stronger suppression, so that we do not expect a significant deterioration of the WFB signal by these color exchange effects.Comment: 9 pages, 8 figures (21 included ps- and eps-files

NLO corrections to e+e- to WWZ and e+e- to ZZZ

We calculate the one-loop electroweak corrections to e+e- to WWZ and e+e- to ZZZ and analyse their impacts on both the total cross section and some key distributions. These processes are important for the measurements of the quartic couplings of the massive gauge bosons which can be a window on the mechanism of spontaneous symmetry breaking. We find that even after subtracting the leading QED corrections, the electroweak corrections can still be large especially as the energy increases. We compare and implement different methods of dealing with potential instabilities in the routines pertaining to the loop integrals. For the real corrections we apply a dipole subtraction formalism and compare it to a phase-space slicing method.Comment: 19 pages, a few comments and references added, version published in PRD

Local thermodynamical equilibrium and the equation of state of hot, dense matter created in Au+Au collisions at AGS

Local kinetic and chemical equilibration is studied for Au+Au collisions at 10.7 AGeV in the microscopic Ultrarelativistic Quantum Molecular Dynamics model (UrQMD). The UrQMD model exhibits dramatic deviations from equilibrium during the high density phase of the collision. Thermal and chemical equilibration of the hadronic matter seems to be established in the later stages during a quasiisentropic expansion, observed in the central reaction cell with volume 125 fm3. For t > 10 fm/c the hadron energy spectra in the cell are nicely reproduced by Boltzmann distributions with a common rapidly dropping temperature. Hadron yields change drastically and at the late expansion stage follow closely those of an ideal gas statistical model. The equation of state seems to be simple at late times: P = 0.12 Epsilon. The time evolution of other thermodynamical variables in the cell is also presented

Effects of oxidized low density lipoprotein, lipid mediators and statins on vascular cell interactions

The integrin heterodimer CD11b/CD18 (alpha M beta 2, Mac-1, CR3) expressed on monocytes or polymorphonuclear leukocytes (PMN) is a receptor for iC3b, fibrinogen, heparin, and for intercellular adhesion molecule (ICAM)-1 on endothelium, crucially contributing to vascular cell interactions in inflammation and atherosclerosis. In this report, we summarize our findings on the effects of lipid mediators and lipid-lowering drugs. Exposure of endothelial cells to oxidized low density lipoprotein (oxLDL) induces upregulation of ICAM-1 and increases adhesion of monocytic cells expressing Mac-1. Inhibition experiments show that monocytes use distinct ligands, i.e. ICAM-1 and heparan sulfate proteoglycans for adhesion to oxLDL-treated endothelium. An albumin-transferable oxLDL activity is inhibited by the antioxidant pyrrolidine dithiocarbamate (PDTC), while 8-epi-prostaglandin F2 alpha (8-epi-PGF2 alpha) or lysophosphatidylcholine had no effect, implicating yet unidentified radicals. Sequential adhesive! and signaling events lead to the firm adhesion of rolling PMN on activated and adherent platelets, which may occupy areas of endothelial denudation. Shear resistant arrest of PMN on thrombin-stimulated platelets in flow conditions requires distinct regions of Mac-1, involving its interactions with fibrinogen bound to platelet alpha llb beta 3, and with other platelet ligands. Both arrest and adhesion strengthening under flow are stimulated by platelet-activating factor and leukotriene B4, but not by the chemokine receptor CXCR2. We tested whether Mac-1-dependent monocyte adhesiveness is affected by inhibitors of hydroxy-methylglutaryl-Coenzyme A reductase (statins) which improve morbidity and survival of patients with coronary heart disease. As compared to controls, adhesion of isolated monocytes to endothelium ex vivo was increased in patients with hypercholesterolemia. Treatment with statins decreased total and low density lipoprotein (LDL) cholesterol plasma levels, surface expression of Mac-1, and resulted in a dramatic reduction of Mac,mediated monocyte adhesion to endothelium. The inhibition of monocyte adhesion was reversed by mevalonate but not LDL in vitro,indicating that isoprenoid precursors are crucial for adhesiveness of Mac-1. Such effects may crucially contribute to the clinical benefit of statins, independent of cholesterol-lowering, and may represent a paradigm for novel, anti-inflammatory mechanisms of action by this class of drugs

SOX5 is involved in balanced MITF regulation in human melanoma cells

Background: Melanoma is a cancer with rising incidence and new therapeutics are needed. For this, it is necessary to understand the molecular mechanisms of melanoma development and progression. Melanoma differs from other cancers by its ability to produce the pigment melanin via melanogenesis; this biosynthesis is essentially regulated by microphthalmia-associated transcription factor (MITF). MITF regulates various processes such as cell cycling and differentiation. MITF shows an ambivalent role, since high levels inhibit cell proliferation and low levels promote invasion. Hence, well-balanced MITF homeostasis is important for the progression and spread of melanoma. Therefore, it is difficult to use MITF itself for targeted therapy, but elucidating its complex regulation may lead to a promising melanoma-cell specific therapy. Method: We systematically analyzed the regulation of MITF with a novel established transcription factor based gene regulatory network model. Starting from comparative transcriptomics analysis using data from cells originating from nine different tumors and a melanoma cell dataset, we predicted the transcriptional regulators of MITF employing ChIP binding information from a comprehensive set of databases. The most striking regulators were experimentally validated by functional assays and an MITF-promoter reporter assay. Finally, we analyzed the impact of the expression of the identified regulators on clinically relevant parameters of melanoma, i.e. the thickness of primary tumors and patient overall survival. Results: Our model predictions identified SOX10 and SOX5 as regulators of MITF. We experimentally confirmed the role of the already well-known regulator SOX10. Additionally, we found that SOX5 knockdown led to MITF up-regulation in melanoma cells, while double knockdown with SOX10 showed a rescue effect; both effects were validated by reporter assays. Regarding clinical samples, SOX5 expression was distinctively up-regulated in metastatic compared to primary melanoma. In contrast, survival analysis of melanoma patients with predominantly metastatic disease revealed that low SOX5 levels were associated with a poor prognosis. Conclusion: MITF regulation by SOX5 has been shown only in murine cells, but not yet in human melanoma cells. SOX5 has a strong inhibitory effect on MITF expression and seems to have a decisive clinical impact on melanoma during tumor progression

Deducing corticotropin-releasing hormone receptor type 1 signaling networks from gene expression data by usage of genetic algorithms and graphical Gaussian models

<p>Abstract</p> <p>Background</p> <p>Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is a hallmark of complex and multifactorial psychiatric diseases such as anxiety and mood disorders. About 50-60% of patients with major depression show HPA axis dysfunction, i.e. hyperactivity and impaired negative feedback regulation. The neuropeptide corticotropin-releasing hormone (CRH) and its receptor type 1 (CRHR1) are key regulators of this neuroendocrine stress axis. Therefore, we analyzed CRH/CRHR1-dependent gene expression data obtained from the pituitary corticotrope cell line AtT-20, a well-established <it>in vitro </it>model for CRHR1-mediated signal transduction. To extract significantly regulated genes from a genome-wide microarray data set and to deduce underlying CRHR1-dependent signaling networks, we combined supervised and unsupervised algorithms.</p> <p>Results</p> <p>We present an efficient variable selection strategy by consecutively applying univariate as well as multivariate methods followed by graphical models. First, feature preselection was used to exclude genes not differentially regulated over time from the dataset. For multivariate variable selection a maximum likelihood (MLHD) discriminant function within GALGO, an R package based on a genetic algorithm (GA), was chosen. The topmost genes representing major nodes in the expression network were ranked to find highly separating candidate genes. By using groups of five genes (chromosome size) in the discriminant function and repeating the genetic algorithm separately four times we found eleven genes occurring at least in three of the top ranked result lists of the four repetitions. In addition, we compared the results of GA/MLHD with the alternative optimization algorithms greedy selection and simulated annealing as well as with the state-of-the-art method random forest. In every case we obtained a clear overlap of the selected genes independently confirming the results of MLHD in combination with a genetic algorithm.</p> <p>With two unsupervised algorithms, principal component analysis and graphical Gaussian models, putative interactions of the candidate genes were determined and reconstructed by literature mining. Differential regulation of six candidate genes was validated by qRT-PCR.</p> <p>Conclusions</p> <p>The combination of supervised and unsupervised algorithms in this study allowed extracting a small subset of meaningful candidate genes from the genome-wide expression data set. Thereby, variable selection using different optimization algorithms based on linear classifiers as well as the nonlinear random forest method resulted in congruent candidate genes. The calculated interacting network connecting these new target genes was bioinformatically mapped to known CRHR1-dependent signaling pathways. Additionally, the differential expression of the identified target genes was confirmed experimentally.</p