| 1. |
- Altheimer, A., et al.
(författare)
-
Boosted objects and jet substructure at the LHC. Report of BOOST2012, held at IFIC Valencia, 23rd-27th of July 2012
- 2014
-
Ingår i: European Physical Journal C. Particles and Fields. - : Springer Science and Business Media LLC. - 1434-6044. ; 74:3
-
Tidskriftsartikel (refereegranskat)abstract
- This report of the BOOST2012 workshop presents the results of four working groups that studied key aspects of jet substructure. We discuss the potential of first-principle QCD calculations to yield a precise description of the substructure of jets and study the accuracy of state-of-the-art Monte Carlo tools. Limitations of the experiments' ability to resolve substructure are evaluated, with a focus on the impact of additional (pile-up) proton proton collisions on jet substructure performance in future LHC operating scenarios. A final section summarizes the lessons learnt from jet substructure analyses in searches for new physics in the production of boosted top quarks.
|
|
| 2. |
|
|
| 3. |
- Nagel, B., et al.
(författare)
-
Communication in aircraft design : Can we establish a common language?
- 2012
-
Ingår i: 28th Congress of the International Council of the Aeronautical Sciences 2012, ICAS 2012. - 9781622767540 ; , s. 443-455
-
Konferensbidrag (refereegranskat)abstract
- A standardized data model as common language for disciplinary communication in aircraft design could have a significant impact on the efficiency of conceptual/preliminary design efforts and collaborative research in aircraft design. This paper discusses if such a standard could be established and under which circumstances this would make sense. The Common Parametric Aircraft Configuration Scheme (CPACS) is introduced as one potential step towards a unified data model. Experiences in coupling established Multidisciplinary Design Optimization (MDO) environments with CPACS are presented and requirements for setting a standard are discussed.
|
|
| 4. |
|
|
| 5. |
- Salvi, Erika, et al.
(författare)
-
Genomewide Association Study Using a High-Density Single Nucleotide Polymorphism Array and Case-Control Design Identifies a Novel Essential Hypertension Susceptibility Locus in the Promoter Region of Endothelial NO Synthase.
- 2012
-
Ingår i: Hypertension. - 1524-4563. ; 59:2, s. 248-248
-
Tidskriftsartikel (refereegranskat)abstract
- Essential hypertension is a multifactorial disorder and is the main risk factor for renal and cardiovascular complications. The research on the genetics of hypertension has been frustrated by the small predictive value of the discovered genetic variants. The HYPERGENES Project investigated associations between genetic variants and essential hypertension pursuing a 2-stage study by recruiting cases and controls from extensively characterized cohorts recruited over many years in different European regions. The discovery phase consisted of 1865 cases and 1750 controls genotyped with 1M Illumina array. Best hits were followed up in a validation panel of 1385 cases and 1246 controls that were genotyped with a custom array of 14 055 markers. We identified a new hypertension susceptibility locus (rs3918226) in the promoter region of the endothelial NO synthase gene (odds ratio: 1.54 [95% CI: 1.37-1.73]; combined P=2.58 · 10(-13)). A meta-analysis, using other in silico/de novo genotyping data for a total of 21 714 subjects, resulted in an overall odds ratio of 1.34 (95% CI: 1.25-1.44; P=1.032 · 10(-14)). The quantitative analysis on a population-based sample revealed an effect size of 1.91 (95% CI: 0.16-3.66) for systolic and 1.40 (95% CI: 0.25-2.55) for diastolic blood pressure. We identified in silico a potential binding site for ETS transcription factors directly next to rs3918226, suggesting a potential modulation of endothelial NO synthase expression. Biological evidence links endothelial NO synthase with hypertension, because it is a critical mediator of cardiovascular homeostasis and blood pressure control via vascular tone regulation. This finding supports the hypothesis that there may be a causal genetic variation at this locus.
|
|
