NLO Higgs Effective Field Theory and kappa-framework

A consistent framework for studying Standard Model deviations is developed. It assumes that New Physics becomes relevant at some scale beyond the present experimental reach and uses the Effective Field Theory approach by adding higher-dimensional operators to the Standard Model Lagrangian and by computing relevant processes at the next-to-leading order, extending the original kappa-framework.Comment: 33 pages + appendice

eHDECAY: an Implementation of the Higgs Effective Lagrangian into HDECAY

We present eHDECAY, a modified version of the program HDECAY which includes the full list of leading bosonic operators of the Higgs effective Lagrangian with a linear or non-linear realization of the electroweak symmetry and implements two benchmark composite Higgs models.Comment: 28 pages. Manual of the eHEDCAY code that can be downloaded at the http://www-itp.particle.uni-karlsruhe.de/~maggie/eHDECAY/ Submitted to Comput. Phys. Commun. Companion paper: arXiv:1303.3876, JHEP 1307 (2013) 03

Refinements of the Bottom and Strange MSSM Higgs Yukawa Couplings at NNLO

We extend the already existing two-loop calculation of the effective bottom-Yukawa coupling in the MSSM. In addition to the resummation of the dominant corrections for large values of tg$\beta$, we include the subleading terms related to the trilinear Higgs coupling $A_b$ and contributions induced by the electroweak gauge couplings. This calculation has been extended to the NNLO corrections to the MSSM strange-Yukawa coupling. Our analysis leads to residual theoretical uncertainties of the effective Yukawa couplings at the per-cent level.Comment: 23 pages, 9 figures, extension of the work described in arxiv:1001.1935 and arxiv:0808.0087, reference added, substantial upgrade to the full Delta_b results at NNL

Effective Lagrangian for a light Higgs-like scalar

We reconsider the effective Lagrangian that describes a light Higgs-like boson and better clarify a few issues which were not exhaustively addressed in the previous literature. In particular we highlight the strategy to determine whether the dynamics responsible for the electroweak symmetry breaking is weakly or strongly interacting. We also discuss how the effective Lagrangian can be implemented into automatic tools for the calculation of Higgs decay rates and production cross sections.Comment: 40 pages + 14 pages of Appendix, 2 figures. v3: Shortened version following the recommendation of the journal. The technical description of the code eHDECAY appeared as a separate paper now available on arXiv. v4: typos corrected and extended discussion on CP-violating Higgs coupling

Low- and high-energy phenomenology of a doubly charged scalar

We explore the phenomenology of an $SU(2)$-singlet doubly charged scalar at the high and low energy frontier. Such a particle is predicted in different new physics models, like left-right symmetric models or the Zee-Babu model. Nonetheless, since its interactions with Standard Model (SM) leptons are gauge invariant, it can be consistently studied as a UV complete SM extension. Its signatures range from same-sign di-lepton pairs to flavour changing decays of charged leptons to muonium-antimuonium oscillations. In this article, we use a systematic effective-field-theory approach for studying the low-energy observables and comparing them consistently to collider bounds. For this purpose, experimental searches for doubly charged scalars at the Large Hadron Collider are reinterpreted, including large width effects, and projections for exclusion and discovery reaches in the high-luminosity phase are provided. The sensitivities of the future International Linear Collider and Compact Linear Collider for the doubly charged scalar are presented with focus on di-lepton final states and resonant production. Theoretically and phenomenologically motivated benchmark scenarios are considered showing the different impact of low- and high-energy observables. We find that future low- and high-energy experiments display strong complementarity in studying the parameter space of the model.Comment: 22 pages, 18 figures. v2: minor revisions, it matches the version published in Physical Review

Hadronic production of top-quark pairs in association with a pair of leptons in the POWHEG BOX framework

We present an implementation of $t\bar t \ell^+\ell^-$ ($\ell=e,\mu$) hadronic production at next-to-leading order in QCD matched to parton-shower event generators in the POWHEG BOX framework. The program we developed includes all leading-order contributions of order $\alpha_s^2\alpha^2$ for the specified final state, as well as the corresponding first-order QCD corrections. Decays of the top quarks have been simulated retaining spin-correlations in all tree-level matrix elements. We consider the case of the Large Hadron Collider at $\sqrt{s}=13$ TeV and compare results for $t\bar t \ell^+\ell^-$ production in the fiducial volume where the invariant mass of the lepton pairs is centered around the $Z$-boson mass to corresponding predictions for $t\bar{t}Z$ on-shell production with $Z\rightarrow \ell^+\ell^-$. We find that off-shell effects in $t\bar t \ell^+\ell^-$ are in general small at the level of the total cross section, but can decrease the tail of the leptons' transverse momentum distributions by 10-20% and, in these regions, they are visible beyond the scale uncertainty due to renormalization and factorization scale variation. Moreover, we find that accounting for top-quark decays in the narrow-width approximation with tree-level spin correlations also gives origin to 10-20% effects in specific regions of the kinematic distributions of the $t\bar t \ell^+\ell^-$ decayed final state.Comment: 22 pages, 13 figure

The zebrafish orthologue of the human hepatocerebral disease gene MPV17 plays pleiotropic roles in mitochondria

Mitochondrial DNA depletion syndromes (MDS) are a group of rare autosomal recessive disorders with early onset and no cure available. MDS are caused by mutations in nuclear genes involved in mitochondrial DNA (mtDNA) maintenance, and characterized by both a strong reduction in mtDNA content and severe mitochondrial defects in affected tissues. Mutations in MPV17, a nuclear gene encoding a mitochondrial inner membrane protein, have been associated with hepatocerebral forms of MDS. The zebrafish mpv17 null mutant lacks the guanine-based reflective skin cells named iridophores and represents a promising model to clarify the role of Mpv17. In this study, we characterized the mitochondrial phenotype of mpv17-/- larvae and found early and severe ultrastructural alterations in liver mitochondria, as well as significant impairment of the respiratory chain, leading to activation of the mitochondrial quality control. Our results provide evidence for zebrafish Mpv17 being essential for maintaining mitochondrial structure and functionality, while its effects on mtDNA copy number seem to be subordinate. Considering that a role in nucleotide availability had already been postulated for MPV17, that embryos blocked in pyrimidine synthesis do phenocopy mpv17-/- knockouts (KOs) and that mpv17-/- KOs have impaired Dihydroorotate dehydrogenase activity, we provided mpv17 mutants with the pyrimidine precursor orotic acid (OA). Treatment with OA, an easily available food supplement, significantly increased both iridophore number and mtDNA content in mpv17-/- mutants, thus linking the loss of Mpv17 to pyrimidine de novo synthesis and opening a new simple therapeutic approach for MPV17-related MDS

Testing the 2018 NIA-AA research framework in a retrospective large cohort of patients with cognitive impairment: From biological biomarkers to clinical syndromes

Background According to the 2018 NIA-AA research framework, Alzheimer's disease (AD) is not defined by the clinical consequences of the disease, but by its underlying pathology, measured by biomarkers. Evidence of both amyloid-beta (A beta) and phosphorylated tau protein (p-tau) deposition-assessed interchangeably with amyloid-positron emission tomography (PET) and/or cerebrospinal fluid (CSF) analysis-is needed to diagnose AD in a living person. Our aim was to test the new NIA-AA research framework in a large cohort of cognitively impaired patients to evaluate correspondence between the clinical syndromes and the underlying pathologic process testified by biomarkers. Methods We retrospectively analysed 628 subjects referred to our centre in suspicion of dementia, who underwent CSF analysis, together with neuropsychological assessment and neuroimaging, and were diagnosed with different neurodegenerative dementias according to current criteria, or as cognitively unimpaired. Subjects were classified considering CSF biomarkers, and the prevalence of normal, AD-continuum and non-AD profiles in each clinical syndrome was calculated. The positivity threshold of each CSF biomarker was first assessed by receiver operating characteristic analysis, using A beta-positive/negative status as determined by amyloid-PET visual reads. The agreement between CSF and amyloid-PET data was also evaluated. Results Among patients with a clinical diagnosis of AD, 94.1% were in the AD-continuum, whereas 5.5% were classified as non-AD and 0.4% were normal. The AD-continuum profile was found also in 26.2% of frontotemporal dementia, 48.6% of Lewy body dementia, 25% of atypical parkinsonism and 44.7% of vascular dementia. Biomarkers' profile did not differ in amnestic and not amnestic mild cognitive impairment. CSF A beta levels and amyloid-PET tracer binding negatively correlated, and the concordance between the two A beta biomarkers was 89%. Conclusions The examination of the 2018 NIA-AA research framework in our clinical setting revealed a good, but incomplete, correspondence between the clinical syndromes and the underlying pathologic process measured by CSF biomarkers. The AD-continuum profile resulted to be a sensitive, but non-specific biomarker with regard to the clinical AD diagnosis. CSF and PET A beta biomarkers were found to be not perfectly interchangeable to quantify the A beta burden, possibly because they measure different aspects of AD pathology