Charged Higgs Observability Through Associated Production With W at a Muon Collider

The observability of a charged Higgs boson produced in association with a W boson at future muon colliders is studied. The analysis is performed within the MSSM framework. The charged Higgs is assumed to decay to tb and a fully hadronic final state is analyzed, i.e., mu+mu- \rightarrow H\pmW\mp \rightarrow tbW \rightarrow WbbW \rightarrow jjjjbb. The main background is tt production in fully hadronic final state which is an irreducible background with very similar kinematic features. It is shown that although the discovery potential is almost the same for a charged Higgs mass in the range 200 GeV < mH\pm < 400 GeV, the signal significance is about 1sigma for tanbeta = 50 at integrated luminosity of 50 fb-1. The signal rate is well above that at e+e- linear colliders with the same center of mass energy and enough data (O(1 ab-1)) will provide the same discovery potential for all heavy charged Higgs masses up to mH\pm \sim 400 GeV, however, the muon collider cannot add anything to the LHC findings.Comment: 18 pages, 11 figure

New angles on top quark decay to a charged Higgs

To properly discover a charged Higgs Boson ($H^\pm$) requires its spin and couplings to be determined. We investigate how to utilize \ttbar spin correlations to analyze the $H^\pm$ couplings in the decay $t\to bH^+\to b\tau^+\nu_\tau$. Within the framework of a general Two-Higgs-Doublet Model, we obtain results on the spin analyzing coefficients for this decay and study in detail its spin phenomenology, focusing on the limits of large and small values for $\tan\beta$. Using a Monte Carlo approach to simulate full hadron-level events, we evaluate systematically how the $H^\pm\to\tau^\pm\nu_\tau$ decay mode can be used for spin analysis. The most promising observables are obtained from azimuthal angle correlations in the transverse rest frames of $t(\bar{t})$. This method is particularly useful for determining the coupling structure of $H^\pm$ in the large $\tan\beta$ limit, where differences from the SM are most significant.Comment: 28 pages, 13 figures. Uses JHEP forma

Likelihood Functions for Supersymmetric Observables in Frequentist Analyses of the CMSSM and NUHM1

On the basis of frequentist analyses of experimental constraints from electroweak precision data, g-2, B physics and cosmological data, we investigate the parameters of the constrained MSSM (CMSSM) with universal soft supersymmetry-breaking mass parameters, and a model with common non-universal Higgs masses (NUHM1). We present chi^2 likelihood functions for the masses of supersymmetric particles and Higgs bosons, as well as b to s gamma, b to mu mu and the spin-independent dark matter scattering cross section. In the CMSSM we find preferences for sparticle masses that are relatively light. In the NUHM1 the best-fit values for many sparticle masses are even slightly smaller, but with greater uncertainties. The likelihood functions for most sparticle masses are cut off sharply at small masses, in particular by the LEP Higgs mass constraint. Both in the CMSSM and the NUHM1, the coannihilation region is favoured over the focus-point region at about the 3-sigma level, largely but not exclusively because of g-2. Many sparticle masses are highly correlated in both the CMSSM and NUHM1, and most of the regions preferred at the 95% C.L. are accessible to early LHC running. Some slepton and chargino/neutralino masses should be in reach at the ILC. The masses of the heavier Higgs bosons should be accessible at the LHC and the ILC in portions of the preferred regions in the (M_A, tan beta) plane. In the CMSSM, the likelihood function for b to mu mu is peaked close to the Standard Model value, but much larger values are possible in the NUHM1. We find that values of the DM cross section > 10^{-10} pb are preferred in both the CMSSM and the NUHM1. We study the effects of dropping the g-2, b to s gamma, relic density and M_h constraints.Comment: 34 pages, 24 figure

Systemic Inflammation in Preclinical Ulcerative Colitis

Background & Aims: Preclinical ulcerative colitis is poorly defined. We aimed to characterize the preclinical systemic inflammation in ulcerative colitis, using a comprehensive set of proteins. Methods: We obtained plasma samples biobanked from individuals who developed ulcerative colitis later in life (n = 72) and matched healthy controls (n = 140) within a population-based screening cohort. We measured 92 proteins related to inflammation using a proximity extension assay. The biologic relevance of these findings was validated in an inception cohort of patients with ulcerative colitis (n = 101) and healthy controls (n = 50). To examine the influence of genetic and environmental factors on these markers, a cohort of healthy twin siblings of patients with ulcerative colitis (n = 41) and matched healthy controls (n = 37) were explored. Results: Six proteins (MMP10, CXCL9, CCL11, SLAMF1, CXCL11 and MCP-1) were up-regulated (P < .05) in preclinical ulcerative colitis compared with controls based on both univariate and multivariable models. Ingenuity Pathway Analyses identified several potential key regulators, including interleukin-1ß, tumor necrosis factor, interferon-gamma, oncostatin M, nuclear factor-¿B, interleukin-6, and interleukin-4. For validation, we built a multivariable model to predict disease in the inception cohort. The model discriminated treatment-naïve patients with ulcerative colitis from controls with leave-one-out cross-validation (area under the curve = 0.92). Consistently, MMP10, CXCL9, CXCL11, and MCP-1, but not CCL11 and SLAMF1, were significantly up-regulated among the healthy twin siblings, even though their relative abundances seemed higher in incident ulcerative colitis. Conclusions: A set of inflammatory proteins are up-regulated several years before a diagnosis of ulcerative colitis. These proteins were highly predictive of an ulcerative colitis diagnosis, and some seemed to be up-regulated already at exposure to genetic and environmental risk factors. © 2021 The Author

The Molecular Genetic Architecture of Self-Employment

Economic variables such as income, education, and occupation are known to affect mortality and morbidity, such as cardiovascular disease, and have also been shown to be partly heritable. However, very little is known about which genes influence economic variables, although these genes may have both a direct and an indirect effect on health. We report results from the first large-scale collaboration that studies the molecular genetic architecture of an economic variable-entrepreneurship-that was operationalized using self-employment, a widely-available proxy. Our results suggest that common SNPs when considered jointly explain about half of the narrow-sense heritability of self-employment estimated in twin data (σg2/σP2= 25%, h2= 55%). However, a meta-analysis of genome-wide association studies across sixteen studies comprising 50,627 participants did not identify genome-wide significant SNPs. 58 SNPs with p<10-5were tested in a replication sample (n = 3,271), but none replicated. Furthermore, a gene-based test shows that none of the genes that were previously suggested in the literature to influence entrepreneurship reveal significant associations. Finally, SNP-based genetic scores that use results from the meta-analysis capture less than 0.2% of the variance in self-employment in an independent sample (p≥0.039). Our results are consistent with a highly polygenic molecular genetic architecture of self-employment, with many genetic variants of small effect. Although self-employment is a multi-faceted, heavily environmentally influenced, and biologically distal trait, our results are similar to those for other genetically complex and biologically more proximate outcomes, such as height, intelligence, personality, and several diseases

Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels.

Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P&lt;10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P&lt;5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health

True substrates: The exceptional resolution and unexceptional preservation of deep time snapshots on bedding surfaces

Abstract: Rock outcrops of the sedimentary–stratigraphic record often reveal bedding planes that can be considered to be true substrates: preserved surfaces that demonstrably existed at the sediment–water or sediment–air interface at the time of deposition. These surfaces have high value as repositories of palaeoenvironmental information, revealing fossilized snapshots of microscale topography from deep time. Some true substrates are notable for their sedimentary, palaeontological and ichnological signatures that provide windows into key intervals of Earth history, but countless others occur routinely throughout the sedimentary–stratigraphic record. They frequently reveal patterns that are strikingly familiar from modern sedimentary environments, such as ripple marks, animal trackways, raindrop impressions or mudcracks: all phenomena that are apparently ephemeral in modern settings, and which form on recognizably human timescales. This paper sets out to explain why these short‐term, transient, small‐scale features are counter‐intuitively abundant within a 3.8 billion year‐long sedimentary–stratigraphic record that is known to be inherently time‐incomplete. True substrates are fundamentally related to a state of stasis in ancient sedimentation systems, and distinguishable from other types of bedding surfaces that formed from a dominance of states of deposition or erosion. Stasis is shown to play a key role in both their formation and preservation, rendering them faithful and valuable archives of palaeoenvironmental and temporal information. Further, the intersection between the time–length scale of their formative processes and outcrop expressions can be used to explain why they are so frequently encountered in outcrop investigations. Explaining true substrates as inevitable and unexceptional by‐products of the accrual of the sedimentary–stratigraphic record should shift perspectives on what can be understood about Earth history from field studies of the sedimentary–stratigraphic record. They should be recognized as providing high‐definition information about the mundane day to day operation of ancient environments, and critically assuage the argument that the incomplete sedimentary–stratigraphic record is unrepresentative of the geological past