The Minimal Scale Invariant Extension of the Standard Model

We perform a systematic analysis of an extension of the Standard Model that includes a complex singlet scalar field and is scale invariant at the tree level. We call such a model the Minimal Scale Invariant extension of the Standard Model (MSISM). The tree-level scale invariance of the model is explicitly broken by quantum corrections, which can trigger electroweak symmetry breaking and potentially provide a mechanism for solving the gauge hierarchy problem. Even though the scale invariant Standard Model is not a realistic scenario, the addition of a complex singlet scalar field may result in a perturbative and phenomenologically viable theory. We present a complete classification of the flat directions which may occur in the classical scalar potential of the MSISM. After calculating the one-loop effective potential of the MSISM, we investigate a number of representative scenarios and determine their scalar boson mass spectra, as well as their perturbatively allowed parameter space compatible with electroweak precision data. We discuss the phenomenological implications of these scenarios, in particular, whether they realize explicit or spontaneous CP violation, neutrino masses or provide dark matter candidates. In particular, we find a new minimal scale-invariant model of maximal spontaneous CP violation which can stay perturbative up to Planck-mass energy scales, without introducing an unnaturally large hierarchy in the scalar-potential couplings.Comment: 71 pages, 34 eps figures, numerical error corrected, clarifying comments adde

New Physics Signals in Longitudinal Gauge Boson Scattering at the LHC

We introduce a novel technique designed to look for signatures of new physics in vector boson fusion processes at the TeV scale. This functions by measuring the polarization of the vector bosons to determine the relative longitudinal to transverse production. In studying this ratio we can directly probe the high energy E^2-growth of longitudinal vector boson scattering amplitudes characteristic of models with non-Standard Model (SM) interactions. We will focus on studying models parameterized by an effective Lagrangian that include a light Higgs with non-SM couplings arising from TeV scale new physics associated with the electroweak symmetry breaking, although our technique can be used in more general scenarios. We will show that this technique is stable against the large uncertainties that can result from variations in the factorization scale, improving upon previous studies that measure cross section alone

Intra-specific variation of sperm length in the malaria vector Anopheles gambiae: males with shorter sperm have higher reproductive success

<p>Abstract</p> <p>Background</p> <p>Intra-specific variation in sperm length influences male reproductive success in several species of insects. In males of the malaria vector <it>Anopheles gambiae</it>, sperm length is highly variable but the significance of this variation is unknown. Understanding what determines the reproductive success of male mosquitoes is critical for controlling malaria, and in particular for replacing natural populations with transgenic, malaria-resistant mosquitoes.</p> <p>Methods</p> <p>A laboratory population of <it>A. gambiae </it>males was tested for intra-specific variation in sperm length. A full-sib quantitative genetic design was used to test for a genetic component of sperm length in <it>A. gambiae </it>males and estimate its heritability. This study also tested for a relationship between sperm length and male reproductive success in <it>A. gambiae</it>. Male reproductive success was measured as the proportions of inseminated and ovipositing females.</p> <p>Results</p> <p>There was intra-specific variation of sperm length in <it>A. gambiae</it>. There was no significant genetic variation in sperm length and its heritability was low (h²= 0.18) compared to other insects. Sperm length was correlated with male body size (measured as wing length). Males with short sperm had significantly higher reproductive success than males with long sperm and this was independent of body size.</p> <p>Conclusion</p> <p>This is the first study to demonstrate intra-specific variation in sperm length in <it>A. gambiae </it>and that males with short sperm have higher reproductive success. That sperm length influences female oviposition is important for any strategy considering the release of transgenic males.</p

Long-range corrected DFT calculations of charge-transfer integrals in model metal-free phthalocyanine complexes

An assessment of several widely used exchange--correlation potentials in computing charge-transfer integrals is performed. In particular, we employ the recently proposed Coulomb-attenuated model which was proven by other authors to improve upon conventional functionals in the case of charge-transfer excitations. For further validation, two distinct approaches to compute the property in question are compared for a phthalocyanine dimer

The sperm factor: paternal impact beyond genes

The fact that sperm carry more than the paternal DNA has only been discovered just over a decade ago. With this discovery, the idea that the paternal condition may have direct implications for the fitness of the offspring had to be revisited. While this idea is still highly debated, empirical evidence for paternal effects is accumulating. Male condition not only affects male fertility but also offspring early development and performance later in life. Several factors have been identified as possible carriers of non-genetic information, but we still know little about their origin and function and even less about their causation. I consider four possible non-mutually exclusive adaptive and non-adaptive explanations for the existence of paternal effects in an evolutionary context. In addition, I provide a brief overview of the main non-genetic components found in sperm including DNA methylation, chromatin modifications, RNAs and proteins. I discuss their putative functions and present currently available examples for their role in transferring non-genetic information from the father to the offspring. Finally, I identify some of the most important open questions and present possible future research avenues

QCD and strongly coupled gauge theories : challenges and perspectives

We highlight the progress, current status, and open challenges of QCD-driven physics, in theory and in experiment. We discuss how the strong interaction is intimately connected to a broad sweep of physical problems, in settings ranging from astrophysics and cosmology to strongly coupled, complex systems in particle and condensed-matter physics, as well as to searches for physics beyond the Standard Model. We also discuss how success in describing the strong interaction impacts other fields, and, in turn, how such subjects can impact studies of the strong interaction. In the course of the work we offer a perspective on the many research streams which flow into and out of QCD, as well as a vision for future developments.Peer reviewe

Loss of function mutations in GEMIN5 cause a neurodevelopmental disorder.

GEMIN5, an RNA-binding protein is essential for assembly of the survival motor neuron (SMN) protein complex and facilitates the formation of small nuclear ribonucleoproteins (snRNPs), the building blocks of spliceosomes. Here, we have identified 30 affected individuals from 22 unrelated families presenting with developmental delay, hypotonia, and cerebellar ataxia harboring biallelic variants in the GEMIN5 gene. Mutations in GEMIN5 perturb the subcellular distribution, stability, and expression of GEMIN5 protein and its interacting partners in patient iPSC-derived neurons, suggesting a potential loss-of-function mechanism. GEMIN5 mutations result in disruption of snRNP complex assembly formation in patient iPSC neurons. Furthermore, knock down of rigor mortis, the fly homolog of human GEMIN5, leads to developmental defects, motor dysfunction, and a reduced lifespan. Interestingly, we observed that GEMIN5 variants disrupt a distinct set of transcripts and pathways as compared to SMA patient neurons, suggesting different molecular pathomechanisms. These findings collectively provide evidence that pathogenic variants in GEMIN5 perturb physiological functions and result in a neurodevelopmental delay and ataxia syndrome