Enhancing Tc in field-doped Fullerenes by applying uniaxial stress

Capitalizing on the two-dimensional nature of superconductivity in field-effect doped C60, we show that it should be possible to increase the transition temperature Tc by applying uniaxial stress perpendicular to the gate electrode. This method not only holds the promise of substantially enhancing Tc (by about 30 K per GPa), but also provides a sensitive check of the current understanding of superconductivity in the doped Fullerenes.Comment: 3 pages RevTe

Instant preheating mechanism and UHECR

Top-down models assume that the still unexplained Ultra High Energy Cosmic Rays (UHECR's) are the decay products of superheavy particles. Such particles may have been produced by one of the post-inflationary reheating mechanisms and may account for a fraction of the cold dark matter. In this paper, we assess the phenomenological applicability of the simplest instant preheating framework not to describe a reheating process, but as a mechanism to generate relic supermassive particles as possible sources of UHECR's. We use cosmic ray flux and cold dark matter observational data to constrain the parameters of the model.Comment: 7 pages, 2 figures, submitted to PR

Bimodal Expansion of the Lymphatic Vessels Is Regulated by the Sequential Expression of IL-7 and Lymphotoxin α1β2 in Newly Formed Tertiary Lymphoid Structures.

Lymphangiogenesis associated with tertiary lymphoid structure (TLS) has been reported in numerous studies. However, the kinetics and dynamic changes occurring to the lymphatic vascular network during TLS development have not been studied. Using a viral-induced, resolving model of TLS formation in the salivary glands of adult mice we demonstrate that the expansion of the lymphatic vascular network is tightly regulated. Lymphatic vessel expansion occurs in two distinct phases. The first wave of expansion is dependent on IL-7. The second phase, responsible for leukocyte exit from the glands, is regulated by lymphotoxin (LT)βR signaling. These findings, while highlighting the tight regulation of the lymphatic response to inflammation, suggest that targeting the LTα1β2/LTβR pathway in TLS-associated pathologies might impair a natural proresolving mechanism for lymphocyte exit from the tissues and account for the failure of therapeutic strategies that target these molecules in diseases such as rheumatoid arthritis

Tests of Higgs Boson Couplings at a mu+mu- Collider

We investigate the potential of a muon collider for testing the presence of anomalous Higgs boson couplings. We consider the case of a light (less than $160 GeV$) Higgs boson and study the effects on the Higgs branching ratios and total width, which could be induced by the non standard couplings created by a class of dim=6 $SU(3)\times SU(2)\times U(1)$ gauge invariant operators satisfying the constraints imposed by the present and future hadronic and $e^-e^+$ colliders. For each operator we give the minimal value of the $\mu^+\mu^-$ integrated luminosity needed for the muon collider ($\mu C$) to improve these constraints. Depending on the operator and the Higgs mass, this minimal $\mu C$ luminosity lies between $0.1 fb^{-1}$ and $100 fb^{-1}$.Comment: 18 pages and 4 figures; version to be published in Phys. Rev.D. e-mail: [email protected]

Mutations in the heat-shock protein A9 (HSPA9) gene cause the EVEN-PLUS syndrome of congenital malformations and skeletal dysplasia.

We and others have reported mutations in LONP1, a gene coding for a mitochondrial chaperone and protease, as the cause of the human CODAS (cerebral, ocular, dental, auricular and skeletal) syndrome (MIM 600373). Here, we delineate a similar but distinct condition that shares the epiphyseal, vertebral and ocular changes of CODAS but also included severe microtia, nasal hypoplasia, and other malformations, and for which we propose the name of EVEN-PLUS syndrome for epiphyseal, vertebral, ear, nose, plus associated findings. In three individuals from two families, no mutation in LONP1 was found; instead, we found biallelic mutations in HSPA9, the gene that codes for mHSP70/mortalin, another highly conserved mitochondrial chaperone protein essential in mitochondrial protein import, folding, and degradation. The functional relationship between LONP1 and HSPA9 in mitochondrial protein chaperoning and the overlapping phenotypes of CODAS and EVEN-PLUS delineate a family of "mitochondrial chaperonopathies" and point to an unexplored role of mitochondrial chaperones in human embryonic morphogenesis

Inflation and late time acceleration in braneworld cosmological models with varying brane tension

Braneworld models with variable brane tension $\lambda$ introduce a new degree of freedom that allows for evolving gravitational and cosmological constants, the latter being a natural candidate for dark energy. We consider a thermodynamic interpretation of the varying brane tension models, by showing that the field equations with variable $\lambda$ can be interpreted as describing matter creation in a cosmological framework. The particle creation rate is determined by the variation rate of the brane tension, as well as by the brane-bulk energy-matter transfer rate. We investigate the effect of a variable brane tension on the cosmological evolution of the Universe, in the framework of a particular model in which the brane tension is an exponentially dependent function of the scale factor. The resulting cosmology shows the presence of an initial inflationary expansion, followed by a decelerating phase, and by a smooth transition towards a late accelerated de Sitter type expansion. The varying brane tension is also responsible for the generation of the matter in the Universe (reheating period). The physical constraints on the model parameters, resulted from the observational cosmological data, are also investigated.Comment: 25 pages, 8 figures, accepted for publication in European Physical Journal

Developmental pathways to autism: a review of prospective studies of infants at risk

Autism Spectrum Disorders (ASDs) are neurodevelopmental disorders characterized by impairments in social interaction and communication, and the presence of restrictive and repetitive behaviors. Symptoms of ASD likely emerge from a complex interaction between pre-existing neurodevelopmental vulnerabilities and the child's environment, modified by compensatory skills and protective factors. Prospective studies of infants at high familial risk for ASD (who have an older sibling with a diagnosis) are beginning to characterize these developmental pathways to the emergence of clinical symptoms. Here, we review the range of behavioral and neurocognitive markers for later ASD that have been identified in high-risk infants in the first years of life. We discuss theoretical implications of emerging patterns, and identify key directions for future work, including potential resolutions to several methodological challenges for the field. Mapping how ASD unfolds from birth is critical to our understanding of the developmental mechanisms underlying this disorder. A more nuanced understanding of developmental pathways to ASD will help us not only to identify children who need early intervention, but also to improve the range of interventions available to them