Gauge singlet scalar as inflaton and thermal relic dark matter

We show that, by adding a gauge singlet scalar S to the standard model which is nonminimally coupled to gravity, S can act both as the inflaton and as thermal relic dark matter. We obtain the allowed region of the (m_s, m_h) parameter space which gives a spectral index in agreement with observational bounds and also produces the observed dark matter density while not violating vacuum stability or nonperturbativity constraints. We show that, in contrast to the case of Higgs inflation, once quantum corrections are included the spectral index is significantly larger than the classical value (n = 0.966 for N = 60) for all allowed values of the Higgs mass m_h. The range of Higgs mass compatible with the constraints is 145 GeV < m_h < 170 GeV. The S mass lies in the range 45 GeV < ms < 1 TeV for the case of a real S scalar with large quartic self-coupling lambdas, with a smaller upper bound for smaller lambdas. A region of the parameter space is accessible to direct searches at the LHC via h-->SS, while future direct dark matter searches should be able to significantly constrain the model.Comment: 13 pages, 7 figures. Published versio

Quantifying the effects of pediatric obesity on musculoskeletal function and biomechanical loading during walking

2015 Spring.Includes bibliographical references.With the high prevalence of pediatric obesity worldwide, there is a critical need for structured physical activity interventions during childhood. However, obese children exhibit altered walking mechanics that are associated with decreased gait stability, reduced walking performance and an increased prevalence of musculoskeletal pain and pathology. Left unaddressed, the increased pain and orthopedic conditions associated with pediatric obesity may lead to reduced physical activity and a cycle of perpetual weight gain for the child and future adult. To enhance the efficacy of health and weight loss interventions, clinicians could benefit from an improved understanding of how pediatric obesity affects the neuromuscular and musculoskeletal systems during walking, the most common form of daily activity. The mechanisms for the altered gait and associated risks to the developing musculoskeletal system in obese children are not well understood, particularly as they relate to excess adiposity and exercise related fatigue. This void in the literature may be attributed in part to the lack of experimental and computational tools necessary to accurately quantify muscle function and joint loads during walking in obese and healthy-weight adults and children. Therefore, to improve our understanding of the musculoskeletal mechanisms for the altered gait mechanics and orthopedic disorders exhibited by obese children, this dissertation sought to first, establish the proper methods to adequately quantify the necessary biomechanical measures in obese and healthy-weight individuals, and second, determine the effects of obesity and duration on muscle function and tibiofemoral loading during walking in children. The accuracy of muscle and joint contact forces estimated from dynamic musculoskeletal simulations is dependent upon the experimental kinematic data used as inputs. Subcutaneous adipose tissue makes the measurement of representative kinematics from motion analysis particularly challenging in overweight and obese individuals. We developed an obesity-specific kinematic marker set and methodology that accounted for subcutaneous adiposity. Next, we determined how this methodology affected muscle and joint contact forces predicted from musculoskeletal simulations of walking in obese individuals. The marker set methodology had a significant effect on model quantified lower-extremity kinematics, muscle forces, and hip and knee joint contact forces. We demonstrated the need for biomechanists to account for subcutaneous adiposity during kinematic data collection and proposed a feasible solution that likely improves the accuracy of musculoskeletal simulations in overweight and obese people. Understanding orthopedic disorders of biological and prosthetic knee joints requires knowledge of the in-vivo loading environment during activities of daily living. Anthropometric and orthopedic differences between individuals make accurate predictions from generic musculoskeletal models a challenge. We developed a knee mechanism within a full-body OpenSim musculoskeletal model that incorporated subject-specific knee parameters to predict medial and lateral tibiofemoral contact forces. To assess the accuracy of our model, we compared measured to predicted medial and lateral compartment contact forces during walking in an individual with an instrumented knee replacement. We determined the importance of specifying subject-specific tibiofemoral alignment and contact locations and validated a simple approach to measure and specify these parameters on a subject-specific basis using radiography. The biomechanical mechanisms responsible for the altered gait mechanics in obese children are not well understood. We investigated the relationship between adiposity and lower extremity kinematics, muscle force requirements, and individual muscle contributions to whole body dynamics by generating musculoskeletal simulations of walking in a group of children with a range of adiposity. Body fat percentage was correlated with average knee flexion angle during stance and pelvic obliquity range of motion, as well as with relative vasti, gluteus medius and soleus force production. The functional demands and relative force requirements of the hip abductors during walking in pediatric obesity likely contribute to the altered gait mechanics in obese children. The combination of larger magnitude and altered application of tibiofemoral loads during physical activity in obese children is commonly theorized to contribute to their increased risk of orthopedic disorders of the knee, such as growth-plate suppression leading to conditions of malalignment. To evaluate this theory and determine how prolonged activity affects knee loading, we quantified the effects of pediatric obesity and walking duration on medial and lateral tibiofemoral contact forces. We found that obese children have elevated medial compartment magnitudes, loading rates, and load share, which further increased with walking duration. The altered tibiofemoral loading environment during walking in obese children likely contributes to their increased risk of knee pain and pathology. These risks may increase with activity duration. This dissertation provides a foundation for improved understanding of the effects of pediatric obesity on the neuromuscular and musculoskeletal systems during walking. The main research outcomes from this dissertation aim to improve rehabilitation and activity guidelines that minimize the risk of musculoskeletal pain and pathology in obese children, address degenerative gait mechanics, and assist in breaking the cycle of weight gain

Impurity Scattering in Luttinger Liquid with Electron-Phonon Coupling

We study the influence of electron-phonon coupling on electron transport through a Luttinger liquid with an embedded weak scatterer or weak link. We derive the renormalization group (RG) equations which indicate that the directions of RG flows can change upon varying either the relative strength of the electron-electron and electron-phonon coupling or the ratio of Fermi to sound velocities. This results in the rich phase diagram with up to three fixed points: an unstable one with a finite value of conductance and two stable ones, corresponding to an ideal metal or insulator.Comment: 4 pages, 2 figure

Dimensional Crossover of the Dephasing Time in Disordered Mesoscopic Rings: From Diffusive through Ergodic to 0D Behavior

We analyze dephasing by electron interactions in a small disordered quasi-one dimensional (1D) ring weakly coupled to leads, where we recently predicted a crossover for the dephasing time \tPh(T) from diffusive or ergodic 1D (\tPh^{-1} \propto T^{2/3}, T^{1}) to $0D$ behavior (\tPh^{-1} \propto T^{2}) as $T$ drops below the Thouless energy \ETh. We provide a detailed derivation of our results, based on an influence functional for quantum Nyquist noise, and calculate all leading and subleading terms of the dephasing time in the three regimes. Explicitly taking into account the Pauli blocking of the Fermi sea in the metal allows us to describe the $0D$ regime on equal footing as the others. The crossover to $0D$, predicted by Sivan, Imry and Aronov for 3D systems, has so far eluded experimental observation. We will show that for T \ll \ETh, $0D$ dephasing governs not only the $T$-dependence for the smooth part of the magnetoconductivity but also for the amplitude of the Altshuler-Aronov-Spivak oscillations, which result only from electron paths winding around the ring. This observation can be exploited to filter out and eliminate contributions to dephasing from trajectories which do not wind around the ring, which may tend to mask the $T^{2}$ behavior. Thus, the ring geometry holds promise of finally observing the crossover to $0D$ experimentally.Comment: in "Perspectives of Mesoscopic Physics - Dedicated to Yoseph Imry's 70th Birthday", edited by Amnon Aharony and Ora Entin-Wohlman (World Scientific, 2010), chap. 20, p. 371-396, ISBN-13 978-981-4299-43-

Unitarizing Higgs Inflation

We consider a simple extension of the Standard Model Higgs inflation with one new real scalar field which preserves unitarity up to the Planck scale. The new scalar field (called sigma) completes in the ultraviolet the theory of Higgs inflation by linearizing the Higgs kinetic term in the Einstein frame, just as the non-linear sigma model is unitarized into its linear version. The unitarity cutoff of the effective theory, obtained by integrating out the sigma field, varies with the background value of the Higgs field. In our setup, both the Higgs field and the sigma field participate in the inflationary dynamics, following the flat direction of the potential. We obtain the same slow-roll parameters and spectral index as in the original Higgs inflation but we find that the Hubble rate during inflation depends not only on the Higgs self-coupling, but also on the unknown couplings of the sigma field.Comment: 16 page

Splitting of Long-Wavelength Modes of the Fractional Quantum Hall Liquid at ν=1/3\nu=1/3

Resonant inelastic light scattering experiments at $\nu=1/3$ reveal a novel splitting of the long wavelength modes in the low energy spectrum of quasiparticle excitations in the charge degree of freedom. We find a single peak at small wavevectors that splits into two distinct modes at larger wavevectors. The evidence of well-defined dispersive behavior at small wavevectors indicates a coherence of the quantum fluid in the micron length scale. We evaluate interpretations of long wavelength modes of the electron liquid.Comment: 4 pages, 4 figure

Gene identification for the cblD defect of vitamin B12 metabolism

Background Vitamin B12 (cobalamin) is an essential cofactor in several metabolic pathways. Intracellular conversion of cobalamin to its two coenzymes, adenosylcobalamin in mitochondria and methylcobalamin in the cytoplasm, is necessary for the homeostasis of methylmalonic acid and homocysteine. Nine defects of intracellular cobalamin metabolism have been defined by means of somatic complementation analysis. One of these defects, the cblD defect, can cause isolated methylmalonic aciduria, isolated homocystinuria, or both. Affected persons present with multisystem clinical abnormalities, including developmental, hematologic, neurologic, and metabolic findings. The gene responsible for the cblD defect has not been identified. Methods We studied seven patients with the cblD defect, and skin fibroblasts from each were investigated in cell culture. Microcell-mediated chromosome transfer and refined genetic mapping were used to localize the responsible gene. This gene was transfected into cblD fibroblasts to test for the rescue of adenosylcobalamin and methylcobalamin synthesis. Results The cblD gene was localized to human chromosome 2q23.2, and a candidate gene, designated MMADHC (methylmalonic aciduria, cblD type, and homocystinuria), was identified in this region. Transfection of wild-type MMADHC rescued the cellular phenotype, and the functional importance of mutant alleles was shown by means of transfection with mutant constructs. The predicted MMADHC protein has sequence homology with a bacterial ATP-binding cassette transporter and contains a putative cobalamin binding motif and a putative mitochondrial targeting sequence. Conclusions Mutations in a gene we designated MMADHC are responsible for the cblD defect in vitamin B12 metabolism. Various mutations are associated with each of the three biochemical phenotypes of the disorder

Magnetic field generation in Higgs inflation model

We study the generation of magnetic field in Higgs-inflation models where the Standard Model Higgs boson has a large coupling to the Ricci scalar. We couple the Higgs field to the Electromagnetic fields via a non- renormalizable dimension six operator suppressed by the Planck scale in the Jordan frame. We show that during Higgs inflation magnetic fields with present value $10^{-6}$ Gauss and comoving coherence length of $100 kpc$ can be generated in the Einstein frame. The problem of large back-reaction which is generic in the usual inflation models of magneto-genesis is avoided as the back-reaction is suppressed by the large Higgs-curvature coupling.Comment: 10 pages, RevTeX

Fluctuation-induced traffic congestion in heterogeneous networks

In studies of complex heterogeneous networks, particularly of the Internet, significant attention was paid to analyzing network failures caused by hardware faults or overload, where the network reaction was modeled as rerouting of traffic away from failed or congested elements. Here we model another type of the network reaction to congestion -- a sharp reduction of the input traffic rate through congested routes which occurs on much shorter time scales. We consider the onset of congestion in the Internet where local mismatch between demand and capacity results in traffic losses and show that it can be described as a phase transition characterized by strong non-Gaussian loss fluctuations at a mesoscopic time scale. The fluctuations, caused by noise in input traffic, are exacerbated by the heterogeneous nature of the network manifested in a scale-free load distribution. They result in the network strongly overreacting to the first signs of congestion by significantly reducing input traffic along the communication paths where congestion is utterly negligible.Comment: 4 pages, 3 figure

Loss of AND-34/BCAR3 Expression in Mice Results in Rupture of the Adult Lens

PURPOSE. AND-34/BCAR3 (Breast Cancer Anti-Estrogen Resistance 3) associates with the focal adhesion adaptor protein, p130CAS/BCAR1. Expression of AND-34 regulates epithelial cell growth pattern, motility, and growth factor dependence. We sought to establish the effects of the loss of AND-34 expression in a mammalian organism. METHODS. AND-34−/− mice were generated by homologous recombination. Histopathology, in situ hybridization, and western blotting were performed on murine tissues. RESULTS. Western analyses confirmed total loss of expression in AND-34−/− splenic lymphocytes. Mice lacking AND-34 are fertile and have normal longevity. While AND-34 is widely expressed in wild type mice, histologic analysis of multiple organs in AND-34−/− mice is unremarkable and analyses of lymphocyte development show no overt changes. A small percentage of AND-34−/− mice show distinctive small white eye lesions resulting from the migration of ruptured cortical lens tissue into the anterior chamber. Following initial vacuolization and liquefaction of the lens cortex first observed at postnatal day three, posterior lens rupture occurs in all AND-34−/− mice, beginning as early as three weeks and seen in all mice at three months. Western blot analysis and in situ hybridization confirmed the presence of AND-34 RNA and protein in lens epithelial cells, particularly at the lens equator. Prior data link AND-34 expression to the activation of Akt signaling. While Akt Ser 473 phosphorylation was readily detectable in AND-34+/+ lens epithelial cells, it was markedly reduced in the AND-34−/− lens epithelium. Basal levels of p130Cas phosphorylation were higher in AND-34+/+ than in AND-34−/− lens epithelium. CONCLUSIONS. These results demonstrate the loss of AND-34 dysregulates focal adhesion complex signaling in lens epithelial cells and suggest that AND-34-mediated signaling is required for maintenance of the structural integrity of the adult ocular lens.National Institutes of Health (RO1 CA114094); Logica Foundatio