Interaction of sine-Gordon kinks with defects: The two-bounce resonance

A model of soliton-defect interactions in the sine-Gordon equations is studied using singular perturbation theory. Melnikov theory is used to derive a critical velocity for strong interactions, which is shown to be exponentially small for weak defects. Matched asymptotic expansions for nearly heteroclinic orbits are constructed for the initial value problem, which are then used to derive analytical formulas for the locations of the well known two- and three-bounce resonance windows, as well as several other phenomena seen in numerical simulations.Comment: 26 pages, 17 figure

Vector-soliton collision dynamics in nonlinear optical fibers

We consider the interactions of two identical, orthogonally polarized vector solitons in a nonlinear optical fiber with two polarization directions, described by a coupled pair of nonlinear Schroedinger equations. We study a low-dimensional model system of Hamiltonian ODE derived by Ueda and Kath and also studied by Tan and Yang. We derive a further simplified model which has similar dynamics but is more amenable to analysis. Sufficiently fast solitons move by each other without much interaction, but below a critical velocity the solitons may be captured. In certain bands of initial velocities the solitons are initially captured, but separate after passing each other twice, a phenomenon known as the two-bounce or two-pass resonance. We derive an analytic formula for the critical velocity. Using matched asymptotic expansions for separatrix crossing, we determine the location of these "resonance windows." Numerical simulations of the ODE models show they compare quite well with the asymptotic theory.Comment: 32 pages, submitted to Physical Review

Do people with risky behaviours participate in biomedical cohort studies?

BACKGROUND: Analysis was undertaken on data from randomly selected participants of a bio-medical cohort study to assess representativeness. The research hypotheses was that there was no difference in participation and non-participations in terms of health-related indicators (smoking, alcohol use, body mass index, physical activity, blood pressure and cholesterol readings and overall health status) and selected socio-demographics (age, sex, area of residence, education level, marital status and work status). METHODS: Randomly selected adults were recruited into a bio-medical representative cohort study based in the north western suburbs of the capital of South Australia – Adealide. Comparison data was obtained from cross-sectional surveys of randomly selected adults in the same age range and in the same region. The cohort participants were 4060 randomly selected adults (18+ years). RESULTS: There were no major differences between study participants and the comparison population in terms of current smoking status, body mass index, physical activity, overall health status and proportions with current high blood pressure and cholesterol readings. Significantly more people who reported a medium to very high alcohol risk participated in the study. There were some demographic differences with study participants more likely to be in the middle level of household income and education level. CONCLUSION: People with risky behaviours participated in this health study in the same proportions as people without these risk factors

Control of TH17 cells occurs in the small intestine

Interleukin (IL)-17-producing T helper cells (TH17) are a recently identified CD4+ T cell subset distinct from T helper type 1 (TH1) and T helper type 2 (TH2) cells1. TH17 cells can drive antigen specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE)2, the mouse model for multiple sclerosis. The factors that are needed for the generation of TH17 cells have been well-characterized3–6. However, where and how the immune system controls TH17 cells in vivo remains unclear.Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory TH17 cells can be redirected to and controlled in the small intestine. TH17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that TH17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen and simultaneously pro-inflammatory TH17 cells acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rTH17). These results identify mechanisms limiting TH17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of TH17 cells

In-sample forecasting: A brief review and new algorithms

Statistical methods often distinguish between in-sample and out-of-sample approaches. In particular this is the case when time is involved. Then often time series methods are proposed that extrapolate past patterns into the future via complicated recursion formulas. Standard statistical inference is on the other hand concerned with estimating parameters within the given sample. This review paper is about a statistical methodology, where all parameters are estimated in-sample while producing a forecast out-of-sample without recursion or extrapolation. A new super-simulation algorithm ensures a faster implementation of the simplest and perhaps most important version of in-sample forecasting

Forty years of carabid beetle research in Europe - from taxonomy, biology, ecology and population studies to bioindication, habitat assessment and conservation

Volume: 100Start Page: 55End Page: 14