206 research outputs found

    Toward Comprehensive Refugee Legislation in Hong Kong? Reflections on Reform of the 'Torture Screening' Procedures

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    Wavelet penalized likelihood estimation in generalized functional models

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    The paper deals with generalized functional regression. The aim is to estimate the influence of covariates on observations, drawn from an exponential distribution. The link considered has a semiparametric expression: if we are interested in a functional influence of some covariates, we authorize others to be modeled linearly. We thus consider a generalized partially linear regression model with unknown regression coefficients and an unknown nonparametric function. We present a maximum penalized likelihood procedure to estimate the components of the model introducing penalty based wavelet estimators. Asymptotic rates of the estimates of both the parametric and the nonparametric part of the model are given and quasi-minimax optimality is obtained under usual conditions in literature. We establish in particular that the LASSO penalty leads to an adaptive estimation with respect to the regularity of the estimated function. An algorithm based on backfitting and Fisher-scoring is also proposed for implementation. Simulations are used to illustrate the finite sample behaviour, including a comparison with kernel and splines based methods

    A Genome-Wide Association Study of Psoriasis and Psoriatic Arthritis Identifies New Disease Loci

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    A genome-wide association study was performed to identify genetic factors involved in susceptibility to psoriasis (PS) and psoriatic arthritis (PSA), inflammatory diseases of the skin and joints in humans. 223 PS cases (including 91 with PSA) were genotyped with 311,398 single nucleotide polymorphisms (SNPs), and results were compared with those from 519 Northern European controls. Replications were performed with an independent cohort of 577 PS cases and 737 controls from the U.S., and 576 PSA patients and 480 controls from the U.K.. Strongest associations were with the class I region of the major histocompatibility complex (MHC). The most highly associated SNP was rs10484554, which lies 34.7 kb upstream from HLA-C (P = 7.8×10−11, GWA scan; P = 1.8×10−30, replication; P = 1.8×10−39, combined; U.K. PSA: P = 6.9×10−11). However, rs2395029 encoding the G2V polymorphism within the class I gene HCP5 (combined P = 2.13×10−26 in U.S. cases) yielded the highest ORs with both PS and PSA (4.1 and 3.2 respectively). This variant is associated with low viral set point following HIV infection and its effect is independent of rs10484554. We replicated the previously reported association with interleukin 23 receptor and interleukin 12B (IL12B) polymorphisms in PS and PSA cohorts (IL23R: rs11209026, U.S. PS, P = 1.4×10−4; U.K. PSA: P = 8.0×10−4; IL12B:rs6887695, U.S. PS, P = 5×10−5 and U.K. PSA, P = 1.3×10−3) and detected an independent association in the IL23R region with a SNP 4 kb upstream from IL12RB2 (P = 0.001). Novel associations replicated in the U.S. PS cohort included the region harboring lipoma HMGIC fusion partner (LHFP) and conserved oligomeric golgi complex component 6 (COG6) genes on chromosome 13q13 (combined P = 2×10−6 for rs7993214; OR = 0.71), the late cornified envelope gene cluster (LCE) from the Epidermal Differentiation Complex (PSORS4) (combined P = 6.2×10−5 for rs6701216; OR 1.45) and a region of LD at 15q21 (combined P = 2.9×10−5 for rs3803369; OR = 1.43). This region is of interest because it harbors ubiquitin-specific protease-8 whose processed pseudogene lies upstream from HLA-C. This region of 15q21 also harbors the gene for SPPL2A (signal peptide peptidase like 2a) which activates tumor necrosis factor alpha by cleavage, triggering the expression of IL12 in human dendritic cells. We also identified a novel PSA (and potentially PS) locus on chromosome 4q27. This region harbors the interleukin 2 (IL2) and interleukin 21 (IL21) genes and was recently shown to be associated with four autoimmune diseases (Celiac disease, Type 1 diabetes, Grave's disease and Rheumatoid Arthritis)

    Development of a practice guideline for dietary counselling of children with IgE-mediated food allergy

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    Purpose The incidence of food allergy is increasing globally and whilst there is consensus that dietitians should be involved in its management, the roles that dietitians should fulfill differ between different guidelines and the description of tasks remains unclear. Currently, no Swiss guideline exists to assist dietitians in counselling children with food allergies. There is a need for recommendations that will guide dietitians through the counselling process. The aim of this project was to create a practice guideline for dietary counselling of children with food allergy. Methods Practice guidelines were developed following the Academy of Nutrition and Dietetics stepwise approach. The process consisted of six steps: (1) Determine the scope oft he guideline. (2) Conduct a systematic review. (3) Draft the guideline recommendations using the Nutrition Care Process (NCP) as a framework. (4) Finalise the guideline during a face-to-face meeting. (5) Conduct internal and external review and revise accordingly. (6) Publish guideline. Results The process resulted in 25 recommendations for dietary counselling. Most recommendations are based on expert opinion only, due to the lack of studies in this field and showed similar levels of consensus between the expert group and external review by allergists. However, there were nine recommendations where the consensus differed. Conclusion This guideline provides a comprehensive guide to dietary counselling for food allergy by dietitians in Switzerland. It will inform best practice and improve patient-centred care and encourage a consistent approach, but it will need to be reviewed and updated as more robust evidence is produced

    Testing theories of post-error slowing

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    People tend to slow down after they make an error. This phenomenon, generally referred to as post-error slowing, has been hypothesized to reflect perceptual distraction, time wasted on irrelevant processes, an a priori bias against the response made in error, increased variability in a priori bias, or an increase in response caution. Although the response caution interpretation has dominated the empirical literature, little research has attempted to test this interpretation in the context of a formal process model. Here, we used the drift diffusion model to isolate and identify the psychological processes responsible for post-error slowing. In a very large lexical decision data set, we found that post-error slowing was associated with an increase in response caution and—to a lesser extent—a change in response bias. In the present data set, we found no evidence that post-error slowing is caused by perceptual distraction or time wasted on irrelevant processes. These results support a response-monitoring account of post-error slowing
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