Activation of TLR3 in keratinocytes increases expression of genes involved in formation of the epidermis, lipid accumulation, and epidermal organelles.

Injury to the skin, and the subsequent release of noncoding double-stranded RNA (dsRNA) from necrotic keratinocytes, has been identified as an endogenous activator of Toll-like receptor 3 (TLR3). As changes in keratinocyte growth and differentiation follow injury, we hypothesized that TLR3 might trigger some elements of the barrier repair program in keratinocytes. dsRNA was observed to induce TLR3-dependent increases in human keratinocyte mRNA abundance for ABCA12 (ATP-binding cassette, sub-family A, member 12), glucocerebrosidase, acid sphingomyelinase, and transglutaminase 1. Additionally, treatment with dsRNA resulted in increases in sphingomyelin and morphologic changes including increased epidermal lipid staining by Oil Red O and TLR3-dependent increases in lamellar bodies and keratohyalin granules. These observations show that dsRNA can stimulate some events in keratinocytes that are important for skin barrier repair and maintenance

Effect of Applied Orthorhombic Lattice Distortion on the Antiferromagnetic Phase of CeAuSb2_2

We study the response of the antiferromagnetism of CeAuSb$_2$ to orthorhombic lattice distortion applied through in-plane uniaxial pressure. The response to pressure applied along a $\langle 110 \rangle$ lattice direction shows a first-order transition at zero pressure, which shows that the magnetic order lifts the $(110)/(1\bar{1}0)$ symmetry of the unstressed lattice. Sufficient $\langle 100 \rangle$ pressure appears to rotate the principal axes of the order from $\langle 110 \rangle$ to $\langle 100 \rangle$. At low $\langle 100 \rangle$ pressure, the transition at $T_N$ is weakly first-order, however it becomes continuous above a threshold $\langle 100 \rangle$ pressure. We discuss the possibility that this behavior is driven by order parameter fluctuations, with the restoration of a continuous transition a result of reducing the point-group symmetry of the lattice.Comment: 6 pages, 7 figure

ENVIRONMENTAL POLICY INFLUENCES ON LIVESTOCK STOCKING AND LOCATION DECISIONS

This paper explores the relationship between state level environmental regulations and stocking and location decisions in the U.S livestock and poultry industry (beef, chicken, dairy and hogs). Rather than conduct this analysis on a species-by-species basis, we choose to focus upon the overall size of the livestock industry (expressed in animal units) and the size of industry found on large, medium and small operations by state (48) and over time (28 yrs). Results indicate that industry may drive policy rather than the converse. However, since we also find that existing policy rules have differential impacts on the industry by operation size, we conclude that structural change in the industry may be driven in part by size or legal structure discriminating regulations.Demand and Price Analysis, Livestock Production/Industries,

Predictability of helminth parasite host range using information on geography, host traits and parasite community structure

© Cambridge University Press 2016. Host-parasite associations are complex interactions dependent on aspects of hosts (e.g. traits, phylogeny or coevolutionary history), parasites (e.g. traits and parasite interactions) and geography (e.g. latitude). Predicting the permissive host set or the subset of the host community that a parasite can infect is a central goal of parasite ecology. Here we develop models that accurately predict the permissive host set of 562 helminth parasites in five different parasite taxonomic groups. We developed predictive models using host traits, host taxonomy, geographic covariates, and parasite community composition, finding that models trained on parasite community variables were more accurate than any other covariate group, even though parasite community covariates only captured a quarter of the variance in parasite community composition. This suggests that it is possible to predict the permissive host set for a given parasite, and that parasite community structure is an important predictor, potentially because parasite communities are interacting non-random assemblages

Effect of uniaxial stress on the magnetic phases of CeAuSb2_2

We present results of measurements of resistivity of \CAS{} under the combination of $c$-axis magnetic field and in-plane uniaxial stress. In unstressed \CAS{} there are two magnetic phases. The low-field A phase is a single-component spin-density wave (SDW), with $\mathbf{q} = (\eta, \pm \eta, 1/2)$, and the high-field B phase consists of microscopically coexisting $(\eta, \eta, 1/2)$ and $(\eta, -\eta, 1/2)$ spin-density waves. Pressure along a $\langle 100 \rangle$ lattice direction is a transverse field to both of these phases, and so initially has little effect, however eventually induces new low- and high-field phases in which the principal axes of the SDW components appear to have rotated to the $\langle 100 \rangle$ directions. Under this strong $\langle 100 \rangle$ compression, the field evolution of the resistivity is much smoother than at zero strain: In zero strain, there is a strong first-order transition, while under strong $\langle 100 \rangle$ it becomes much broader. We hypothesize that this is a consequence of the uniaxial stress lifting the degeneracy between the (100) and (010) directions.Comment: 8 pages, 7 figure

Vector species richness increases haemorrhagic disease prevalence through functional diversity modulating the duration of seasonal transmission

© Copyright Cambridge University Press 2015. SUMMARY Although many parasites are transmitted between hosts by a suite of arthropod vectors, the impact of vector biodiversity on parasite transmission is poorly understood. Positive relationships between host infection prevalence and vector species richness (SR) may operate through multiple mechanisms, including (i) increased vector abundance, (ii) a sampling effect in which species of high vectorial capacity are more likely to occur in species-rich communities, and (iii) functional diversity whereby communities comprised species with distinct phenologies may extend the duration of seasonal transmission. Teasing such mechanisms apart is impeded by a lack of appropriate data, yet could highlight a neglected role for functional diversity in parasite transmission. We used statistical modelling of extensive host, vector and microparasite data to test the hypothesis that functional diversity leading to longer seasonal transmission explained variable levels of disease in a wildlife population. We additionally developed a simple transmission model to guide our expectation of how an increased transmission season translates to infection prevalence. Our study demonstrates that vector SR is associated with increased levels of disease reporting, but not via increases in vector abundance or via a sampling effect. Rather, the relationship operates by extending the length of seasonal transmission, in line with theoretical predictions

Erratum: Vector species richness increases haemorrhagic disease prevalence through functional diversity modulating the duration of seasonal transmission (Parasitology (2015) 143 (874-879) DOI: 10.1017/S0031182015000578)

© Cambridge University Press 2016. The publisher apologises for the link to the Supplementary Material being incorrect. On page 878, the Supplementary Material section should read as follows: SUPPLEMENTARY MATERIAL To view supplementary material for this article, please visit https://doi.org/10.1017/S0031182015000578

Estimating parasite host range

© 2017 The Author(s) Published by the Royal Society. All rights reserved. Estimating the number of host species that a parasite can infect (i.e. host range) provides key insights into the evolution of host specialism and is a central concept in disease ecology. Host range is rarely estimated in real systems, however, because variation in species relative abundance and the detection of rare species makes it challenging to confidently estimate host range. We applied a non-parametric richness indicator to estimate host range in simulated and empirical data, allowing us to assess the influence of sampling heterogeneity and data completeness. After validating our method on simulated data, we estimated parasite host range for a sparsely sampled global parasite occurrence database (Global Mammal Parasite Database) and a repeatedly sampled set of parasites of small mammals from New Mexico (Sevilleta Long Term Ecological Research Program). Estimation accuracy varied strongly with parasite taxonomy, number of parasite occurrence records, and the shape of host species-abundance distribution (i.e. the dominance and rareness of species in the host community). Our findings suggest that between 20% and 40% of parasite host ranges are currently unknown, highlighting a major gap in our understanding of parasite specificity, host–parasite network structure, and parasite burdens

G2A Attenuates Propionibacterium acnes Induction of Inflammatory Cytokines in Human Monocytes.

Background:Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. Objective:To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. Methods:Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. Results:G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. Conclusion:G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium