Scaling laws for magnetic fields on the quiet Sun

The Sun's magnetic field is structured over a range of scales that span approximately seven orders of magnitudes, four of which lie beyond the resolving power of current telescopes. Here we have used a Hinode SOT/SP deep mode data set for the quiet-sun disk center in combination with constraints from the Hanle effect to derive scaling laws that describe how the magnetic structuring varies from the resolved scales down to the magnetic diffusion limit, where the field ceases to be frozen-in. The focus of the analysis is a derivation of the magnetic energy spectrum, but we also discuss the scale dependence of the probability density function (PDF) for the flux densities and the role of the cancellation function for the average unsigned flux density. Analysis of the Hinode data set with the line-ratio method reveals a collapsed flux population in the form of flux tubes with a size distribution that is peaked in the 10-100 km range. Magnetic energy is injected into this scale range by the instability mechanism of flux tube collapse, which is driven by the external gas pressure in the superadiabatic region at the top of the convection zone. This elevates the magnetic energy spectrum just beyond the telescope resolution limit. Flux tube decay feeds an inertial range that cascades down the scale spectrum to the magnetic diffusion limit, and which contains the tangled, "hidden" flux that is known to exist from observations of the Hanle effect. The observational constraints demand that the total magnetic energy in the hidden flux must be of the same order as the total energy in the kG flux tubes. Both the flux tubes and the hidden flux are found to be preferentially located in the intergranular lanes, which is to be expected since they are physically related.Comment: accepted for publication in Astronomy & Astrophysic

A Recombinant Blood-Stage Malaria Vaccine Reduces Plasmodium falciparum Density and Exerts Selective Pressure on Parasite Populations in a Phase 1-2b Trial in Papua New Guinea

The malaria vaccine Combination B comprises recombinant Plasmodium falciparum ring-infected erythrocyte surface antigen and 2 merozoite surface proteins (MSP1 and MSP2) formulated in oil-based adjuvant. A phase 1-2b double-blind, randomized, placebo-controlled trial in 120 children (5-9 years old) in Papua New Guinea demonstrated a 62% (95% confidence limits: 13%, 84%) reduction in parasite density in children not pretreated with sulfadoxine-pyrimethamine. Vaccinees had a lower prevalence of parasites carrying the MSP2-3D7 allelic form (corresponding to that in the vaccine) and a higher incidence of morbid episodes associated with FC27-type parasites. These results demonstrate functional activity of Combination B against P. falciparum in individuals with previous malaria exposure. The specific effects on parasites with particular msp2 genotypes suggest that the MSP2 component, at least in part, accounted for the activity. The vaccine-induced selection pressure exerted on the parasites and its consequences for morbidity strongly argue for developing vaccines comprising conserved antigens and/or multiple components covering all important allelic type

Inselect: Automating the Digitization of Natural History Collections

Copyright: © 2015 Hudson et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The attached file is the published version of the article

IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome

Expansion of the polyglutamine repeat within the protein Huntingtin (Htt) causes Huntington's disease, a neurodegenerative disease associated with aging and the accumulation of mutant Htt in diseased neurons. Understanding the mechanisms that influence Htt cellular degradation may target treatments designed to activate mutant Htt clearance pathways. We find that Htt is phosphorylated by the inflammatory kinase IKK, enhancing its normal clearance by the proteasome and lysosome. Phosphorylation of Htt regulates additional post-translational modifications, including Htt ubiquitination, SUMOylation, and acetylation, and increases Htt nuclear localization, cleavage, and clearance mediated by lysosomal-associated membrane protein 2A and Hsc70. We propose that IKK activates mutant Htt clearance until an age-related loss of proteasome/lysosome function promotes accumulation of toxic post-translationally modified mutant Htt. Thus, IKK activation may modulate mutant Htt neurotoxicity depending on the cell's ability to degrade the modified species

The fruits of collaboration in a multidisciplinary field

Collaboration between researchers and between research organizations is generally considered a desirable course of action, in particular by some funding bodies. However, collaboration within a multidisciplinary community, such as the Computer–Human Interaction (CHI) community, can be challenging. We performed a bibliometric analysis of the CHI conference proceedings to determine if papers that have authors from different organization or countries receive more citations than papers that are authored by members of the same organization. There was no significant difference between these three groups, indicating that there is no advantage for collaboration in terms of citation frequency. Furthermore, we tested if papers written by authors from different organizations or countries receive more best paper awards or at least award nominations. Papers from only one organization received significantly fewer nominations than collaborative papers

Bioactive Hydrogel Substrates: Probing Leukocyte Receptor–Ligand Interactions in Parallel Plate Flow Chamber Studies

The binding of activated integrins on the surface of leukocytes facilitates the adhesion of leukocytes to vascular endothelium during inflammation. Interactions between selectins and their ligands mediate rolling, and are believed to play an important role in leukocyte adhesion, though the minimal recognition motif required for physiologic interactions is not known. We have developed a novel system using poly(ethylene glycol) (PEG) hydrogels modified with either integrin-binding peptide sequences or the selectin ligand sialyl Lewis X (SLe(X)) within a parallel plate flow chamber to examine the dynamics of leukocyte adhesion to specific ligands. The adhesive peptide sequences arginine–glycine–aspartic acid–serine (RGDS) and leucine–aspartic acid–valine (LDV) as well as sialyl Lewis X were bound to the surface of photopolymerized PEG diacrylate hydrogels. Leukocytes perfused over these gels in a parallel plate flow chamber at physiological shear rates demonstrate both rolling and firm adhesion, depending on the identity and concentration of ligand bound to the hydrogel substrate. This new system provides a unique polymer-based model for the study of interactions between leukocytes and endothelium as well as a platform to develop improved scaffolds for cardiovascular tissue engineering

First measurement of direct f0(980)f_0(980) photoproduction on the proton

We report on the results of the first measurement of exclusive $f_0(980)$ meson photoproduction on protons for $E_\gamma=3.0 - 3.8$ GeV and $-t = 0.4-1.0$ GeV$^2$. Data were collected with the CLAS detector at the Thomas Jefferson National Accelerator Facility. The resonance was detected via its decay in the $\pi^+ \pi^-$ channel by performing a partial wave analysis of the reaction $\gamma p \to p \pi^+ \pi^-$. Clear evidence of the $f_0(980)$ meson was found in the interference between $P$ and $S$ waves at $M_{\pi^+ \pi^-}\sim 1$ GeV. The $S$-wave differential cross section integrated in the mass range of the $f_0(980)$ was found to be a factor of 50 smaller than the cross section for the $\rho$ meson. This is the first time the $f_0(980)$ meson has been measured in a photoproduction experiment

A Catering Theory of Analyst Bias

We posit a theory that runs counter to how conventional wisdom thinks about analyst bias, that it is the result of distorted incentives by "the system" - especially upstream factors like the analysts' employers. We suggest that analysts are also heavily influenced by what investors believe, the purported victims of analyst bias. We adapt Mullainathan-Shleifer's theory of media bias to build a theory of how analysts cater to what investors believe. The theory also predicts that competition among analysts does not reduce their bias. We provide empirical support for this theory, using an enormous dataset built from over 6.5 million analyst estimates and 42.8 million observations on investor holdings, which we argue is a proxy for what they believe. We use a simultaneous-equations model for estimation, with instruments to rule out alternative interpretations of the direction of causality. For additional robustness, we investigate the time series of analyst bias and heterogeneity in investor beliefs from 1987 through 2003. Dickey-Fuller tests show that both have unit roots, but we establish that cointegration hold. Further, we employ a vector-autoregressive model to show Granger - causality between the two