A summary of the BARREL campaigns: Technique for studying electron precipitation.

BARREL observed electron precipitation over wide range of energy and timescalesPrecipitating electron distribution is determined using spectroscopy for 19 January 2013 eventBARREL timing data has accuracy within sampling interval of 0.05 s

O-3, NOY, AND NOX/NOY IN THE UPPER TROPOSPHERE OF THE EQUATORIAL PACIFIC

No abstract available

The Drinfel'd twisted XYZ model

We construct a factorizing Drinfel'd twist for a face type model equivalent to the XYZ model. Completely symmetric expressions for the operators of the monodromy matrix are obtained.Comment: 15 pages, 4 figures, second preprint no. added, reference [14] added, typos correcte

Effect of terbutaline on hyperpnoea-induced bronchoconstriction and urinary club cell protein 16 in athletes

This article is made available through the Brunel Open Access Publishing Fund and is distributed by the Creative Commons CC-BY 3.0 license, under which all are free to reuse or distribute the article under the condition that this original publication must be cited.Repeated injury of the airway epithelium caused by hyperpnoea of poorly conditioned air has been proposed as a key factor in the pathogenesis of exercise-induced bronchoconstriction (EIB) in athletes. In animals, the short-acting β2-agonist terbutaline has been shown to reduce dry airflow-induced bronchoconstriction and the associated shedding of airway epithelial cells. Our aim was to test the efficacy of inhaled terbutaline in attenuating hyperpnoea-induced bronchoconstriction and airway epithelial injury in athletes. Twenty-seven athletes with EIB participated in a randomized, double-blind, placebo-controlled, crossover study. Athletes completed an 8-min eucapnic voluntary hyperpnoea (EVH) test with dry air on two separate days 15 min after inhaling 0.5 mg terbutaline or a matching placebo. Forced expiratory volume in 1 s (FEV1) and urinary concentration of the club cell (Clara cell) protein 16 (CC16, a marker of airway epithelial perturbation) were measured before and up to 60 min after EVH. The maximum fall in FEV1 of 17 ± 8% (SD) on placebo was reduced to 8 ± 5% following terbutaline (P < 0.001). Terbutaline gave bronchoprotection (i.e., post-EVH FEV1 fall <10%) to 22 (81%) athletes. EVH caused an increase in urinary excretion of CC16 in both conditions (P < 0.001), and terbutaline significantly reduced this rise (pre- to postchallenge CC16 increase 416 ± 495 pg/μmol creatinine after placebo vs. 315 ± 523 pg/μmol creatinine after terbutaline, P = 0.016). These results suggest that the inhalation of a single therapeutic dose of terbutaline offers significant protection against hyperpnoea-induced bronchoconstriction and attenuates acute airway epithelial perturbation in athletes.World Anti Doping Agenc

Power-dependent speciation of volatile organic compounds in aircraft exhaust

As part of the third NASA Aircraft Particle Emissions Experiment (APEX-3, November 2005), whole air samples were collected to determine the emission rates of volatile organic compounds (VOCs) from aircraft equipped with three different gas-turbine engines (an Allison Engine 3007-A1E, a Pratt-Whitney 4158, and a Rolls-Royce RB211-535E4B). Samples were collected 1 m behind the engine exhaust plane of the engines while they were operated at powers ranging from idle up to 30% of maximum rated thrust.Exhaust emission indices (mass emitted per kilogram of fuel used) for CO and non-methane hydrocarbons (NMHCs) were calculated based on enhancements over background relative to CO 2. Emissions of all NMHCs were greatest at low power with values decreasing by an order of magnitude with increasing power. Previous studies have shown that scaling idle hydrocarbon emissions to formaldehyde or ethene (which are typically emitted at a ratio of 1-to-1 at idle) reduces variability amongst engine types. NMHC emissions were found to scale at low power, with alkenes contributing over 50% of measured NMHCs. However, as the power increases hydrocarbon emissions no longer scale to ethene, as the aromatics become the dominant species emitted. This may be due in part to a shift in combustion processes from thermal cracking (producing predominantly alkenes) to production of new molecules (producing proportionally more aromatics) as power increases. The formation of these aromatics is an intermediate step in the production of soot, which also increases with increasing power. The increase in aromatics relative to alkenes additionally results in a decrease in the hydroxyl radical reactivity and ozone formation potential of aircraft exhaust.Samples collected 30 m downwind of the engine were also analyzed for NMHCs and carbonyl compounds (acetone, 2-butanone and C 1-C 9 aldehydes). Formaldehyde was the predominant carbonyl emitted; however, the ratio of ethene-to-formaldehyde varied between the aircraft, possibly due to the sampling of transient emissions such as engine start-up and power changes. A large portion of the measured emissions (27-42% by mass) in the plume samples was made up of hazardous air pollutants (HAPs) with oxygenated compounds being most significant. © 2012

Methods for estimating the case fatality ratio for a novel, emerging infectious disease.

During the course of an epidemic of a potentially fatal disease, it is important that the case fatality ratio be well estimated. The authors propose a novel method for doing so based on the Kaplan-Meier survival procedure, jointly considering two outcomes (death and recovery), and evaluate its performance by using data from the 2003 epidemic of severe acute respiratory syndrome in Hong Kong, People's Republic of China. They compare this estimate obtained at various points in the epidemic with the case fatality ratio eventually observed; with two commonly quoted, naïve estimates derived from cumulative incidence and mortality statistics at single time points; and with estimates in which a parametric mixture model is used. They demonstrate the importance of patient characteristics regarding outcome by analyzing subgroups defined by age at admission to the hospital

Role of dystrophin in airway smooth muscle phenotype, contraction and lung function

Dystrophin links the transmembrane dystrophin-glycoprotein complex to the actin cytoskeleton. We have shown that dystrophin-glycoprotein complex subunits are markers for airway smooth muscle phenotype maturation and together with caveolin-1, play an important role in calcium homeostasis. We tested if dystrophin affects phenotype maturation, tracheal contraction and lung physiology. We used dystrophin deficient Golden Retriever dogs (GRMD) and mdx mice vs healthy control animals in our approach. We found significant reduction of contractile protein markers: smooth muscle myosin heavy chain (smMHC) and calponin and reduced Ca2+ response to contractile agonist in dystrophin deficient cells. Immunocytochemistry revealed reduced stress fibers and number of smMHC positive cells in dystrophin-deficient cells, when compared to control. Immunoblot analysis of Akt1, GSK3β and mTOR phosphorylation further revealed that downstream PI3K signaling, which is essential for phenotype maturation, was suppressed in dystrophin deficient cell cultures. Tracheal rings from mdx mice showed significant reduction in the isometric contraction to methacholine (MCh) when compared to genetic control BL10ScSnJ mice (wild-type). In vivo lung function studies using a small animal ventilator revealed a significant reduction in peak airway resistance induced by maximum concentrations of inhaled MCh in mdx mice, while there was no change in other lung function parameters. These data show that the lack of dystrophin is associated with a concomitant suppression of ASM cell phenotype maturation in vitro, ASM contraction ex vivo and lung function in vivo, indicating that a linkage between the DGC and the actin cytoskeleton via dystrophin is a determinant of the phenotype and functional properties of ASM. © 2014 Sharma et al

Reduction in both seasonal mortality and longer term mortality trends following restrictions on the sulphur content of fuel oil in Hong Kong (Abstract)

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