Observation of different spin behavior with temperature variation and Cr substitution in a multiferroic compound YMn2_2O5_5

In this article, the collective response of the spins is explored through low field bulk magnetic measurement for the series YMn$_{2-x}$Cr$_x$O$_5$ (x= 0.0, 0.05). Low field ac susceptibility and dc magnetization of YMn$_2$O$_5$ shows multiple transition in analogy to those observed in electrical measurement of the compound. Using various time dependent magnetization protocols it has been observed that the behavior of spins in commensurate and incommensurate phase are drastically different. YMn$_{1.95}$Cr$_{0.05}$O$_5$ undergoes a ferrimagnetic ordering with an enhanced magnetic ordering temperature as compared to the parent, which undergoes an antiferromagnetic ordering. Appearance of spontaneous magnetization without any major change in the atomic structure is rather significant since the parent compound is an important multiferroic material. In addition, magnetic memory effect is observed in the Cr substituted compound whereas it is absent in the parent compound

Determining the extragalactic extinction law with SALT

We present CCD imaging observations of early-type galaxies with dark lanes obtained with the Southern African Large Telescope (SALT) during its performance-verification phase. We derive the extinction law by the extragalactic dust in the dark lanes in the spectral range 1.11mu m^{-1} < lambda^{-1} < 2.94 mu m^{-1} by fitting model galaxies to the unextinguished parts of the image, and subtracting from these the actual images. We find that the extinction curves run parallel to the Galactic extinction curve, which implies that the properties of dust in the extragalactic enviroment are similar to those of the Milky Way. The ratio of the total V band extinction to the selective extinction between the V and B bands is derived for each galaxy with an average of 2.82+-0.38, compared to a canonical value of 3.1 for the Milky Way. The similar values imply that galaxies with well-defined dark lanes have characteristic dust grain sizes similar to those of Galactic dust.Comment: 20 pages, 15 figures and 4 tables. Accepted for publication in MNRA

4-Formyl­phenyl 2,3,4,6-tetra-O-acetyl-β-d-glucopyran­oside

The pyran­oside ring in the title compound, C21H24O11, has a chair conformation with the substituted benzene ring occupying an equatorial position. The crystal packing is dominated by C—H⋯O inter­actions that lead to the formation of supra­molecular layers in the ab plane

An essential function for the ATR-Activation-Domain (AAD) of TopBP1 in mouse development and cellular senescence

ATR activation is dependent on temporal and spatial interactions with partner proteins. In the budding yeast model, three proteins – Dpb11TopBP1, Ddc1Rad9 and Dna2 - all interact with and activate Mec1ATR. Each contains an ATR activation domain (ADD) that interacts directly with the Mec1ATR:Ddc2ATRIP complex. Any of the Dpb11TopBP1, Ddc1Rad9 or Dna2 ADDs is sufficient to activate Mec1ATR in vitro. All three can also independently activate Mec1ATR in vivo: the checkpoint is lost only when all three AADs are absent. In metazoans, only TopBP1 has been identified as a direct ATR activator. Depletion-replacement approaches suggest the TopBP1-AAD is both sufficient and necessary for ATR activation. The physiological function of the TopBP1 AAD is, however, unknown. We created a knock-in point mutation (W1147R) that ablates mouse TopBP1-AAD function. TopBP1-W1147R is early embryonic lethal. To analyse TopBP1-W1147R cellular function in vivo, we silenced the wild type TopBP1 allele in heterozygous MEFs. AAD inactivation impaired cell proliferation, promoted premature senescence and compromised Chk1 signalling following UV irradiation. We also show enforced TopBP1 dimerization promotes ATR-dependent Chk1 phosphorylation. Our data suggest that, unlike the yeast models, the TopBP1-AAD is the major activator of ATR, sustaining cell proliferation and embryonic development

Scale-up of an RF heated micro trickle bed reactor to a kg/day production scale

The scale-up of a radiofrequency (RF) heated micro trickle bed reactor for hydrogenation of 2-methyl-3-butyne-2-ol (MBY) over a Pd/TiO2 catalyst has been performed. The axial and radial temperature profiles were calculated using a 2D convection and conduction heat transfer model. The effect of the reactor length, tube diameter and number of parallel tubes on the temperature non-uniformity parameter has been studied. The axial scale-up was achieved by repeating a single periodic unit consisting of one heating and one catalytic zone along the reactor length. The catalyst loading can be increased by an order of magnitude following this approach. A radial temperature difference of 2 K was developed in a reactor with an inner diameter of 15 mm. The scale-up by numbering up allows the accommodation of seven parallel tubes inside a single RF coil. It creates a 7 K difference in the average temperature between the central and the outer tubes which results in a 5% difference in MBY conversion. An overall scale-up factor of near 700 is achieved which corresponds to a production rate of 0.5 kg of product/day

Chemical and Metabolic Aspects of Antimetabolite Toxins Produced by Pseudomonas syringae Pathovars

Pseudomonas syringae is a phytopathogenic bacterium present in a wide variety of host plants where it causes diseases with economic impact. The symptoms produced by Pseudomonas syringae include chlorosis and necrosis of plant tissues, which are caused, in part, by antimetabolite toxins. This category of toxins, which includes tabtoxin, phaseolotoxin and mangotoxin, is produced by different pathovars of Pseudomonas syringae. These toxins are small peptidic molecules that target enzymes of amino acids’ biosynthetic pathways, inhibiting their activity and interfering in the general nitrogen metabolism. A general overview of the toxins’ chemistry, biosynthesis, activity, virulence and potential applications will be reviewed in this work

Data and 2D scaling relations for galaxies in Abell 1689: a hint of size evolution at z~0.2

{abridged} We present imaging and spectroscopy of Abell 1689 (z=0.183) from GEMINI/GMOS-N and HST/ACS. We measure integrated photometry from the GMOS g' and r' images (for 531 galaxies) and surface photometry from the HST F625W image (for 43 galaxies) as well as velocities and velocity dispersions from the GMOS spectra (for 71 galaxies). We construct the Kormendy relation (KR), Faber-Jackson relation (FJR) and colour-magnitude relation (CMR) for early-type galaxies in Abell 1689 using this data and compare them to those of the Coma cluster. We measure the intrinsic scatter of the CMR in Abell 1689 to be 0.054 \pm 0.004 mag which places degenerate constraints on the ratio of the assembly timescale to the time available (beta) and the age of the population. Making the assumption that galaxies in Abell 1689 will evolve into those of Coma over an interval of 2.26 Gyr breaks this degeneracy and limits beta to be > 0.6 and the age of the red sequence to be > 5.5 Gyr (formed at z > 0.55). Without corrections for size evolution but accounting for magnitude cuts and selection effects, the KR & FJR are inconsistent and disagree at the 2 sigma level regarding the amount of luminosity evolution in the last 2.26 Gyr. However, after correcting for size evolution the KR & FJR show similar changes in luminosity (0.22 \pm 0.11 mag) that are consistent with the passive evolution of the stellar populations from a single burst of star formation 10.2 \pm 3.3 Gyr ago (z = 1.8+inf-0.9). Thus the changes in the KR, FJR & CMR of Abell 1689 relative to Coma all agree and suggest old galaxy populations with little or no synchronisation in the star formation histories. Furthermore, the weak evidence for size evolution in the cluster environment in the last 2.26 Gyr places interesting constraints on the possible mechanisms at work, favouring harassment or secular processes over merger scenarios.Comment: Accepted for publication in MNRA

A statistical framework for genetic association studies of power curves in bird flight

How the power required for bird flight varies as a function of forward speed can be used to predict the flight style and behavioral strategy of a bird for feeding and migration. A U-shaped curve was observed between the power and flight velocity in many birds, which is consistent to the theoretical prediction by aerodynamic models. In this article, we present a general genetic model for fine mapping of quantitative trait loci (QTL) responsible for power curves in a sample of birds drawn from a natural population. This model is developed within the maximum likelihood context, implemented with the EM algorithm for estimating the population genetic parameters of QTL and the simplex algorithm for estimating the QTL genotype-specific parameters of power curves. Using Monte Carlo simulation derived from empirical observations of power curves in the European starling (Sturnus vulgaris), we demonstrate how the underlying QTL for power curves can be detected from molecular markers and how the QTL detected affect the most appropriate flight speeds used to design an optimal migration strategy. The results from our model can be directly integrated into a conceptual framework for understanding flight origin and evolution

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation