Drugs in sport

This article addresses the controversial issue of the use of performance enhancing drugs in sport. It looks at the legal basis for regulation via the World Anti-Doping Code and the nature of a sports participant's relationship with their governing body and the anti-doping organisations. It explains in the context of proportionality, the measures designed to combat doping in sport and the importance to the Code of the central principle of strict liability. It also, highlights the use of non-analytical positives as a further method of detection of doping violations, whilst taking consideration of the impact of these measures on the human rights of participants

On the role of articulatory prosodies in German message decoding

A theoretical framework for speech reduction is outlined in which 'coarticulation' and 'articulatory control' operate on sequences of 'opening-closing gestures' in linguistic and communicative settings, leading to suprasegmental properties - 'articulatory prosodies' - in the acoustic output. In linking this gestalt perspective in speech production to the role of phonetic detail in speech understanding, this paper reports on perception experiments that test listeners' reactions to varying extension of an 'articulatory prosody of palatality' in message identification. The point of departure for the experimental design was the German utterance ich kann Ihnen das ja mal sagen 'I can mention this to you' from the Kiel Corpus of Spontaneous Speech, which contains the palatalized stretch [k̟(h)ε̈n(j)n(j)əs] for the sequence of function words /kan i.n(kə)n das/ kann Ihnen das. The utterance also makes sense without the personal pronoun Ihnen. Systematic experimental variation has shown that the extent of palatality has a highly significant influence on the decoding of Ihnen and that the effect of nasal consonant duration depends on the extension of palatality. These results are discussed in a plea to base future speech perception research on a paradigm that makes the traditional segment-prosody divide more permeable, and moves away from the generally practised phoneme orientation

Cosmological Parameter Estimation Using 21 cm Radiation from the Epoch of Reionization

A number of radio interferometers are currently being planned or constructed to observe 21 cm emission from reionization. Not only will such measurements provide a detailed view of that epoch, but, since the 21 cm emission also traces the distribution of matter in the Universe, this signal can be used to constrain cosmological parameters at 6 < z < 20. The sensitivity of an interferometer to the cosmological information in the signal may depend on how precisely the angular dependence of the 21 cm 3-D power spectrum can be measured. Utilizing an analytic model for reionization, we quantify all the effects that break the spherical symmetry of the 3-D 21 cm power spectrum and produce physically motivated predictions for this power spectrum. We find that upcoming observatories will be sensitive to the 21 cm signal over a wide range of scales, from larger than 100 to as small as 1 comoving Mpc. We consider three methods to measure cosmological parameters from the signal: (1) direct fitting of the density power spectrum to the signal, (2) using only the velocity field fluctuations in the signal, (3) looking at the signal at large enough scales such that all fluctuations trace the density field. With the foremost method, the first generation of 21 cm observations should moderately improve existing constraints on cosmological parameters for certain low-redshift reionization scenarios, and a two year observation with the second generation interferometer MWA5000 can improve constraints on Omega_w, Omega_m h^2, Omega_b h^2, Omega_nu, n_s, and alpha_s. If the Universe is substantially ionized by z = 12 or if spin temperature fluctuations are important, we show that it will be difficult to place competitive constraints on cosmological parameters with any of the considered methods.Comment: 20 pages, 12 figures, accepted by Ap

Berufliches Lernen von Wissenschaftler(inne)n: Zeitmanagement als Moderator des Zusammenhangs zwischen Lernzielen und Lernergebnis

Berufliches Lernen zur Erweiterung eigener Kompetenzen in Lehre und Forschung gilt als wichtige Bedingung für erfolgreiche Arbeit von Wissenschaftler(inne)n. Bisherige Forschung belegt einen positiven, jedoch heterogenen Zusammenhang von Lernzielen (dem Streben nach Kompetenzerweiterung) und Lernergebnissen (Payne, Youngcourt & Beaubien, 2007). Moderatoren, die die Enge des Zusammenhangs erklären, wurden bisher kaum ausreichend untersucht. Da Wissenschaftler(innen) sich ihre Zeit oft frei einteilen können und die eigene Arbeitszeit daher selbstbestimmt nutzen, scheint die Fähigkeit zum Zeitmanagement eine wichtige Voraussetzung für das erfolgreiche Verfolgen eigener Lernziele im Spannungsfeld zwischen Lehre und Forschung zu sein. Die Ausprägung des Zeitmanagements sollte daher den Zusammenhang zwischen Lernzielen und dem Lernergebnis stärken und so zur Aufklärung der Schwankungen innerhalb der gefundenen Zusammenhänge beitragen können. Außerdem sollte nach dem Selbstregulationsmodell von Schmitz und Wiese (2006) neben den Lernzielen das Zeitmanagement als Indikator für selbstreguliertes Lernverhalten im Beruf den Lernerfolg auch direkt beeinflussen nämlich dergestalt, dass ein besseres Zeitmanagement mit stärkeren Wissenszuwächsen einhergeht. Diesen theoretischen Überlegungen folgend untersucht die vorliegende Studie das Zeitmanagement als Moderator zwischen Lernzielen und -ergebnissen und als Prädiktor der Lernergebnisse im Beruf von Wissenschaftler(inne)n. Hierfür schätzte eine Stichprobe von 264 an Hochschulen in Baden-Württemberg beschäftigten Wissenschaftler(inne)n getrennt für die Tätigkeitsbereiche Lehre und Forschung die eigenen aktuellen Lernziele, das kurz- und langfristige Zeitmanagement und den eigenen Lernzuwachs in einem Kurzfragebogen ein. Strukturgleichungsmodelle bestätigen positive Zusammenhänge von aktuellen Lernzielen und dem selbstberichteten Lernergebnis, welche wie theoretisch postuliert von dem Zeitmanagement sowohl in der Lehre als auch in der Forschung moderiert wurden. Die positiven Zusammenhänge zwischen dem Zeitmanagement und dem selbstberichteten Lernergebnis bestätigten sich nur im Bereich der Lehre. Die Fähigkeit zum Zeitmanagement ist ein möglicher Ansatzpunkt für zukünftige Schulungen von Wissenschaftler(inne)n, um das selbstregulierte Lernen im Beruf zu fördern. Zukünftige Forschung könnte diese Zusammenhänge in Experimenten oder Interventionsstudien prüfen

The type-2 Streptococcus canis M protein SCM-2 binds fibrinogen and facilitates antiphagocytic properties

Streptococcus canis is a zoonotic agent that causes severe invasive diseases in domestic animals and humans, but little is known about its pathogenesis and virulence mechanisms so far. SCM, the M-like protein expressed by S. canis, is considered one of the major virulence determinants. Here, we report on the two distinct groups of SCM. SCM-1 proteins were already described to interact with its ligands IgG and plasminogen as well as with itself and confer antiphagocytic capability of SCM-1 expressing bacterial isolates. In contrast, the function of SCM-2 type remained unclear to date. Using whole-genome sequencing and subsequent bioinformatics, FACS analysis, fluorescence microscopy and surface plasmon resonance spectrometry, we demonstrate that, although different in amino acid sequence, a selection of diverse SCM-2-type S. canis isolates, phylogenetically representing the full breadth of SCM-2 sequences, were able to bind fibrinogen. Using targeted mutagenesis of an SCM-2 isolate, we further demonstrated that this strain was significantly less able to survive in canine blood. With respect to similar studies showing a correlation between fibrinogen binding and survival in whole blood, we hypothesize that SCM-2 has an important contribution to the pathogenesis of S. canis in the host

Deletion of the Zinc Transporter Lipoprotein AdcAII Causes Hyperencapsulation of Streptococcus pneumoniae Associated with Distinct Alleles of the Type I Restriction-Modification System.

The capsule is the dominant Streptococcus pneumoniae virulence factor, yet how variation in capsule thickness is regulated is poorly understood. Here, we describe an unexpected relationship between mutation of adcAII, which encodes a zinc uptake lipoprotein, and capsule thickness. Partial deletion of adcAII in three of five capsular serotypes frequently resulted in a mucoid phenotype that biochemical analysis and electron microscopy of the D39 adcAII mutants confirmed was caused by markedly increased capsule thickness. Compared to D39, the hyperencapsulated ΔadcAII mutant strain was more resistant to complement-mediated neutrophil killing and was hypervirulent in mouse models of invasive infection. Transcriptome analysis of D39 and the ΔadcAII mutant identified major differences in transcription of the Sp_0505-0508 locus, which encodes an SpnD39III (ST5556II) type I restriction-modification system and allelic variation of which correlates with capsule thickness. A PCR assay demonstrated close linkage of the SpnD39IIIC and F alleles with the hyperencapsulated ΔadcAII strains. However, transformation of ΔadcAII with fixed SpnD39III alleles associated with normal capsule thickness did not revert the hyperencapsulated phenotype. Half of hyperencapsulated ΔadcAII strains contained the same single nucleotide polymorphism in the capsule locus gene cps2E, which is required for the initiation of capsule synthesis. These results provide further evidence for the importance of the SpnD39III (ST5556II) type I restriction-modification system for modulating capsule thickness and identified an unexpected linkage between capsule thickness and mutation of ΔadcAII Further investigation will be needed to characterize how mutation of adcAII affects SpnD39III (ST5556II) allele dominance and results in the hyperencapsulated phenotype.IMPORTANCE The Streptococcus pneumoniae capsule affects multiple interactions with the host including contributing to colonization and immune evasion. During infection, the capsule thickness varies, but the mechanisms regulating this are poorly understood. We have identified an unsuspected relationship between mutation of adcAII, a gene that encodes a zinc uptake lipoprotein, and capsule thickness. Mutation of adcAII resulted in a striking hyperencapsulated phenotype, increased resistance to complement-mediated neutrophil killing, and increased S. pneumoniae virulence in mouse models of infection. Transcriptome and PCR analysis linked the hyperencapsulated phenotype of the ΔadcAII strain to specific alleles of the SpnD39III (ST5556II) type I restriction-modification system, a system which has previously been shown to affect capsule thickness. Our data provide further evidence for the importance of the SpnD39III (ST5556II) type I restriction-modification system for modulating capsule thickness and identify an unexpected link between capsule thickness and ΔadcAII, further investigation of which could further characterize mechanisms of capsule regulation

Astrobites as a Community-led Model for Education, Science Communication, and Accessibility in Astrophysics

Support for early career astronomers who are just beginning to explore astronomy research is imperative to increase retention of diverse practitioners in the field. Since 2010, Astrobites has played an instrumental role in engaging members of the community -- particularly undergraduate and graduate students -- in research. In this white paper, the Astrobites collaboration outlines our multi-faceted online education platform that both eases the transition into astronomy research and promotes inclusive professional development opportunities. We additionally offer recommendations for how the astronomy community can reduce barriers to entry to astronomy research in the coming decade

Whole-genome analysis of histone H3 lysine 27 trimethylation in Arabidopsis

Trimethylation of histone H3 lysine 27 (H3K27me3) plays critical roles in regulating animal development, and in several cases, H3K27me3 is also required for the proper expression of developmentally important genes in plants. However, the extent to which H3K27me3 regulates plant genes on a genome-wide scale remains unknown. In addition, it is not clear whether the establishment and spreading of H3K27me3 occur through the same mechanisms in plants and animals. We identified regions containing H3K27me3 in the genome of the flowering plant Arabidopsis thaliana using a high-density whole-genome tiling microarray. The results suggest that H3K27me3 is a major silencing mechanism in plants that regulates an unexpectedly large number of genes in Arabidopsis (~4,400), and that the maintenance of H3K27me3 is largely independent of other epigenetic pathways, such as DNA methylation or RNA interference. Unlike in animals, where H3K27m3 occupies large genomic regions, in Arabidopsis, we found that H3K27m3 domains were largely restricted to the transcribed regions of single genes. Furthermore, unlike in animals systems, H3K27m3 domains were not preferentially associated with low-nucleosome density regions. The results suggest that different mechanisms may underlie the establishment and spreading of H3K27me3 in plants and animals

A structural model of the active ribosome-bound membrane protein insertase YidC

The integration of most membrane proteins into the cytoplasmic membrane of bacteria occurs co-translationally. The universally conserved YidC protein mediates this process either individually as a membrane protein insertase, or in concert with the SecY complex. Here, we present a structural model of YidC based on evolutionary co-variation analysis, lipid-versus-protein-exposure and molecular dynamics simulations. The model suggests a distinctive arrangement of the conserved five transmembrane domains and a helical hairpin between transmembrane segment 2 (TM2) and TM3 on the cytoplasmic membrane surface. The model was used for docking into a cryo-electron microscopy reconstruction of a translating YidC-ribosome complex carrying the YidC substrate F(O)c. This structure reveals how a single copy of YidC interacts with the ribosome at the ribosomal tunnel exit and identifies a site for membrane protein insertion at the YidC protein-lipid interface. Together, these data suggest a mechanism for the co-translational mode of YidC-mediated membrane protein insertion