GALEX J201337.6+092801: The lowest gravity subdwarf B pulsator

We present the recent discovery of a new subdwarf B variable (sdBV), with an exceptionally low surface gravity. Our spectroscopy of J20136+0928 places it at Teff = 32100 +/- 500, log(g) = 5.15 +/- 0.10, and log(He/H) = -2.8 +/- 0.1. With a magnitude of B = 12.0, it is the second brightest V361 Hya star ever found. Photometry from three different observatories reveals a temporal spectrum with eleven clearly detected periods in the range 376 to 566 s, and at least five more close to our detection limit. These periods are unusually long for the V361 Hya class of short-period sdBV pulsators, but not unreasonable for p- and g-modes close to the radial fundamental, given its low surface gravity. Of the ~50 short period sdB pulsators known to date, only a single one has been found to have comparable spectroscopic parameters to J20136+0928. This is the enigmatic high-amplitude pulsator V338 Ser, and we conclude that J20136+0928 is the second example of this rare subclass of sdB pulsators located well above the canonical extreme horizontal branch in the HR diagram.Comment: 5 pages, accepted for publication in ApJ Letter

Paternal effects on early embryogenesis

Historically, less attention has been paid to paternal effects on early embryogenesis than maternal effects. However, it is now apparent that certain male factor infertility phenotypes are associated with increased DNA fragmentation and/or chromosome aneuploidies that may compromise early embryonic development. In addition, there is a growing body of evidence that the fertilizing sperm has more function than just carrying an intact, haploid genome. The paternally inherited centrosome is essential for normal fertilization, and the success of higher order chromatin packaging may impact embryogenesis. Epigenetic modifications of sperm chromatin may contribute to the reprogramming of the genome, and sperm delivered mRNA has also been hythesized to be necessary for embryogenesis. There is less information about the epigenetic factors affecting embryogenesis than genetic factors, but the epigenetics of gamete and early embryogenesis is a rapidly advancing field

An analysis of the quality of experimental design and reliability of results in tribology research

In recent years several high profile projects have questioned the repeatability and validity of scientific research in the fields of psychology and medicine. In general, these studies have shown or estimated that less than 50% of published research findings are true or replicable even when no breaches of ethics are made. This high percentage stems from widespread poor study design; either through the use of underpowered studies or designs that allow the introduction of bias into the results. In this work, we have aimed to assess, for the first time, the prevalence of good study design in the field of tribology. A set of simple criteria for factors such as randomisation, blinding, use of control and repeated tests has been made. These criteria have been used in a mass review of the output of five highly regarded tribology journals for the year 2017. In total 379 papers were reviewed by 26 reviewers, 28% of the total output of the journals selected for 2017. Our results show that the prevalence of these simple aspects of study design is poor. Out of 290 experimental studies, 2.2% used any form of blinding, 3.2% used randomisation of either the tests or the test samples, while none randomised both. 30% repeated experiments 3 or more times and 86% of those who repeated tests used single batches of test materials. 4.4% completed statistical tests on their data. Due to the low prevalence of repeated tests and statistical analysis it is impossible to give a realistic indication of the percentage of the published works that are likely to be false positives, however these results compare poorly to other more well studied fields. Finally, recommendations for improved study design for researchers and group design for research group leaders are given

Academic Performance and Behavioral Patterns

Identifying the factors that influence academic performance is an essential part of educational research. Previous studies have documented the importance of personality traits, class attendance, and social network structure. Because most of these analyses were based on a single behavioral aspect and/or small sample sizes, there is currently no quantification of the interplay of these factors. Here, we study the academic performance among a cohort of 538 undergraduate students forming a single, densely connected social network. Our work is based on data collected using smartphones, which the students used as their primary phones for two years. The availability of multi-channel data from a single population allows us to directly compare the explanatory power of individual and social characteristics. We find that the most informative indicators of performance are based on social ties and that network indicators result in better model performance than individual characteristics (including both personality and class attendance). We confirm earlier findings that class attendance is the most important predictor among individual characteristics. Finally, our results suggest the presence of strong homophily and/or peer effects among university students

Hereditary alpha-1-antitrypsin deficiency and its clinical consequences

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that manifests as pulmonary emphysema, liver cirrhosis and, rarely, as the skin disease panniculitis, and is characterized by low serum levels of AAT, the main protease inhibitor (PI) in human serum. The prevalence in Western Europe and in the USA is estimated at approximately 1 in 2,500 and 1 : 5,000 newborns, and is highly dependent on the Scandinavian descent within the population. The most common deficiency alleles in North Europe are PI Z and PI S, and the majority of individuals with severe AATD are PI type ZZ. The clinical manifestations may widely vary between patients, ranging from asymptomatic in some to fatal liver or lung disease in others. Type ZZ and SZ AATD are risk factors for the development of respiratory symptoms (dyspnoea, coughing), early onset emphysema, and airflow obstruction early in adult life. Environmental factors such as cigarette smoking, and dust exposure are additional risk factors and have been linked to an accelerated progression of this condition. Type ZZ AATD may also lead to the development of acute or chronic liver disease in childhood or adulthood: prolonged jaundice after birth with conjugated hyperbilirubinemia and abnormal liver enzymes are characteristic clinical signs. Cirrhotic liver failure may occur around age 50. In very rare cases, necrotizing panniculitis and secondary vasculitis may occur. AATD is caused by mutations in the SERPINA1 gene encoding AAT, and is inherited as an autosomal recessive trait. The diagnosis can be established by detection of low serum levels of AAT and isoelectric focusing. Differential diagnoses should exclude bleeding disorders or jaundice, viral infection, hemochromatosis, Wilson's disease and autoimmune hepatitis. For treatment of lung disease, intravenous alpha-1-antitrypsin augmentation therapy, annual flu vaccination and a pneumococcal vaccine every 5 years are recommended. Relief of breathlessness may be obtained with long-acting bronchodilators and inhaled corticosteroids. The end-stage liver and lung disease can be treated by organ transplantation. In AATD patients with cirrhosis, prognosis is generally grave

Self-Organization and Regulation of Intrinsically Disordered Proteins with Folded N-Termini

How do mostly disordered proteins coordinate the specific assembly of very large signal transduction protein complexes? A newly emerging hypothesis may provide some clues towards a molecular mechanism

Uptake of the Necrotic Serpin in Drosophila melanogaster via the Lipophorin Receptor-1

The humoral response to fungal and Gram-positive infections is regulated by the serpin-family inhibitor, Necrotic. Following immune-challenge, a proteolytic cascade is activated which signals through the Toll receptor. Toll activation results in a range of antibiotic peptides being synthesised in the fat-body and exported to the haemolymph. As with mammalian serpins, Necrotic turnover in Drosophila is rapid. This serpin is synthesised in the fat-body, but its site of degradation has been unclear. By “freezing” endocytosis with a temperature sensitive Dynamin mutation, we demonstrate that Necrotic is removed from the haemolymph in two groups of giant cells: the garland and pericardial athrocytes. Necrotic uptake responds rapidly to infection, being visibly increased after 30 mins and peaking at 6–8 hours. Co-localisation of anti-Nec with anti-AP50, Rab5, and Rab7 antibodies establishes that the serpin is processed through multi-vesicular bodies and delivered to the lysosome, where it co-localises with the ubiquitin-binding protein, HRS. Nec does not co-localise with Rab11, indicating that the serpin is not re-exported from athrocytes. Instead, mutations which block late endosome/lysosome fusion (dor, hk, and car) cause accumulation of Necrotic-positive endosomes, even in the absence of infection. Knockdown of the 6 Drosophila orthologues of the mammalian LDL receptor family with dsRNA identifies LpR1 as an enhancer of the immune response. Uptake of Necrotic from the haemolymph is blocked by a chromosomal deletion of LpR1. In conclusion, we identify the cells and the receptor molecule responsible for the uptake and degradation of the Necrotic serpin in Drosophila melanogaster. The scavenging of serpin/proteinase complexes may be a critical step in the regulation of proteolytic cascades