Glueball mass measurements from improved staggered fermion simulations

We present the first 2+1 flavour spectrum measurements of glueball states using high statistics simulations with improved staggered fermions. We find a spectrum consistent with quenched measurements of scalar, pseudoscalar andtensor glueball states. The measurements were made using 5000 configurations at a lattice spacing of 0.123 fm and pion mass of 280 MeV and 3000 configurations at 0.092 fm with a pion mass of 360 MeV. We see some evidence of coupling to 2 pion states. We compare our results with the experimental glueball candidate spectrum as well as quenched glueball estimates.Comment: 22 pages, 19 figures and 8 tables, minor additions on mixing post-refere

The impact of in-season national team soccer play on injury and player availability in a professional club

This study investigated the impact of in-season national team duty on injury rates and player availability in a professional soccer club. Time-loss injuries and exposure time during club and national team duties were recorded prospectively over 5 seasons (2009–2014). A time-loss injury was sustained by 37.7% of squad members participating in national duty, all injuries occurring in match-play. The incidence (per 1000 h exposure) for national team player match-play injuries did not differ (P = 0.608) to that for all players in club competitions: 48.0 (95% CI 20.9–75.5) vs. 41.9 (95% CI 36.5–47.4), incidence rate ratio = 1.2 (CI: 0.8–2.4). The majority (58%) of national team injuries resulted in a layoff ≤1 week. Of all working days lost to injury generally, 5.2% were lost through injury on national duty. Injury incidence in the week following national duty was comparable (P = 0.818) in players participating or not: 7.8 (95% CI 3.6–12.0) vs. 7.1 (95% CI: 4.6–9.6), incidence rate ratio = 1.1 (CI: 0.7–2.7). While approximately 40% of participating players incurred a time-loss injury on national duty, no training injuries were sustained and injuries made up a negligible part of overall club working days lost to injury. Following duty, players had a similar injury risk to peers without national obligations

Loss of nonsense mediated decay suppresses mutations in Saccharomyces cerevisiae TRA1

<p>Abstract</p> <p>Background</p> <p>Tra1 is an essential protein in <it>Saccharomyces cerevisiae</it>. It was first identified in the SAGA and NuA4 complexes, both with functions in multiple aspects of gene regulation and DNA repair, and recently found in the ASTRA complex. Tra1 belongs to the PIKK family of proteins with a C-terminal PI3K domain followed by a FATC domain. Previously we found that mutation of leucine to alanine at position 3733 in the FATC domain of Tra1 (<it>tra1-L3733A</it>) results in transcriptional changes and slow growth under conditions of stress. To further define the regulatory interactions of Tra1 we isolated extragenic suppressors of the <it>tra1-L3733A </it>allele.</p> <p>Results</p> <p>We screened for suppressors of the ethanol sensitivity caused by <it>tra1-L3733A</it>. Eleven extragenic recessive mutations, belonging to three complementation groups, were identified that partially suppressed a subset of the phenotypes caused by tra<it>1-L3733A</it>. Using whole genome sequencing we identified one of the mutations as an opal mutation at tryptophan 165 of <it>UPF1/NAM7</it>. Partial suppression of the transcriptional defect resulting from <it>tra1-L3733A </it>was observed at <it>GAL10</it>, but not at <it>PHO5</it>. Suppression was due to loss of nonsense mediated decay (NMD) since deletion of any one of the three NMD surveillance components (<it>upf1/nam7, upf2/nmd2</it>, or <it>upf3</it>) mediated the effect. Deletion of <it>upf1 </it>suppressed a second FATC domain mutation, <it>tra1-F3744A</it>, as well as a mutation to the PIK3 domain. In contrast, deletions of SAGA or NuA4 components were not suppressed.</p> <p>Conclusions</p> <p>We have demonstrated a genetic interaction between <it>TRA1 </it>and genes of the NMD pathway. The suppression is specific for mutations in <it>TRA1</it>. Since NMD and Tra1 generally act reciprocally to control gene expression, and the FATC domain mutations do not directly affect NMD, we suggest that suppression occurs as the result of overlap and/or crosstalk in these two broad regulatory networks.</p

Diffusional and microstructural profiles in metallic-to-UHTC conversion by carbonization

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Macropinocytosis is decreased in diabetic mouse macrophages and is regulated by AMPK

<p>Abstract</p> <p>Background</p> <p>Macrophages (MΦs) utilize macropinocytosis to integrate immune and metabolic signals in order to initiate an effective immune response. Diabetes is characterized by metabolic abnormalities and altered immune function. Here we examine the influence of diabetes on macropinocytosis in primary mouse macrophages and in an <it>in vitro </it>diabetes model.</p> <p>Results</p> <p>The data demonstrate that peritoneal MΦs from diabetic (<it>db/db</it>) mice had reduced macropinocytosis when compared to MΦs from non-diabetic (<it>db/+</it>) mice. Additionally, MΦs cultured in hyperglycemic conditions were less adept at macropinocytosis than those cultured in low glucose. Notably, AMP-activated protein kinase (AMPK) activity was decreased in MΦs cultured in hyperglycemic conditions. Activation of AMPK with leptin or 5-aminoimidazole-4-carboxamide-1-β-riboside (AICAR) increased macropinocytosis and inhibition of AMPK with compound C decreased macropinocytosis.</p> <p>Conclusion</p> <p>Taken together, these findings indicate that MΦs from diabetic mice have decreased macropinocytosis. This decrease appears dependent on reduced AMPK activity. These results demonstrate a previously unrealized role for AMPK in MΦs and suggest that increasing AMPK activity in diabetic MΦs could improve innate immunity and decrease susceptibility to infection.</p