Space debris: Orbital microparticulates impacting LDEF experiments favour a natural extraterrestrial origin

The results of work carried out at the Unit for Space Sciences at the University of Kent at Canterbury, United Kingdom, on the micrometeoroid and space debris environment of near Earth space are described. The primary data for the research program is supplied by an examination of several types of exposed surface from the NASA Long Duration Exposure Facility (LDEF), including an experiment dedicated to the detection of micrometeoroids and space debris provided by the University

Towards an understanding of configurational and national influences on international integration in the HR function in MNCs

The human resource (HR) function plays a critical role in how multinational companies (MNCs) centralise decision-making or coordinate and exploit expertise internationally. However, there has been limited attention on the extent to which the HR function in MNCs is integrated internationally and the influencing factors behind this. Using nationally representative, cross-country comparative data, this paper identifies the degree to which internationally integrated HR functions exist and test the extent to which this is shaped by the strategy, structure and nationality of the MNC. We demonstrate the multidimensionality of an internationally integrated HR function; with the structural configuration, level of inter-dependencies between MNC operations and country of origin each partially impacting its nature. A key implication concerns the need to move beyond solely focusing on either nationality as per institutionalist theory, or corporate strategy and structure as characterised in the strategic international HRM literature, towards an integrated explanation that incorporates both sets of factors

Inhibition of major integrin αVβ3 reduces Staphylococcus aureus attachment to sheared human endothelial cells.

BACKGROUND: Vascular endothelial dysfunction with associated oedema and organ failure is one of the hallmarks of sepsis. While a large number of microorganisms can cause sepsis, Staphylococcus aureus is one of the primary etiological agents. Currently there are no approved specific treatments for sepsis and therefore the initial management bundle focuses on cardiorespiratory resuscitation and mitigation against the immediate threat of uncontrolled infection. The continuous emergence of antibiotic resistant strains of bacteria urges the development of new therapeutic approaches for this disease. OBJECTIVE: The objective of this study was to identify the molecular mechanisms leading to endothelial dysfunction as a result of Staphylococcus aureus binding. METHODS: Stahpylococcus aureus Newman and clumping factor A-deficient binding to endothelium were measured in vitro and in the mesenteric circulation of C57Bl/6 mice. The effect of the αVβ3 blocker, cilengitide, on bacterial binding, endothelial VE-cadherin expression, apoptosis, proliferation and permeability were assessed. RESULTS: Here we show that the major Staphylococcus aureus cell wall protein clumping factor A binds to endothelial cell integrin αVβ3 in the presence of fibrinogen. This interaction results in disturbances in barrier function mediated by VE-cadherin in endothelial cell monolayers and ultimately cell death by apoptosis. Using a low concentration of cilengitide, ClfA binding to αVβ3 was significantly inhibited both in vitro and in vivo. Moreover, preventing Staphylococcus aureus from attaching to αVβ3 resulted in a significant reduction in endothelial dysfunction following infection. CONCLUSION: Inhibition of Staphylococcus aureus ClfA binding to endothelial cell αVβ3 using cilengitide prevents endothelial dysfunction. This article is protected by copyright. All rights reserved

The Lantern, 2010-2011

• The Graterford Department of Corrections • Visiting Room: Lewis Considers the Space & Time Continuum • String • The Tale of Lad Wadley • The Devout • One Moment in the Garden • Water, Focused and Tumbling • Bomber • Another • I Walked Home • Perhe • I Describe the Last Time My Parents Had Sex • Butterflies • Ship Without Fools • The Interview • Cyane • An Imaginary Portrait of Stella as a Young Girl • At the Farm Market in Early Autumn • Victor Jorgenson\u27s Photograph of the V-J Day Kiss • Lightning • The Citadel • Whenever You Come Home From School • It Came in a Dream • What I Know About Fission • Please Don\u27t Fire Me for Saying Such Things • Femina Irata • Thank You For Shopping • Sunday, November 27th • An Introduction to The Lifestyle • Laid-Off Perception • Good-Night, Sweet Prince • Requiem for a Marriage • Gertrude\u27s Book • Passing • Elk Run II • Shady Tides • A Quiet House • Tell Him. A Manual • Silence • Google This • The Dinner Table Dance • The Inevitable Extinction of Filing Cabinets • Chateau d\u27If • Man Smoking in Charcoal • Inside Auschwitz • Bark Glow • Anticipation • Look Up • Major News Networks • Others Wage War • Insert Bible Verse Here • The Empress • Candy Castle • Venice, Italy • Quebec • Bhutanese Child • Jumper • Pomegranates • Cover Image: Octopus Hathttps://digitalcommons.ursinus.edu/lantern/1176/thumbnail.jp

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely