Completions of Z/(p)-Tate cohomology of periodic spectra

We construct splittings of some completions of the Z/(p)-Tate cohomology of E(n) and some related spectra. In particular, we split (a completion of) tE(n) as a (completion of) a wedge of E(n-1)'s as a spectrum, where t is shorthand for the fixed points of the Z/(p)-Tate cohomology spectrum (ie Mahowald's inverse limit of P_{-k} smash SE(n)). We also give a multiplicative splitting of tE(n) after a suitable base extension.Comment: 30 pages. Published copy, also available at http://www.maths.warwick.ac.uk/gt/GTVol2/paper8.abs.htm

Bleomycin increases neutrophil adhesion to human vascular endothelial cells independently of upregulation of ICAM-1 and E-selectin

© 2016 Taylor & Francis. Aim of the Study: Bleomycin-induced lung disease is a serious complication of therapy characterized by alveolar injury, cytokine release, inflammatory cell recruitment, and eventually pulmonary fibrosis. The mechanisms underlying bleomycin-induced pulmonary fibrosis may be relevant to other progressive scarring diseases of the lungs. Pulmonary vascular endothelial cells are critically involved in immune cell extravasation at sites of injury through adhesion molecule expression and cytokine release. We sought to determine the effects of bleomycin on adhesion molecule expression and cytokine release by pulmonary vascular endothelial cells, and their functional relevance to inflammatory cell recruitment. Materials and Methods: The effects of pharmacologically relevant concentrations of bleomycin on adhesion molecule expression and cytokine release by human vascular endothelial cells in vitro were studied by flow cytometry, quantitative polymerase chain reaction, and enzyme-linked immunosorbent assay. A flow chamber model was used to assess the functional consequences on adhesion of flowing human neutrophils to endothelial cell monolayers. Results: Bleomycin increased intercellular adhesion molecule 1 (ICAM-1; CD54), vascular cell adhesion molecule (VCAM-1; CD106), and E-selectin (CD62E) expression, and increased monocyte chemoattractant protein (MCP-1) and interleukin (IL-8) release by endothelial cells. Increases in protein expression were accompanied by increased mRNA transcription. In contrast, there was no direct effect of bleomycin on the profibrotic cytokines transforming growth factor-beta (TGF-β), platelet-derived growth factor-BB (PDGF-BB), or endothelin-1. Under flow conditions, endothelial cells exposed to bleomycin supported increased neutrophil adhesion which was independent of ICAM-1 or E-selectin. Conclusion: Our findings demonstrate that bleomycin promotes endothelial-mediated inflammation and neutrophil adhesion. These mechanisms may contribute to the development of pulmonary fibrosis by supporting immune cell recruitment in the lungs

Dieudonn\'e modules and pp-divisible groups associated with Morava KK-theory of Eilenberg-Mac Lane spaces

We study the structure of the formal groups associated to the Morava $K$-theories of integral Eilenberg-Mac Lane spaces. The main result is that every formal group in the collection $\{K(n)^*K({\mathbb Z}, q), q=2,3,...\}$ for a fixed $n$ enters in it together with its Serre dual, an analogue of a principal polarization on an abelian variety. We also identify the isogeny class of each of these formal groups over an algebraically closed field. These results are obtained with the help of the Dieudonn\'e correspondence between bicommutative Hopf algebras and Dieudonn\'e modules. We extend P. Goerss's results on the bilinear products of such Hopf algebras and corresponding Dieudonn\'e modules.Comment: 23 page

PromOTing Quality of Life for Individuals with Huntington’s Disease

Objectives of Presentation: Describe the symptoms of Huntington’s disease and their impact on functional performance. Recognize the role of occupational therapy in improving quality of life for individuals with Huntington’s disease. Discuss how occupational therapy interventions for individuals with Huntington’s disease can be applied in a variety of settings. Clinical Question: What is the effectiveness of occupational therapy interventions in improving quality of life for individuals with Huntington’s disease? Presentation: 46 minute

Nitrogen geochemistry of subducting sediments: new results from the Izu-Bonin-Mariana margin and insights regarding global nitrogen subduction

[1] Toward understanding of the subduction mass balance in the Izu-Bonin-Mariana (IBM) convergent margin, we present an inventory of N and C concentrations and isotopic compositions in sediments obtained on Ocean Drilling Program (ODP) Legs 129 and 185. Samples from Sites 1149, 800, 801, and 802 contain 5 to 661 ppm total N (organic, inorganic combined) with δ15NAir of −0.2 to +8.2‰ (all δ15N values <+2.5‰ from Site 800). At Site 1149, N content is higher in clay-rich layers and lower in chert and carbonate layers, and δ15N shows a distinct down-section decrease from 0 to 120 mbsf (near +8.0 at shallow levels to near +4.0‰). Reduced-C concentration ranges from 0.02 to 0.5 wt.%, with δ13CVPDB of −28.1 to −21.7‰. The down-section decreases in δ15N and N concentration (and variations in concentrations and δ13C of reduced C, and Creduced/N) at Site 1149 could help reconcile differences between δ15N values of modern deep-sea sediments from near the sediment-water interface and values for forearc metasedimentary rocks. At Site 1149, negative shifts in δ15N, from marine organic values (up to ∼+8‰) toward lower values approaching those for the metasedimentary rocks (+1 to +3‰), are most likely caused by complex diagenetic processes, conceivably with minor effects of changes in productivity and differing proportions of marine and terrestrial organic matter. However, the forearc metamorphic suites (e.g., Franciscan Complex) are known to have been deposited nearer continents, and their lower δ15N at least partly reflects larger proportions of lower-δ15N terrestrial organic matter. Subduction at the Izu-Bonin (IB) margin, of a sediment section like that at Site 1149, would deliver an approximate annual subduction flux of 2.5 × 106 g of N and 1.4 × 107 g of reduced C per linear kilometer of trench, with average δ15N of +5.0‰ and δ13C of −24‰. Incorporating the larger C flux of 9.2 × 108 g/yr/linear-km in carbonate-rich layers of 1149B (average δ13C = +2.3‰) provides a total C flux of 9.3 × 108 g/yr/linear-km (δ13C = +1.9‰). Once subducted, sediments are shifted to higher δ15N by N loss during devolatilization, with magnitudes of the shifts depending on the thermal evolution of the margin

Record of forearc devolatilization in low-T, high-P/T metasedimentary suites: Significance for models of convergent margin chemical cycling

[1] The Franciscan Complex (Coast Ranges and Diablo Range, California) and the Western Baja Terrane (WBT; Baja California, Mexico) were metamorphosed along high-P/T paths like those experienced in many active subduction zones, recording peak conditions up to ∼1 GPa and 300°C. Franciscan and WBT metasedimentary rocks are similar in lithology and geochemistry to clastic sediments outboard of many subduction zones. These metamorphic suites provide evidence regarding devolatilization history experienced by subducting sediments, information that is needed to mass-balance the inputs of materials into subduction zones with their respective outputs. Analyzed samples have lower total volatile contents than their likely protoliths. Little variation in LOI among similar lithologies at differing metamorphic grades, suggests that loss of structurally bound water occurred during early clay-mineral transformations. Finely disseminated carbonate is present in the lowest-grade rocks, but absent in all higher-grade rocks. δ13CVPDB of reduced-C is uniform in the lower-grade Franciscan samples (mean = −25.1‰, 1σ = 0.4‰), but varies in higher-grade rocks (−28.8 to −21.9‰). This likely reflects a combination of devolatilization and C-isotope exchange, between organic and carbonate reservoirs. Nitrogen concentration ranges from 102 to 891 ppm, with δ15Nair of +0.1 to +3.0‰ (n = 35); this organic-like δ15N probably represents an efficient transfer of N from decaying organic matter to reacting clay minerals. The lowest-grade rocks in the Coastal Belt have elevated carbonate contents and correlated N-δ15N variations, and exhibit the most uniform δ13C and C/N, all consistent with these rocks having experienced less devolatilization. Most fluid-mobile trace elements are present at concentrations indistinguishable from protoliths. Suggesting that, despite apparent loss of much clay-bound H2O and CO2 from diagenetic cements (combined, <5–10 wt. %), most fluid-mobile trace elements are retained to depths of up to ∼40 km. Organic-like δ15N, lower than that of many seafloor sediments, is consistent with some loss of adsorbed N (perhaps as NO3−) during early stages of diagenesis. The efficient entrainment of fluid-mobile elements to depths of at least 40 km in these relatively cool subduction zone settings lends credence to models invoking transfer of these elements to the subarc mantle

Lunch Talk | Capital Markets: Down and Dirty with IPO Due Diligence

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TRPA1 mediates aromatase inhibitor-evoked pain by the aromatase substrate androstenedione

Aromatase inhibitors (AI) induce painful musculoskeletal symptoms (AIMSS), which are dependent upon the pain transducing receptor TRPA1. However, as the AI concentrations required to engage TRPA1 in mice are higher than those found in the plasma of patients, we hypothesized that additional factors may cooperate to induce AIMSS. Here we report that the aromatase substrate androstenedione, unique among several steroid hormones, targeted TRPA1 in peptidergic primary sensory neurons in rodent and human cells expressing the native or recombinant channel. Androstenedione dramatically lowered the concentration of letrozole required to engage TRPA1. Notably, addition of a minimal dose of androstenedione to physiologically ineffective doses of letrozole and oxidative stress byproducts produces AIMSS-like behaviors and neurogenic inflammatory responses in mice. Elevated androstenedione levels cooperated with low letrozole concentrations and inflammatory mediators were sufficient to provoke AIMSS-like behaviors. The generation of such painful conditions by small quantities of simultaneously administered TRPA1 agonists justifies previous failure to identify a precise link between AIs and AIMSS, underscoring the potential of channel antagonists to treat AIMSS

Molecular pharmacology of the capsaicin receptor (TRPV1) in the airways

The capsaicin receptor (vanilloid receptor I, transient receptor potential vanilloid 1 or TRPV I) is a member of the transient receptor potential (TRP) family of proteins. This cation channel is sensitive to a range of inflammatory mediators such as some lipoxygenase products, as well as the tussive agents capsaicin, resiniferatoxin and protons. It has been proposed that TRPV I is a cough receptor and may be important in airways inflammation.Rat TRPVI (rTRPVI) and human TRPVI (hTRPVl) permanently expressing cell lines were generated and successfully characterised by agonist triggered changes in intracellular calcium levels. Thapsigargin and/or removal of extracellular calcium revealed that, both rTRPVI and hTRPVI are not only expressed on the cell surface but on thapsigargin sensitive and insensitive intracellular stores respectively.Citric acid, an agent routinely used in the clinic for inhalation cough challenges, was investigated for its ability to activate TRPVl permanently expressed in a cell line. rTRPV I was activated by citric acid in a concentration and pH dependent manner. Citric acid activation of TRPVI was inhibited by iodoresiniferatoxin but not capsazepine. Mutation of the TRPVI putative proton binding site (E648 to A648) abolished citric acid activation of the channel without reducing the capsaicin evoked response. Thus, citric acid activates rTRPV I by a proton dependent mechanism.The role of N-linked glycosylation and sialylation on rTRPVI and hTRPVI was investigated. Treatment of rTRPVl with neuraminidase or tunicamycin dramatically reduced the channels' maximal responses to capsaicin. In addition mutation of the rTRPVI N-linked glycosylation site (N604 to Q604) or expression ofrTRPVI in the glycosylation mutant cell line, Lec2, also resulted in a striking reduction in the receptors' maximal calcium response to capsaicin. Flow cytometry data indicated that these differences in TRPVI function were unlikely to be linked to differences in receptor cell surface expression. Human TRPV I also displayed significant reductions in responsiveness to capsaicin following either neuraminidase or tunicamycin treatment. Thus, receptor sialylation regulates TRPVI activation by capsaicin.Finally, TRPVI expression on human primary bronchial fibroblasts (HPBF) was investigated. Negligible endogenous TRPVI expression was detected in HPBF. Interestingly, the inflammatory mediators tumour necrosis factor (TNF-a), lipopolysaccharide (LPS) and interleukin Ia (IL-Ia) all induced TRPVI expression in HPBF, as assessed by RT-PCR, flow cytometry and calcium signalling. TRPVI functional expression was observed as early as 6 hrs (for TNF-a) post challenge and remained elevated upto the final time point tested (96 hrs for IL-Ia). Thus, TRPVI may play an important role in the inflammatory process.In conclusion, TRPV I may play an important role in conditions where cough and inflammation have been implicated