Study and development of acoustic treatment for jet engine tailpipes

A study and development program was accomplished to attenuate turbine noise generated in the JT3D turbofan engine. Analytical studies were used to design an acoustic liner for the tailpipe. Engine ground tests defined the tailpipe environmental factors and laboratory tests were used to support the analytical studies. Furnace-brazed, stainless steel, perforated sheet acoustic liners were designed, fabricated, installed, and ground tested in the tailpipe of a JT3D engine. Test results showed the turbine tones were suppressed below the level of the jet exhaust for most far field polar angles

Nitrite Generation in Interleukin-4—Treated Human Macrophage Cultures Does Not Involve the Nitric Oxide Synthase Pathway

The search continues for high-output nitric oxide biosynthesis in human macrophages analogous to murine phagocytes. Recently, generation of nitrite in culture supernatants of human macrophages exposed to interferon-γ and interleukin-4 (IFN-γ/IL-4) was reported. The present study reproduces these findings and shows that L-arginine is not consumed and L-citrulline is not produced during this process. Furthermore, the biosynthesis of the obligatory cofactor tetrahydrobiopterin is not coinduced. These biochemical data provide support against a nitric oxide synthase contribution to nitrite accumulation. Nitrite was generated from nitrate salts even in cell-free media. Nitric oxide synthase activity but not nitrate reduction depended on molecular oxygen. Nitrite accumulation in experiments with IFN-γ/IL-4 in human monocytes appears to be an in vitro artifact produced by nitrate-reducing activities contained in cytokine preparation

Comparison of the fragmentation behavior of DNA and LNA single strands and duplexes

DNA and locked nucleic acid (LNA) were characterized as single strands, as well as double stranded DNA‐DNA duplexes and DNA‐LNA hybrids using tandem mass spectrometry with collision‐induced dissociation. Additionally, ion mobility spectrometry was carried out on selected species. Oligonucleotide duplexes of different sequences – bearing mismatch positions and abasic sites of complementary DNA 15‐mers – were investigated to unravel general trends in their stability in the gas phase. Single stranded LNA oligonucleotides were also investigated with respect to their gas phase behavior and fragmentation upon collision‐induced dissociation. In contrast to the collision‐induced dissociation of DNA, almost no base loss was observed for LNAs. Here, backbone cleavages were the dominant dissociation pathways. This finding was further underlined by the need for higher activation energies. Base losses from the LNA strand were also absent in fragmentation experiments of the investigated DNA‐LNA hybrid duplexes. While DNA‐DNA duplexes dissociated easily into single stranded fragments, the high stability of DNA‐LNA hybrids resulted in predominant fragmentation of the DNA part rather than the LNA, while base losses were only observed from the DNA single strand of the hybrid

Hyperglycaemia but not hyperlipidaemia causes beta cell dysfunction and beta cell loss in the domestic cat

Aims/hypothesis: In vitro studies point to a toxic effect of high glucose and non-esterified fatty acids on beta cells. Whether elevated levels of glucose and lipids induce beta cell loss in vivo is less clear. The domestic cat has recently been proposed as a valuable animal model for human type 2 diabetes because feline diabetes shows several similarities with diabetes in humans, including obesity-induced insulin resistance, impaired beta cell function, decreased number of beta cells and pancreatic amyloid deposition. Methods: We infused healthy cats with glucose or lipids for 10days to clamp their blood concentrations at the approximate level found in untreated feline diabetes (glucose: 25-30mmol/l; triacylglycerols: 3-7mmol/l). Results: Glucose and lipid levels were adequately targeted. Plasma non-esterified fatty acids were increased by lipid infusion 1.7-fold. A dramatic and progressive decline of plasma insulin levels was observed in glucose-infused cats beginning after 2days of hyperglycaemic clamp. In contrast, plasma insulin concentration and glucose tolerance test were not affected by hyperlipidaemia. Compared with controls, glucose-infused cats had a 50% decrease in beta cells per pancreatic area. Apoptotic islet cells and cleaved caspase-3-positive beta cells were observed in glucose-infused cats only. Conclusions/interpretation: Sustained hyperglycaemia but not hyperlipidaemia induces early and severe beta cell dysfunction in cats, and excess glucose causes beta cell loss via apoptosis in vivo. Hyperglycaemic clamps in cats may provide a good model to study the pathogenesis of glucose toxicity in beta cell

Hyperglycaemia but not hyperlipidaemia causes beta cell dysfunction and beta cell loss in the domestic cat

AIMS/HYPOTHESIS: In vitro studies point to a toxic effect of high glucose and non-esterified fatty acids on beta cells. Whether elevated levels of glucose and lipids induce beta cell loss in vivo is less clear. The domestic cat has recently been proposed as a valuable animal model for human type 2 diabetes because feline diabetes shows several similarities with diabetes in humans, including obesity-induced insulin resistance, impaired beta cell function, decreased number of beta cells and pancreatic amyloid deposition. METHODS: We infused healthy cats with glucose or lipids for 10 days to clamp their blood concentrations at the approximate level found in untreated feline diabetes (glucose: 25-30 mmol/l; triacylglycerols: 3-7 mmol/l). RESULTS: Glucose and lipid levels were adequately targeted. Plasma non-esterified fatty acids were increased by lipid infusion 1.7-fold. A dramatic and progressive decline of plasma insulin levels was observed in glucose-infused cats beginning after 2 days of hyperglycaemic clamp. In contrast, plasma insulin concentration and glucose tolerance test were not affected by hyperlipidaemia. Compared with controls, glucose-infused cats had a 50% decrease in beta cells per pancreatic area. Apoptotic islet cells and cleaved caspase-3-positive beta cells were observed in glucose-infused cats only. CONCLUSIONS/INTERPRETATION: Sustained hyperglycaemia but not hyperlipidaemia induces early and severe beta cell dysfunction in cats, and excess glucose causes beta cell loss via apoptosis in vivo. Hyperglycaemic clamps in cats may provide a good model to study the pathogenesis of glucose toxicity in beta cells

Towards a global understanding of vegetation-climate dynamics at multiple timescales

Funding Information: Acknowledgements. This paper has been realized within the Earth System Data Lab project funded by the European Space Agency. The authors acknowledge Lina Fürst for initiation of the preliminary study laying the foundation for this project. The authors acknowledge support from Ulrich Weber for data management and preprocessing. Lina M. Estupinan-Suarez acknowledges the support of the DAAD and its Graduate School Scholarship Programme (57395813). Nora Linscheid acknowledges the support of the TUM Graduate School. Lina M. Estupinan-Suarez and Nora Linscheid acknowledge the continuous support of the International Max Planck Research School for Global Biogeochemical Cycles. Felix Cre-mer acknowledges the support of the German Research Foundation project HyperSense (grant no. TH 1435/4-1). Publisher Copyright: © Author(s) 2020. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Climate variables carry signatures of variability at multiple timescales. How these modes of variability are reflected in the state of the terrestrial biosphere is still not quantified or discussed at the global scale. Here, we set out to gain a global understanding of the relevance of different modes of variability in vegetation greenness and its covariability with climate. We used > 30 years of remote sensing records of the normalized difference vegetation index (NDVI) to characterize biosphere variability across timescales from submonthly oscillations to decadal trends using discrete Fourier decomposition. Climate data of air temperature (Tair) and precipitation (Prec) were used to characterize atmosphere-biosphere covariability at each timescale. Our results show that short-term (intra-annual) and longerterm (interannual and longer) modes of variability make regionally highly important contributions to NDVI variability: short-term oscillations focus in the tropics where they shape 27% of NDVI variability. Longer-term oscillations shape 9% of NDVI variability, dominantly in semiarid shrublands. Assessing dominant timescales of vegetation-climate covariation, a natural surface classification emerges which captures patterns not represented by conventional classifications, especially in the tropics. Finally, we find that correlations between variables can differ and even invert signs across timescales. For southern Africa for example, correlation between NDVI and Tair is positive for the seasonal signal but negative for short-term and longer-term oscillations, indicating that both short- and long-term temperature anomalies can induce stress on vegetation dynamics. Such contrasting correlations between timescales exist for 15% of vegetated areas for NDVI with Tair and 27% with Prec, indicating global relevance of scale-specific climate sensitivities. Our analysis provides a detailed picture of vegetation-climate covariability globally, characterizing ecosystems by their intrinsic modes of temporal variability. We find that (i) correlations of NDVI with climate can differ between scales, (ii) nondominant subsignals in climate variables may dominate the biospheric response, and (iii) possible links may exist between short-term and longer-term scales. These heterogeneous ecosystem responses on different timescales may depend on climate zone and vegetation type, and they are to date not well understood and do not always correspond to transitions in dominant vegetation types. These scale dependencies can be a benchmark for vegetation model evaluation and for comparing remote sensing products.publishersversionpublishe

Acute-phase reactants after paediatric cardiac arrest. Procalcitonin as marker of immediate outcome

<p>Abstract</p> <p>Objective</p> <p>Procalcitonin (PCT) and C reactive protein (CRP) have been used as infection parameters. PCT increase correlates with the infection's severity, course, and mortality. Post-cardiocirculatory arrest syndrome may be related to an early systemic inflammatory response, and may possibly be associated with an endotoxin tolerance. Our objective was to report the time profile of PCT and CRP levels after paediatric cardiac arrest and to assess if they could be use as markers of immediate survival.</p> <p>Materials and methods</p> <p>A retrospective observational study set in an eight-bed PICU of a university hospital was performed during a period of two years. Eleven children younger than 14 years were admitted in the PICU after a cardiac arrest. PCT and CRP plasma concentrations were measured within the first 12 and 24 hours of admission.</p> <p>Results</p> <p>In survivors, PCT values increased 12 hours after cardiac arrest without further increase between 12 and 24 hours. In non survivors, PCT values increased 12 hours after cardiac arrest with further increase between 12 and 24 hours. Median PCT values (range) at 24 hours after cardiac arrest were 22.7 ng/mL (0.2 – 41.0) in survivors vs. 205.5 ng/mL (116.6 – 600.0) in non survivors (p < 0.05). CRP levels were elevated in all patients, survivors and non-survivors, at 12 and 24 hours without differences between both groups.</p> <p>Conclusion</p> <p>Measurement of PCT during the first 24 hours after paediatric cardiac arrest could serve as marker of mortality.</p

Procalcitonin for diagnosis of infection and guide to antibiotic decisions: past, present and future

There are a number of limitations to using conventional diagnostic markers for patients with clinical suspicion of infection. As a consequence, unnecessary and prolonged exposure to antimicrobial agents adversely affect patient outcomes, while inappropriate antibiotic therapy increases antibiotic resistance. A growing body of evidence supports the use of procalcitonin (PCT) to improve diagnosis of bacterial infections and to guide antibiotic therapy. For patients with upper and lower respiratory tract infection, post-operative infections and for severe sepsis patients in the intensive care unit, randomized-controlled trials have shown a benefit of using PCT algorithms to guide decisions about initiation and/or discontinuation of antibiotic therapy. For some other types of infections, observational studies have shown promising first results, but further intervention studies are needed before use of PCT in clinical routine can be recommended. The aim of this review is to summarize the current evidence for PCT in different infections and clinical settings, and discuss the reliability of this marker when used with validated diagnostic algorithms