Legacy Effect of Long-Term Elevated CO2 and Warming on Soil Properties Controls Soil Organic Matter Decomposition

Plant litter quality is one of the key factors that control soil organic matter (SOM) decomposition. Under climate change, although significant change in litter quality has been intensively reported, the effect of litter quality change on SOM decomposition is poorly understood. This limits our ability to model the dynamics of soil carbon under climate change. To determine the effect of litter quality and soil property change on SOM decomposition, we performed a controlled, reciprocal transplant and litter decomposition experiments. The soils and plant litters were collected from a long-term field experiment, where four treatments were designed, including: (1) the control without warming at ambient CO2; (2) elevated atmospheric CO2 up to 500 ppm (C); (3) warming plant canopy by 2 degrees C (T); (4) elevated CO2 plus warming (CT). We found that elevated CO2 and warming altered the litter quality significantly in terms of macronutrients' content and their stoichiometry. Elevated CO2 decreased the concentration of N in rice and wheat straw, while warming decreased the concentration of N and K in wheat straw. However, the change in plant litter quality did not lead to a shift in SOM decomposition. On the contrary, the legacy effect of long-term elevated CO2 and warming on soil properties dominated the decomposition rate of SOM. Elevated atmospheric CO2 suppressed SOM decomposition mainly by increasing phosphorous availability and lowering the soil C/N, fungi/bacteria ratio, and N-acetyl-glucosaminidase activity, while warming or elevated CO2 plus warming had no effect on SOM decomposition. Our results demonstrated that the changes in soil property other than litter quality control the decomposition of SOM under climate change, and soil property change in respond to climate change should be considered in model developing to predict terrestrial soil carbon dynamics under elevated atmospheric CO2 and warming

Structural analysis and corrosion studies on an ISO 5832-9 biomedical alloy with TiO2 sol–gel layers

The aim of this study was to demonstrate the relationship between the structural and corrosion properties of an ISO 5832-9 biomedical alloy modified with titanium dioxide (TiO2) layers. These layers were obtained via the sol–gel method by acid-catalyzed hydrolysis of titanium isopropoxide in isopropanol solution. To obtain TiO2 layers with different structural properties, the coated samples were annealed at temperatures of 200, 300, 400, 450, 500, 600 and 800 C for 2 h. For all the prepared samples, accelerated corrosion measurements were performed in Tyrode’s physiological solution using electrochemical methods. The most important corrosion parameters were determined: corrosion potential, polarization resistance, corrosion rate, breakdown and repassivation potentials. Corrosion damage was analyzed using scanning electron microscopy. Structural analysis was carried out for selected TiO2 coatings annealed at 200, 400, 600 and 800 C. In addition, the morphology, chemical composition, crystallinity, thickness and density of the deposited TiO2 layers were determined using suitable electron and X-ray measurement methods. It was shown that the structure and character of interactions between substrate and deposited TiO2 layers depended on annealing temperature. All the obtained TiO2 coatings exhibit anticorrosion properties, but these properties are related to the crystalline structure and character of substrate–layer interaction. From the point of view of corrosion, the best TiO2 sol–gel coatings for stainless steel intended for biomedical applications seem to be those obtained at 400 C.This study was supported by Grant No. N N507 501339 of the National Science Centre. The authors wish to express their thanks to J. Borowski (MEDGAL, Poland) for the Rex 734 alloy

Mapping an atlas of tissue-specific drosophila melanogaster metabolomes by high resolution mass spectrometry

Metabolomics can provide exciting insights into organismal function, but most work on simple models has focussed on the whole organism metabolome, so missing the contributions of individual tissues. Comprehensive metabolite profiles for ten tissues from adult Drosophila melanogaster were obtained here by two chromatographic methods, a hydrophilic interaction (HILIC) method for polar metabolites and a lipid profiling method also based on HILIC, in combination with an Orbitrap Exactive instrument. Two hundred and forty two polar metabolites were putatively identified in the various tissues, and 251 lipids were observed in positive ion mode and 61 in negative ion mode. Although many metabolites were detected in all tissues, every tissue showed characteristically abundant metabolites which could be rationalised against specific tissue functions. For example, the cuticle contained high levels of glutathione, reflecting a role in oxidative defence; the alimentary canal (like vertebrate gut) had high levels of acylcarnitines for fatty acid metabolism, and the head contained high levels of ether lipids. The male accessory gland uniquely contained decarboxylated S-adenosylmethionine. These data thus both provide valuable insights into tissue function, and a reference baseline, compatible with the FlyAtlas.org transcriptomic resource, for further metabolomic analysis of this important model organism, for example in the modelling of human inborn errors of metabolism, aging or metabolic imbalances such as diabetes

Sphingolipid Modulation Activates Proteostasis Programs to Govern Human Hematopoietic Stem Cell Self-Renewal.

Cellular stress responses serve as crucial decision points balancing persistence or culling of hematopoietic stem cells (HSCs) for lifelong blood production. Although strong stressors cull HSCs, the linkage between stress programs and self-renewal properties that underlie human HSC maintenance remains unknown, particularly at quiescence exit when HSCs must also dynamically shift metabolic state. Here, we demonstrate distinct wiring of the sphingolipidome across the human hematopoietic hierarchy and find that genetic or pharmacologic modulation of the sphingolipid enzyme DEGS1 regulates lineage differentiation. Inhibition of DEGS1 in hematopoietic stem and progenitor cells during the transition from quiescence to cellular activation with N-(4-hydroxyphenyl) retinamide activates coordinated stress pathways that coalesce on endoplasmic reticulum stress and autophagy programs to maintain immunophenotypic and functional HSCs. Thus, our work identifies a linkage between sphingolipid metabolism, proteostatic quality control systems, and HSC self-renewal and provides therapeutic targets for improving HSC-based cellular therapeutics.E.L. is supported by Wellcome grant 107630/Z/15/Z and a core support grant from the Wellcome and MRC to the Wellcome-Medical Research Council Cambridge Stem Cell Institute. C.L. is supported by U.S. NIH, NCI Grant P01-CA097132. JED is supported by funds from the Princess Margaret Cancer Centre Foundation, Canadian Institutes for Health Research, Joint Canada-Israel Health Research Program, Terry Fox Foundation, and a Canada Research Chair

Effects of Tillage and Nitrogen Fertilizers on CH4 and CO2 Emissions and Soil Organic Carbon in Paddy Fields of Central China

Quantifying carbon (C) sequestration in paddy soils is necessary to help better understand the effect of agricultural practices on the C cycle. The objective of the present study was to assess the effects of tillage practices [conventional tillage (CT) and no-tillage (NT)] and the application of nitrogen (N) fertilizer (0 and 210 kg N ha−1) on fluxes of CH4 and CO2, and soil organic C (SOC) sequestration during the 2009 and 2010 rice growing seasons in central China. Application of N fertilizer significantly increased CH4 emissions by 13%–66% and SOC by 21%–94% irrespective of soil sampling depths, but had no effect on CO2 emissions in either year. Tillage significantly affected CH4 and CO2 emissions, where NT significantly decreased CH4 emissions by 10%–36% but increased CO2 emissions by 22%–40% in both years. The effects of tillage on the SOC varied with the depth of soil sampling. NT significantly increased the SOC by 7%–48% in the 0–5 cm layer compared with CT. However, there was no significant difference in the SOC between NT and CT across the entire 0–20 cm layer. Hence, our results suggest that the potential of SOC sequestration in NT paddy fields may be overestimated in central China if only surface soil samples are considered

Acid-evoked Ca2+ signalling in rat sensory neurones: effects of anoxia and aglycaemia

Ischaemia excites sensory neurones (generating pain) and promotes calcitonin gene-related peptide release from nerve endings. Acidosis is thought to play a key role in mediating excitation via the activation of proton-sensitive cation channels. In this study, we investigated the effects of acidosis upon Ca2+ signalling in sensory neurones from rat dorsal root ganglia. Both hypercapnic (pHo 6.8) and metabolic–hypercapnic (pHo 6.2) acidosis caused a biphasic increase in cytosolic calcium concentration ([Ca2+]i). This comprised a brief Ca2+ transient (half-time approximately 30 s) caused by Ca2+ influx followed by a sustained rise in [Ca2+]i due to Ca2+ release from caffeine and cyclopiazonic acid-sensitive internal stores. Acid-evoked Ca2+ influx was unaffected by voltage-gated Ca2+-channel inhibition with nickel and acid sensing ion channel (ASIC) inhibition with amiloride but was blocked by inhibition of transient receptor potential vanilloid receptors (TRPV1) with (E)-3-(4-t-butylphenyl)-N-(2,3-dihydrobenzo[b][1,4] dioxin-6-yl)acrylamide (AMG 9810; 1 μM) and N-(4-tertiarybutylphenyl)-4-(3-cholorphyridin-2-yl) tetrahydropryazine-1(2H)-carbox-amide (BCTC; 1 μM). Combining acidosis with anoxia and aglycaemia increased the amplitude of both phases of Ca2+ elevation and prolonged the Ca2+ transient. The Ca2+ transient evoked by combined acidosis, aglycaemia and anoxia was also substantially blocked by AMG 9810 and BCTC and, to a lesser extent, by amiloride. In summary, the principle mechanisms mediating increase in [Ca2+]i in response to acidosis are a brief Ca2+ influx through TRPV1 followed by sustained Ca2+ release from internal stores. These effects are potentiated by anoxia and aglycaemia, conditions also prevalent in ischaemia. The effects of anoxia and aglycaemia are suggested to be largely due to the inhibition of Ca2+-clearance mechanisms and possible increase in the role of ASICs

Improved measurement of the reactor antineutrino flux and spectrum at Daya Bay

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Measurement of electron antineutrino oscillation based on 1230 days of operation of the Daya Bay experiment

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