1,161 research outputs found

    121 SPATIAL CORRELATIONS BETWEEN LOCAL IMPACT STRESS AND CELL DEATH DISTRIBUTIONS

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    Black carbon in the atmosphere and snow, from pre-industrial times until present

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    The distribution of black carbon (BC) in the atmosphere and the deposition of BC on snow surfaces since pre-industrial time until present are modelled with the Oslo CTM2 model. The model results are compared with observations including recent measurements of BC in snow in the Arctic. The global mean burden of BC from fossil fuel and biofuel sources increased during two periods. The first period, until 1920, is related to increases in emissions in North America and Europe, and the last period after 1970 are related mainly to increasing emissions in East Asia. Although the global burden of BC from fossil fuel and biofuel increases, in the Arctic the maximum atmospheric BC burden as well as in the snow was reached in 1960s, with a slight reduction thereafter. The global mean burden of BC from open biomass burning sources has not changed significantly since 1900. With current inventories of emissions from open biomass sources, the modelled burden of BC in snow and in the atmosphere north of 65° N is small compared to the BC burden of fossil fuel and biofuel origin. From the concentration changes radiative forcing time series due to the direct aerosol effect as well as the snow-albedo effect is calculated for BC from fossil fuel and biofuel. The calculated radiative forcing in 2000 for the direct aerosol effect is 0.35 W m<sup>−2</sup> and for the snow-albedo effect 0.016 W m<sup>−2</sup> in this study. Due to a southward shift in the emissions there is an increase in the lifetime of BC as well as an increase in normalized radiative forcing, giving a change in forcing per unit of emissions of 26 % since 1950

    Anthropogenic Space Weather

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    Anthropogenic effects on the space environment started in the late 19th century and reached their peak in the 1960s when high-altitude nuclear explosions were carried out by the USA and the Soviet Union. These explosions created artificial radiation belts near Earth that resulted in major damages to several satellites. Another, unexpected impact of the high-altitude nuclear tests was the electromagnetic pulse (EMP) that can have devastating effects over a large geographic area (as large as the continental United States). Other anthropogenic impacts on the space environment include chemical release ex- periments, high-frequency wave heating of the ionosphere and the interaction of VLF waves with the radiation belts. This paper reviews the fundamental physical process behind these phenomena and discusses the observations of their impacts.Comment: 71 pages, 35 figure

    TCF7L2 rs7903146-macronutrient interaction in obese individuals' responses to a 10-wk randomized hypoenergetic diet

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    BACKGROUND: Transcription factor 7-like 2 (TCF7L2) rs7903146 associates with type 2 diabetes and may operate via impaired glucagon-like peptide 1 secretion, which is stimulated more by fat than by carbohydrate ingestion. OBJECTIVE: The objective was to examine the interaction between TCF7L2 rs7903146 and dietary fat and carbohydrate [high-fat, low-carbohydrate: 40-45% of energy as fat (HF); compared with low-fat, high-carbohydrate: 20-25% of energy as fat (LF)] in obese individuals' responses to a 10-wk hypoenergetic diet (-600 kcal/d). DESIGN: European, obese participants (n = 771) were randomly assigned to receive an HF or an LF diet. Body weight, fat mass (FM), fat-free mass (FFM), waist circumference (WC), resting energy expenditure (REE), fasting fat oxidation in percentage of REE (FatOx), homeostasis model assessed insulin release (HOMA-beta), and HOMA-insulin resistance (HOMA-IR) were determined at baseline and after the intervention; 739 individuals were genotyped for rs7903146. RESULTS: Average weight loss was 6.9 kg with the LF and 6.6 kg with the HF (difference between diets, NS) diet. Among individuals who were homozygous for the T-risk allele, those in the HF diet group experienced smaller weight losses (Deltaweight) (2.6 kg; P = 0.009; n = 622), smaller DeltaFFM (1.6 kg; P = 0.027; n = 609), smaller DeltaWC (3.3 cm; P = 0.010; n = 608), and a smaller DeltaHOMA-IR (1.3 units; P = 0.004; n = 615) than did the LF diet group. For C allele carriers, there were no differences between the HF and LF diet groups. For the HF diet group, each additional T allele was associated with a reduced loss of FM (0.67 kg; P = 0.019; n = 609). TCF7L2 rs7903146 was not associated with DeltaREE, DeltaFatOx, DeltaHOMA-beta, or dropout. CONCLUSION: Our results suggest that obese individuals who are homozygous for the TCF7L2 rs7903146 T-risk allele are more sensitive to LF than to HF weight-loss diets

    Enteroendocrine K-cells exert complementary effects to control bone quality and mass in mice

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    International audienceThe involvement of a gut-bone axis in controlling bone physiology has been long suspected, although the exact mechanisms are unclear. We explored whether glucose-dependent insulinotropic polypeptide (GIP)-producing enteroendocrine K-cells were involved in this process. The bone phenotype of transgenic mouse models lacking GIP secretion (GIP-GFP-KI) or enteroendocrine K-cells (GIP-DT) was investigated. Mice deficient in GIP secretion exhibited lower bone strength, trabecular bone mass, trabecula number and cortical thickness, notably due to higher bone resorption. Alterations of microstructure, modifications of bone compositional parameters, represented by lower collagen cross-linking were also apparent. None of these alterations were observed in GIP-DT mice lacking enteroendocrine K-cells, suggesting that other K-cell secretory product acts to counteract GIP action. To assess this, stable analogues of the known K-cell peptide hormones, xenin and GIP, were administered to mature NIH Swiss male mice. Both were capable of modulating bone strength mostly by altering bone microstructure, bone gene expression and bone compositional parameters. However, the two molecules exhibited opposite actions on bone physiology, with evidence that xenin effects are mediated indirectly, possibly via neural networks. Our data highlight a previously unknown interaction between GIP and xenin, which both moderate gut-bone connectivity
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