88 research outputs found

    Numerical Modeling of Hyperconcentrated Turbidity Currents

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    Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

    A Study of the Merger History of the Galaxy Group HCG 62 Based on X-Ray Observations and SPH Simulations

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    We choose the bright compact group HCG 62, which was found to exhibit both excess X-ray emission and high Fe abundance to the southwest of its core, as an example to study the impact of mergers on chemical enrichment in the intragroup medium. We first reanalyze the high-quality Chandra and XMM-Newton archive data to search for the evidence for additional SN II yields, which is expected as a direct result of the possible merger-induced starburst. We reveal that, similar to the Fe abundance, the Mg abundance also shows a high value in both the innermost region and the southwest substructure, forming a high-abundance plateau, meanwhile all the SN Ia and SN II yields show rather flat distributions in >0.1r200>0.1r_{200} in favor of an early enrichment. Then we carry out a series of idealized numerical simulations to model the collision of two initially isolated galaxy groups by using the TreePM-SPH GADGET-3 code. We find that the observed X-ray emission and metal distributions, as well as the relative positions of the two bright central galaxies with reference to the X-ray peak, can be well reproduced in a major merger with a mass ratio of 3 when the merger-induced starburst is assumed. The `best-match' snapshot is pinpointed after the third pericentric passage when the southwest substructure is formed due to gas sloshing. By following the evolution of the simulated merging system, we conclude that the effects of such a major merger on chemical enrichment are mostly restricted within the core region when the final relaxed state is reached.Comment: Accepted for publication in the Astrophysical Journa

    Elucidating the role of the TRPM7 alpha-kinase: TRPM7 kinase inactivation leads to magnesium deprivation resistance phenotype in mice

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    TRPM7 is an unusual bi-functional protein containing an ion channel covalently linked to a protein kinase domain. TRPM7 is implicated in regulating cellular and systemic magnesium homeostasis. While the biophysical properties of TRPM7 ion channel and its function are relatively well characterized, the function of the TRPM7 enzymatically active kinase domain is not understood yet. To investigate the physiological role of TRPM7 kinase activity, we constructed mice carrying an inactive TRPM7 kinase. We found that these mice were resistant to dietary magnesium deprivation, surviving three times longer than wild type mice; also they displayed decreased chemically induced allergic reaction. Interestingly, mutant mice have lower magnesium bone content compared to wild type mice when fed regular diet; unlike wild type mice, mutant mice placed on magnesium-depleted diet did not alter their bone magnesium content. Furthermore, mouse embryonic fibroblasts isolated from TRPM7 kinase-dead animals exhibited increased resistance to magnesium deprivation and oxidative stress. Finally, electrophysiological data revealed that the activity of the kinase-dead TRPM7 channel was not significantly altered. Together, our results suggest that TRPM7 kinase is a sensor of magnesium status and provides coordination of cellular and systemic responses to magnesium deprivation

    TRPM7 is essential for Mg2+ homeostasis in mammals

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    Mg2+ is the second-most abundant cation in animal cells and is an essential cofactor in numerous enzymatic reactions. The molecular mechanisms controlling Mg2+ balance in the organism are not well understood. In this study, we report identification of TRPM7, a bifunctional protein containing a protein kinase fused to an ion channel, as a key regulator of whole body Mg2+ homeostasis in mammals. We generated TRPM7-deficient mice with the deletion of the kinase domain. Homozygous TRPM7Δkinase mice demonstrated early embryonic lethality, whereas heterozygous mice were viable, but developed signs of hypomagnesaemia and revealed a defect in intestinal Mg2+ absorption. Cells derived from heterozygous TRPM7Δkinase mice demonstrated reduced TRPM7 currents that had increased sensitivity to the inhibition by Mg2+. Embryonic stem cells lacking TRPM7 kinase domain displayed a proliferation arrest phenotype that can be rescued by Mg2+ supplementation. Our results demonstrate that TRPM7 is essential for the control of cellular and whole body Mg2+ homeostasis

    Approximate Solutions for Ideal Dam-Break Sediment-Laden Flows on Uniform Slopes

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    Shallow water hydro-sediment-morphodynamic (SHSM) models have been applied increasingly widely in hydraulic engineering and geomorphological studies over the past few decades. Analytical and approximate solutions are usually sought to verify such models and therefore confirm their credibility. Dam-break flows are often evoked because such flows normally feature shock waves and contact discontinuities that warrant refined numerical schemes to solve. While analytical and approximate solutions to clear-water dam-break flows have been available for some time, such solutions are rare for sediment transport in dam-break flows. Here we aim to derive approximate solutions for ideal dam-break sediment-laden flows resulting from the sudden release of a finite volume of frictionless, incompressible water-sediment mixture on a uniform slope. The approximate solutions are presented for three typical sediment transport scenarios, i.e., pure advection, pure sedimentation, and concurrent entrainment and deposition. Although the cases considered in this paper are not real, the approximate solutions derived facilitate suitable benchmark tests for evaluating SHSM models, especially presently when shock waves can be numerically resolved accurately with a suite of finite volume methods, while the accuracy of the numerical solutions of contact discontinuities in sediment transport remains generally poorer
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