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Abstract
The evolution of mantle composition can be viewed as a process of destruction whereby the initial chemical state is overprinted and reworked with time. Analyses of ocean island basalts reveals that some portion of the mantle has survived this process, retaining a chemically "primitive" signature. A question that remains is how this primitive signature has survived four and a half billion years of vigorous convection. We hypothesize that some of Earth's primitive mantle is buried within a slab graveyard at the core-mantle boundary. We explore this possibility using high-resolution finite element models of mantle convection, in which oceanic lithosphere is produced at zones of plate spreading and subducted at zones of plate convergence. Upon subduction, dense oceanic crust sinks to the base of the mantle and gradually accumulates to form broad, robust thermochemical piles. Sinking oceanic crust entrains the surrounding mantle whose composition is predominantly primitive early in the model's evolution. As a result, thermochemical piles are initially supplied with relatively high concentrations of primitive material-summing up to similar to 30% their total mass. The dense oceanic crust dominating the piles resists efficient mixing and preserves the primitive material that it is intermingled with. The significance of this process is shown to be proportional the rate of mantle processing through time and the excess density of oceanic crust at mantle pressures and temperatures. Unlike other theories for the survival of Earth's primitive mantle, this one does not require the early Earth to have large-scale domains of anomalously high density and/or viscosity.
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Abstract
Tracer methods are widespread in computational geodynamics for modeling the advection of chemical data. However, they present certain numerical challenges, especially when used over long periods of simulation time. We address two of these in this work: the necessity for mass conservation of chemical composition fields and the need for the velocity field to be pointwise divergence free to avoid gaps in tracer coverage. We do this by implementing the hybrid discontinuous Galerkin (HDG) finite element (FE) method combined with a mass conserving constrained projection of the tracer data. To demonstrate the efficacy of this system, we compare it to other common FE formulations of the Stokes system and projections of the chemical composition. We provide a reference of the numerical properties and error convergence rates which should be observed by using these various discretization schemes. This serves as a tool for verification of existing or new implementations. We summarize these data in a reproduction of a published Rayleigh-Taylor instability benchmark, demonstrating the importance of careful choices of appropriate and compatible discretization methods for all aspects of geodynamics simulations.
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Abstract
The composition of Earth's mantle, continental crust, and oceanic crust continuously evolve in response to the dynamic forces of plate tectonics and mantle convection. The classical view of terrestrial geochemistry, where mid-ocean ridges sample mantle previously depleted by continental crust extraction, broadly explains the composition of the oceanic and continental crust but is potentially inconsistent with observed slab subduction to the lower mantle and oceanic crust accumulation in the deep mantle. We develop a box model to explore the key processes controlling crust-mantle chemical evolution. The model mimics behaviors observed in thermochemical convection simulations including subducted oceanic crust separating and accumulating in the deep mantle. We demonstrate that oceanic crust accumulation strongly depletes the mantle independently of continental crust extraction. Slab stalling depths and continental crust recycling rates also affect the extent and location of mantle depletion. We constrain model regimes that reproduce oceanic and continental crust compositions using Markov chain Monte Carlo sampling. Some regimes deplete the lower mantle more than the upper mantle, contradicting the assumption of a more enriched lower mantle. All regimes require oceanic crust accumulation in the mantle. Though a small fraction of the mantle mass, accumulated oceanic crust can sequester trace element budgets exceeding the continental crust, depleting the mantle more than continental crust extraction alone. Oceanic crust accumulation may therefore be as important as continental crust extraction in depleting the mantle, contradicting the paradigmatic complementarity of depleted mantle and continental crust. Instead, depleted mantle is complementary to continental crust plus sequestered oceanic crust.
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Abstract
In prior work we found that precise approximation of the continuity constraint is crucial for accurate propagation of tracer data when advected through a background incompressible velocity field (Sime et al., 2021, ). Here we extend this investigation to compressible flows using the anelastic liquid approximation (ALA) and address four related issues: (a) Exact conservation of tracer discretized fields through a background compressible velocity; (b) Exact mass conservation; (c) Addition and removal of tracers without affecting (exact) conservation to preserve a consistent number of tracers per cell; and (d) the diffusion of tracer data, for example, as induced by thermal or chemical effects. In this process we also present an abstract formulation of the interior penalty hybrid discontinuous Galerkin (HDG) finite element formulation for diffusion problems and apply it to the advection-diffusion and compressible Stokes systems. Finally we present numerical experiments exhibiting the HDG compressible Stokes momentum formulation's superconvergent compressibility approximation and reproduce examples of a community benchmark for the ALA.
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Abstract
Oceanic crust subduction sequesters substantial amounts of argon in the Earth's mantle, while atmosphere-derived argon affects only the isotopic composition and not the overall budget, according to geodynamic-geochemical models of mantle convection.
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SURI 2022
September 06, 2022
Campus News

From chondrite characterization to deep-sea microbes: SURI interns present their research at final symposium

Jens Barosch studies a sample of the Ryugu meteorite under a microscope on campus.
September 06, 2022
Spotlight

Jens Barosch studies stardust to understand our Solar System

The seismology group in 1990. Back row left to right: Fred Pollitz, Paul Silver, Selwyn Sacks, Gotz Bokelmann, Michael Acierno, Craig Bina, David James, Alan Linde. Front row left to right: Satoshi Kaneshima, Randy Kuehnel, and Chris Kincaid. Courtesy of Carnegie Institution for Science.

The seismology group in 1990. Back row left to right: Fred Pollitz, Paul Silver, Selwyn Sacks, Gotz Bokelmann, Michael Acierno, Craig Bina, David James, Alan Linde. Front row left to right: Satoshi Kaneshima, Randy Kuehnel, and Chris Kincaid. Courtesy of Carnegie Institution for Science.

September 06, 2022
Campus News

Michael Acierno's retirement speech

Abstract
Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unexplored. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence and mounts strong systemic inflammation that leads to de-regulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by ageassociated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and de-repression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during aging. Overall design: 17 samples from the fat body, the midgut, or the whole gut with different ages or RNAi treatment. 6 of the samples were wildtype young control. For each experiment, we had two or three biological replicates.
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Abstract
Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unexplored. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence and mounts strong systemic inflammation that leads to de-regulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by ageassociated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and de-repression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during aging. Overall design: 17 samples from the fat body, the midgut, or the whole gut with different ages or RNAi treatment. 6 of the samples were wildtype young control. For each experiment, we had two or three biological replicates.
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