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.

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.

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.

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.

Difficulties to accurately map epigenomes in a few cells sorted or dissected from tissues have hampered our understanding of how chromatin modification regulates development and diseases. Despite recent progress, all reported chromatin-immunoprecipitation-based deep sequencing (ChIP-seq) methods have not achieved high quality mapping of rare cell populations. We report Recovery via Protection (RP)-ChIP-seq and favored amplification RP-ChIP-seq (FARP-ChIP-seq) for as few as 500 cells with superior quality compared to all reported techniques to date. FARP-ChIP-seq accurately mapped histone H3 lysine 4 trimethylation (H3K4me3) and H3K27me3 in long-term hematopoietic stem cells (LT-HSCs), short-term HSCs (ST-HSCs), and multi-potent progenitors (MPPs) sorted from one mouse. These high quality datasets not only implicate genes involved in HSC differentiation but also demonstrate a general lack of H3K4me3/H3K27me3 bivalency on hematopoietic genes in HSCs. Thus the method offers accurate mapping for fewest cells. Overall design: two H3K4me3 replications for mESC, two to three replications of H3K4me3 and H3K27me3 for LT-HSC, ST-HSC and MPP

Difficulties to accurately map epigenomes in a few cells sorted or dissected from tissues have hampered our understanding of how chromatin modification regulates development and diseases. Despite recent progress, all reported chromatin-immunoprecipitation-based deep sequencing (ChIP-seq) methods have not achieved high quality mapping of rare cell populations. We report Recovery via Protection (RP)-ChIP-seq and favored amplification RP-ChIP-seq (FARP-ChIP-seq) for as few as 500 cells with superior quality compared to all reported techniques to date. FARP-ChIP-seq accurately mapped histone H3 lysine 4 trimethylation (H3K4me3) and H3K27me3 in long-term hematopoietic stem cells (LT-HSCs), short-term HSCs (ST-HSCs), and multi-potent progenitors (MPPs) sorted from one mouse. These high quality datasets not only implicate genes involved in HSC differentiation but also demonstrate a general lack of H3K4me3/H3K27me3 bivalency on hematopoietic genes in HSCs. Thus the method offers accurate mapping for fewest cells. Overall design: two H3K4me3 replications for mESC, two to three replications of H3K4me3 and H3K27me3 for LT-HSC, ST-HSC and MPP

We discovered that two mitotic regulators, BuGZ and Bub3, involved in splicing regulation during interphase Overall design: 8 samples from primary Human foreskin fibroblast cells (HFFs) , 12 samples from TOV21G cells. Control siRNA. BuGZ siRNA or Bub3 siRNA were transfected for 48 h before sample collection. Cells treated with pladienolide B served as positive controls. For each RNAi experiment, we had two biological replicates.