A hyperbolic-elliptic PDE model and conservative numerical method for gravity-dominated variably-saturated groundwater flow

Richards equation is often used to represent two-phase fluid flow in an unsaturated porous medium when one phase is much heavier and more viscous than the other. However, it cannot describe the fully saturated flow due to degeneracy in the capillary pressure term. Mathematically, gravity-driven variably saturated flows are interesting because their governing partial differential equation switches from hyperbolic in the unsaturated region to elliptic in the saturated region. Moreover, the presence of wetting fronts introduces strong spatial gradients often leading to numerical instability. In this work, we develop a robust, multidimensional mathematical and computational model for such variably saturated flow in the limit of negligible capillary forces. The elliptic problem for saturated regions is built-in efficiently into our framework for a reduced system corresponding to the saturated cells, with the boundary condition of the fixed head at the unsaturated cells. In summary, this coupled hyperbolic-elliptic PDE framework provides an efficient, physics-based extension of the hyperbolic Richards equation to simulate fully saturated regions. Finally, we provide a suite of easy-to-implement yet challenging benchmark test problems involving saturated flows in one and two dimensions. These simple problems, accompanied by their corresponding analytical solutions, can prove to be pivotal for the code verification, model validation (V&V) and performance comparison of such simulators. Our numerical solutions show an excellent comparison with the analytical results for the proposed problems. The last test problem on two-dimensional infiltration in a stratified, heterogeneous soil shows the formation and evolution of multiple disconnected saturated regions.Comment: 21 pages, 9 figure

Targeting Interleukin-10 Restores Graft Microvascular Supply and Airway Epithelium in Rejecting Allografts

Interleukin-10 (IL-10) is a vital regulatory cytokine, which plays a constructive role in maintaining immune tolerance during an alloimmune inflammation. Our previous study highlighted that IL-10 mediated immunosuppression established the immune tolerance phase and thereby modulated both microvascular and epithelial integrity, which affected inflammation-associated graft malfunctioning and sub-epithelial fibrosis in rejecting allografts. Here, we further investigated the reparative effects of IL-10 on microvasculature and epithelium in a mouse model of airway transplantation. To investigate the IL-10 mediated microvascular and epithelial repair, we depleted and reconstituted IL-10, and monitored graft microvasculature, airway epithelium, and associated repair proteins. Our data demonstrated that both untreated control allografts and IL-10 (−) allografts showed a significant early (d6) increase in microvascular leakiness, drop-in tissue oxygenation, blood perfusion, and denuded airway epithelium, which is associated with loss of adhesion protein Fascin-1 and β-catenin on vascular endothelial cells at d10 post-transplantation. However, IL-10 (+) promotes early microvascular and airway epithelial repair, and a proportional increase in endothelial Fascin-1, and β-catenin at d10 post-transplantation. Moreover, airway epithelial cells also express a significantly higher expression of FOXJ1 and β-catenin in syngrafts and IL-10 (+) allografts as compared to IL-10 (−) and untreated controls at d10 post-transplantation. Collectively, these findings demonstrated that IL-10 mediated microvascular and epithelial changes are associated with the expression of FOXJ1, β-catenin, and Fascin-1 proteins on the airway epithelial and vascular endothelial cells, respectively. These findings establish a potential reparative modulation of IL-10 associated microvascular and epithelial repair, which could provide a vital therapeutic strategy to facilitate graft repair in clinical settings

Texas Open Science Summit (TOSS)

In celebration of 2023 being designated as a Year of Open Science, the University of Texas Libraries – with support from the Office of Vice President for Research, Scholarship and Creative Endeavors – are collaborating with HELIOS and NASA TOPS to organize the Texas Open Science Summit (TOSS). Our half-day program will bring together experts in a variety of disciplines to talk about federal government requirements for sharing research publications and data, the importance of open science to early career researchers, and open science opportunities at UT Austin. We’ll also be introducing the new Open Source Program Office (OSPO) at UT Austin and discussing the role of OSPOs at institutions across the U.S.UT Librarie

IL-10 Mediated Immunomodulation Limits Subepithelial Fibrosis and Repairs Airway Epithelium in Rejecting Airway Allografts

Interleukin-10 plays a vital role in maintaining peripheral immunotolerance and favors a regulatory immune milieu through the suppression of T effector cells. Inflammation-induced microvascular loss has been associated with airway epithelial injury, which is a key pathological source of graft malfunctioning and subepithelial fibrosis in rejecting allografts. The regulatory immune phase maneuvers alloimmune inflammation through various regulatory modulators, and thereby promotes graft microvascular repair and suppresses the progression of fibrosis after transplantation. The present study was designed to investigate the therapeutic impact of IL-10 on immunotolerance, in particular, the reparative microenvironment, which negates airway epithelial injury, and fibrosis in a mouse model of airway graft rejection. Here, we depleted and reconstituted IL-10, and serially monitored the phase of immunotolerance, graft microvasculature, inflammatory cytokines, airway epithelium, and subepithelial collagen in rejecting airway transplants. We demonstrated that the IL-10 depletion suppresses FOXP3+ Tregs, tumor necrosis factor-inducible gene 6 protein (TSG-6), graft microvasculature, and establishes a pro-inflammatory phase, which augments airway epithelial injury and subepithelial collagen deposition while the IL-10 reconstitution facilitates FOXP3+ Tregs, TSG-6 deposition, graft microvasculature, and thereby favors airway epithelial repair and subepithelial collagen suppression. These findings establish a potential reparative modulation of IL-10-associated immunotolerance on microvascular, epithelial, and fibrotic remodeling, which could provide a vital therapeutic option to rescue rejecting transplants in clinical settings