No abstract

We report theoretical and numerical studies of the flow behaviour when a fluid is injected into a confined porous medium saturated with another fluid of different density and viscosity. For a two-dimensional configuration with point source injection, a nonlinear convection–diffusion equation is derived to describe the time evolution of the fluid–fluid interface. In the early time period, the fluid motion is mainly driven by the buoyancy force and the governing equation is reduced to a nonlinear diffusion equation with a well-known self-similar solution. In the late time period, the fluid flow is mainly driven by the injection, and the governing equation is approximated by a nonlinear hyperbolic equation that determines the global spreading rate; a shock solution is obtained when the injected fluid is more viscous than the displaced fluid, whereas a rarefaction wave solution is found when the injected fluid is less viscous. In the late time period, we also obtain analytical solutions including the diffusive term associated with the buoyancy effects (for an injected fluid with a viscosity higher than or equal to that of the displaced fluid), which provide the structure of the moving front. Numerical simulations of the convection–diffusion equation are performed; the various analytical solutions are verified as appropriate asymptotic limits, and the transition processes between the individual limits are demonstrated. The flow behaviour is summarized in a diagram with five distinct dynamical regimes: a nonlinear diffusion regime, a transition regime, a travelling wave regime, an equal-viscosity regime, and a rarefaction regime.

Per‐ and polyfluoroalkyl substances (PFAS) are emerging contaminants of critical concern. As surfactants, PFAS tend to accumulate at air‐water interfaces and may stay in the vadose zone for long times before contaminating groundwater. Yet not well understood, the extent of retention in the vadose zone has critical implications for risk management and remediation strategies. We present the first mathematical model that accounts for surfactant‐induced flow and solid‐phase and air‐water interfacial adsorption. We apply the model to simulate PFOS (a PFAS compound of primary concern) transport in the vadose zone at a model fire‐training area site impacted by aqueous film‐forming foam (AFFF). Air‐water interfacial adsorption is shown to have a significant impact—amplified by the low water content due to gravity drainage—total retardation factors range from 233 to 1,355 for the sand and 146 to 792 for the soil used in the study. The simulations illustrate it can take several decades or longer for PFOS to reach groundwater. Counterintuitively, the lower water content in the sand—due to stronger drainage and weaker capillary retention—leads to retardation factors greater than for the soil. Also, most PFOS is adsorbed at air‐water interfaces with only 1–2% in the aqueous phase. The implications include (1) fine‐texture materials could have lower retardation factors than sand due to higher retained water content, (2) soil PFAS concentrations are likely to be orders of magnitude higher than those in groundwater at source zones. Both implications are consistent with recent field observations at hundreds of AFFF‐impacted sites.

In contrast to Ag-specific αβ T cells, γδ T cells can kill malignantly transformed cells in a manner that does not require the recognition of tumor-specific Ags. Although such observations have contributed to the emerging view that γδ T cells provide protective innate immunosurveillance against certain malignancies, particularly those of epithelial origin, they also provide a rationale for developing novel clinical approaches to exploit the innate antitumor properties of γδ T cells for the treatment of cancer. Using TRAMP, a transgenic mouse model of prostate cancer, proof-of-concept studies were performed to first establish that γδ T cells can indeed provide protective immunosurveillance against spontaneously arising mouse prostate cancer. TRAMP mice, which predictably develop prostate adenocarcinoma, were backcrossed with γδ T cell-deficient mice (TCRδ−/− mice) yielding TRAMP × TCRδ−/− mice, a proportion of which developed more extensive disease compared with control TRAMP mice. By extension, these findings were then used as a rationale for developing an adoptive immunotherapy model for treating prostate cancer. Using TRAMP-C2 cells derived from TRAMP mice (C57BL/6 genetic background), disease was first established in otherwise healthy wild-type C57BL/6 mice. In models of localized and disseminated disease, tumor-bearing mice treated i.v. with supraphysiological numbers of syngeneic γδ T cells (C57BL/6-derived) developed measurably less disease compared with untreated mice. Disease-bearing mice treated i.v. with γδ T cells also displayed superior survival compared with untreated mice. These findings provide a biological rationale for clinical trials designed to adoptively transfer ex vivo expanded autologous γδ T cells for the treatment of prostate cancer.

Ex vivo, expanded human Vgamma9Vdelta2+ gammadelta-T cells are able innately to recognize and kill certain human prostate tumor cell lines in vitro. The recognition and killing of prostate cancer cells occurs in a gammadelta-T-cell receptor dependent manner and it also appears to involve interactions between ICAM-1 and CD18. Because apoptosis resistant human Vgamma9Vdelta2+ gammadelta-T cells can readily be expanded to large numbers (clinical scale), these findings must be considered in the context of developing adoptive immunotherapy strategies to exploit gammadelta-T cell innate immune responses to prostate cancer.