@article{spence_osmond_childres_heitman_robarge_2012, title={Effects of Lawn Maintenance on Nutrient Losses Via Overland Flow During Natural Rainfall Events}, volume={48}, ISSN={1093-474X}, url={http://dx.doi.org/10.1111/j.1752-1688.2012.00658.x}, DOI={10.1111/j.1752-1688.2012.00658.x}, abstractNote={Spence, Porchè L., Deanna L. Osmond, Wesley Childres, Joshua L. Heitman, and Wayne P. Robarge, 2012. Effects of Lawn Maintenance on Nutrient Losses Via Overland Flow During Natural Rainfall Events. Journal of the American Water Resources Association (JAWRA) 48(5): 909‐924. DOI: 10.1111/j.1752‐1688.2012.00658.x}, number={5}, journal={JAWRA Journal of the American Water Resources Association}, publisher={Wiley}, author={Spence, Porchè L. and Osmond, Deanna L. and Childres, Wesley and Heitman, Joshua L. and Robarge, Wayne P.}, year={2012}, month={May}, pages={909–924} }
 @article{bragg_childers_tompkins_tompkins_meeker_2002, title={Infection of the choroid plexus by feline immunodeficiency virus}, volume={8}, ISSN={["1355-0284"]}, DOI={10.1080/13550280290049688}, abstractNote={The human, simian, and feline immunodeficiency viruses rapidly penetrate into the brain and trigger an inflammatory process that can lead to significant neurologic disease. However, the mechanisms that permit efficient trafficking of macrophage-tropic and the more neurotoxic lymphocytotropic isolates are still poorly understood. One potential source of virus entry may be the blood-CSF barrier provided by the choroid plexus. Infected cells are often detected within the choroid plexus but it is unclear whether this reflects trafficking cells or infection of the large macrophage population within the choroidal stroma. To address this issue, we cultured fetal feline choroid plexus and evaluated the ability of feline immunodeficiency virus (FIV) to establish a primary infection. Significant provirus was detected in macrophage-enriche d choroid plexus cultures as well as in the choroid plexus of cats infected in vivo. FIV p24 antigen production in vitro was very low but detectable. Addition of a feline T-cell line to macrophages inoculated with FIV resulted in a dense clustering of the T cells over macrophages with dendritic cell-like morphologies and a robust productive infection. The direct infection of choroid plexus macrophages with FIV, the efficient transfer of the infection to T cells indicate that the choroid plexus can be a highly efficient site of viral infection and perhaps trafficking of both macrophage-tropic and T-cell-tropic viruses into the CNS.}, number={3}, journal={JOURNAL OF NEUROVIROLOGY}, author={Bragg, DC and Childers, TA and Tompkins, MB and Tompkins, WA and Meeker, RB}, year={2002}, month={Jun}, pages={211–224} }
 @article{gebhard_dow_childers_alvelo_tompkins_tompkins_1999, title={Progressive expansion of an L-selectin-negative CD8 cell with anti-feline immunodeficiency virus (FIV) suppressor function in the circulation of FIV-infected cats}, volume={180}, ISSN={["0022-1899"]}, DOI={10.1086/315089}, abstractNote={The acute stage of feline immunodeficiency virus (FIV) infection is characterized by the appearance of a major CD8 subpopulation with reduced expression of the CD8 beta chain (CD8alpha+betalo). CD8 antiviral activity was subsequently shown to be mediated by the CD8alpha+betalo phenotype, which is the dominant CD8 phenotype in long-term infected cats. Two- and three-color flow cytometric analysis demonstrated that the CD8alpha+betalo subset is L-selectin negative (CD62L-) and has increased expression of CD44, CD49d, and CD18, consistent with an activation phenotype. The CD8alpha+betaloCD62L- cells but not the CD8alpha+betahiCD62L+ cells demonstrated strong antiviral activity in the FIV acute-infection assay. The progressive expansion of the CD8alpha+betaloCD62L- effector subset cells in FIV-infected cats parallels that seen in human immunodeficiency virus (HIV)-infected patients, suggesting that failure in homeostatic mechanisms regulating lymphocyte activation or trafficking (or both) may be a consequence of both HIV and FIV infections.}, number={5}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Gebhard, DH and Dow, JL and Childers, TA and Alvelo, JI and Tompkins, MB and Tompkins, WAF}, year={1999}, month={Nov}, pages={1503–1513} }