An experimental system was constructed in order to measure the two distinct components of the effective diffusivity tensor in transversely isotropic, unconsolidated porous media. Measurements were made for porous media consisting of glass spheres, mica particles, and disks made from mylar sheets. Both the particle geometry and the void fraction of the porous media were determined experimentally, and theoretical calculations for the two components of the effective diffusivity tensor were carried out. The comparison between theory and experiment clearly indicates that the void fraction and particle geometry are insufficient to characterize the process of diffusion in anisotropic porous media. ~K Ave a b CA r y C De~ DyyDeft f h interfacial area between y-and r-phases for the macroscopic system, m 2 area of entrances and exits of the r-phase for the macroscopic system, m: interfacial area contained within the averaging volume, m 2 characteristic length of a particle, m average thickness of a particle, m concentration of species A, moles/m 3 reference concentration of species A, moles/m 3 intrinsic phase average concentration of species A, moles/m 3 ca-(CA) v, spatial deviation concentration of species A, moles/m 3 (CA)Y/Co, dimensionless concentration of species A binary molecular diffusion coefficient, m2/s effective diffusivity tensor, m2/s component of the effective diffusivity tensor associated with diffusion parallel to the bedding plane, m2/s component of the effective diffusivity tensor associated with diffusion perpendicular to the bedding plane, m2/s effective diffusivity for isotropic systems, m2/s vector field that maps V (CA) ~ on to ca, m depth of the mixing chamber, m "*Current address:

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Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88-and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.