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The influence of source zone concentration reduction on solute plume detachment and recession times in fractured rock was investigated using new semianalytical solutions to transient solute transport in the presence of advection, dispersion, sorption, matrix diffusion, and first-order decay. Novel aspects of these solutions are: (1) the source zone concentration behavior is simulated using a constant concentration with the option for either an instantaneous reduction to zero concentration or an exponentially decaying source zone concentration initiated at some time (t*) after the source is introduced, and (2) different biodegradation rates in the fracture and rock matrix. These solutions were applied for sandstone bedrock and revealed that biodegradation in the matrix, not the fracture, may be the most significant attenuation mechanism and therefore may dictate remediation time scales. Also, instantaneous and complete source concentration reduction in aged plumes may not be beneficial with respect to plume response because back-diffusion can sustain plume migration for long periods of time. Moderate source zone concentration reduction has a similar impact on the rate of advance of the leading edge of the plume as aggressive concentration reduction. If the source zone concentration reduction half-life is less than the plume decay half-life, then volatile organic compound (VOC) mass sequestered in the rock matrix will ultimately dictate plume persistence and not the presence of the source zone.

Objective To investigate the role of CXCL13 in the development and pathogenesis of collagen-induced arthritis (CIA), and to determine the mechanisms involved in the modulation of arthritogenic response by CXCL13 neutralization. Methods Mice were immunized with type II collagen (CII) and treated with anti-CXCL13 or control antibodies during boosting. Mice were monitored for the development and severity of arthritis. The effects of CXCL13 neutralization on immune response to CII were evaluated by cytokine production by CII-specific T cells and CII-specific antibody production. Follicular response in the spleen and in synovial tissue was determined by in situ immunohistology. Results Mice receiving neutralizing antibodies to CXCL13 developed significantly less severe arthritis compared with mice injected with phosphate buffered saline or control antibodies. Follicular response both in the spleen and in synovial tissue was inhibited by anti-CXCL13 treatment. Injection with anti-CXCL13 antibodies did not significantly affect antigen-specific recall lymphocyte proliferation or type 1 cytokine production in vitro. Antibody response specific to CII was not inhibited by anti-CXCL13 treatment. However, anti-CXCL13 treatment induced significantly higher levels of interleukin-10 production after in vitro CII stimulation. Conclusion Neutralization of CXCL13 inhibits the development of CIA and reduces follicular response in both lymphoid and nonlymphoid tissues. These findings may have important implications regarding the pathogenesis and treatment of autoimmune arthritis.