In order to use urinary EMV for routine SAR131675 VEGFR/PDGFR inhibitor clinical diagnostics, a new method is needed. Recently, we developed a unique 96-well filterplate in order to isolate EMV from human plasma samples for mRNA analysis. Although we were able to detect EMV mRNA in human urine using the same system, it was necessary to process 5–12 mL urine to obtain sufficient sensitivity. A standard 96-well filterplate format is useful for high-throughput assays, but not convenient to process samples with.1 mL sample volumes. On the other hands, a standard centrifuge filter tube format is useful to process large volumes of samples, but not suitable for high-throughput assays. In this study, we developed a unique EMV mRNA quantification method from 10 mL urine samples in a high throughput format, and quantified kidney-specific mRNAs. Analytical validation has been completed, and the system is ready for clinical research, biomarker screening, and the development of molecular diagnostics. Obliterative bronchiolitis is a significant problem in lung transplant and BMT recipients. OB is directly or indirectly responsible for almost 40% of lung transplant related deaths. This is mainly due to chronic allograft dysfunction, manifesting as OB, characterized histologically by inflammation and fibrosis of small airways. In BMT recipients, the incidence of OB has been reported to be as high as 29% with increased risk of mortality and is associated with chronic graft-versus-host disease. After transplant, the host immune system is activated by exposure to allogeneic tissue antigens, resulting in an inflammatory cascade with alloimmune and non-alloimmune dependent factors contributing to the response. The cumulative end result of this cascade is OB. Current management strategies involving immunosuppressive medications have not been very successful. Lack of suitable animal models has limited efforts to understand and develop therapeutic strategies for OB. We have previously reported a new murine BMT model, in which chronic GVHD leads to OB similar to the chronic rejection seen in lung transplantation. MSCs provide a promising management option for this population. They have immunomodulatory properties, among which is their ability to suppress T-lymphocyte activation and proliferation, key events in allograft rejection. MSCs have been shown to inhibit maturation of dendritic cells and promote secretion of anti-inflammatory cytokines, resulting in generation of Tregs. Tregs can suppress effector FoxP3negative cells and antigen presenting cells thereby inhibiting inflammatory responses. MSCs and MSC-induced Tregs are capable of generating alternatively activated macrophages, which are immunosuppressive and inhibit the proliferation of activated CD4+ T cells. MSCs have been used successfully to prolong allograft survival in other animal models of organ transplantation. Donor human lungs infused with MSCs have improved alveolar fluid clearance compared to the current state of the art technique. In the context of BMT, MSCs have shown efficacy in ameliorating graft-versus-host-disease and have been approved for steroid-refractory acute GVHD. They have been used safely as a co-infusion in patients undergoing unrelated allogeneic bone marrow transplant. MSCs have not been previously evaluated as a cell therapy for OB post-BMT although they have been studied many times in other lung injury models where they are given as either a pretreatment or concomitantly with injury induction. In the clinical experience of MSCs for HSCT, the MSCs have been third party. They are considered to be relatively immunoprivileged and their allogenicity has not been an issue in several studies.