294 research outputs found

    A contaminant transport model for wetlands accounting for distinct residence time bimodality

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    Vegetation plays a major role in controlling the fate of contaminants in natural and constructed wetlands. Estimating the efficiency of contaminant removal of a wetland requires separate knowledge of the residence time statistics in the main flow channels, where the flow velocity is relatively higher, and in the more densely vegetated zones, where the velocity is smaller and most of the biochemical transformations occur. A conceptual wetland characterized by a main flow channel (MFC) and lateral vegetated zones (LVZs) is modeled here using a two-dimensional depth-averaged hydrodynamic and advection\u2013dispersion model. The effect of vegetation is described as a flow resistance represented in the hydrodynamic model as a function of the stem density. Simulations are performed for a given flow discharge and for increasing values of the ratio between the vegetation density in the LVZs and in the MFC. Residence time distributions (RTDs) of a nonreactive tracer are derived from numerical simulations of the solute breakthrough curves (BTCs) resulting from a continuous concentration input. Results show that increasing vegetation densities produce an increasingly pronounced bimodality of the RTDs. At longer times, the RTDs decrease exponentially, with different timescales depending on the stem density ratio and other system parameters. The overall residence time distribution can be decomposed into a first component associated with the relatively fast transport in the MFC, and a second component associated with the slower transport in the LVZs. The weight of each temporal component is related to the exchange flux at the MFC-LVZ interface. A one-dimensional transport model is proposed that is capable to reproduce the RTDs predicted by the depth-averaged model, and the relationship between model and system parameters is investigated using a combination of direct and inverse modeling approaches

    label free fluorescence detection of kinase activity using a gold nanoparticle based indicator displacement assay

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    A straightforward fluorescence indicator-displacement assay (IDA) has been developed for the quantitative analysis of ATP→ADP conversion

    Enhanced B-cell differentiation and reduced proliferative capacity in chronic hepatitis C and chronic hepatitis B virus infections

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    BACKGROUND & AIMS: Chronic microial infections aare frequently associated with B-cell activation and polyclonal proliferation, potentially leading to autoimmunity and lymphoproliferative disorders. We assessed B-cell phenotype and function in chronic hepatitis B (HBV) and chronic hepatitis C (HCV) virus infection. METHODS: We studied 70 patients with chronic HCV infection, 34 with chronic HBV infection and 54 healthy controls, B-cell phenotype was assessed by flow cytometry using monoclonal antibodies specific for CD27, the CD69, CD71, and CD86 activation markers and the chemokine receptor CXCR3. Differentiation into immunoglobulin-producing cells (IPC) was analysed by ELISpot upon stimulation and with CD40 ligand+IL-10 as surrogate bystander T-cell help or CpG oligodeoxynucleotide+IL-2, as innate immunity signal. Proliferation was examined by cytometry using carboxyfluorescein diacetate succinimidyl ester (CFSE) after stimulation with CpG. RESULTS: A significantly higher proportion of B cells from both HCV-and HBV-infected patients expressed activation markers compared with controls and a positive correlation was found between CXCR3(+) B cells and HCV RNA values. Memory B cells from patients with chronic HCV and HBV infections showed enhanced differentiation into IPC compared with controls, although this was restricted to IgG and at a lower level in HCV-compared with HBV-infected patients. Moreover, patients' activated B cells displayed significantly lower proliferative ability compared to healthy donors despite low expression of the FcRL4 exhaustin marker. CONCLUSIONS: B-cell activation, but not exhaustion, is common in chronic viral hepatitis. However, enhanced B-cell differentiation and deficient proliferative capacity were not associated with commitment to terminal differentiation
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