46,817 research outputs found
Bio-dependent bed parameters as a proxy tool for sediment stability in mixed habitat intertidal areas
No full textThe stability of cohesive and non-cohesive sediments in a mixed intertidal habitat within the Ria Formosa tidal lagoon, Portugal, was examined during two field campaigns as part of the EU F-ECTS project. The cohesive strength meter Mk III was used to determine critical erosion shear stress (c) within a variety of different intertidal habitats and substrata, including Spartina maritima fields and Zostera noltii beds. The best predictor(s) for c were derived from a range of properties measured for the surface sediments (chlorophyll a, colloidal carbohydrate, water, organic content, % fraction <63 m, and seabed elevation). Pigment biomarkers were used to identify the dominant algal groups within the surface phytobenthic assemblage.Strong, seasonally dependent relationships were found between c and habitat type, chl a, colloidal carbohydrate and bed elevation. Typically, critical erosion thresholds decreased seawards, reflecting a change from biostabilisation by cyanobacteria in the upper intertidal areas, to biostabilisation by diatoms on the bare substrata of the channel edges. In the late summer/early autumn, cyanobacteria were the main sediment stabilisers, and colloidal carbohydrate was the best bio-dependent predictor of c across the entire field area. In the late winter/early spring, cyanobacterial activity was lower, and sediment stabilisation by Enteromorpha clathrata was important; the best predictor of c was bed elevation. The implications and use of proxies for sediment stability are discussed in terms of feedback and sedimentation processes operating across the intertidal area
Expression of Friend leukemia virus and spleen focus-forming virus-specific sequences in erythroid bursts and granulocyte-macrophage colonies from spleen and marrow of mice infected with Friend leukemia virus
No full textA large number of studies have been carried out to identify the Friend leukemia virus (FV) target cell(s). In FV-infected mice, the kinetics of "primitive" erythroid burst-forming units (P-BFU-E) is perturbed, and their proliferative rate is enhanced. These results indirectly suggest, but do not prove, that cycling P-BFU-E may serve as FV target. In vitro infection studies showed that normal erythroid colony forming units (CFU-E) and "mature" erythroid burst-forming units (M-BFU-E) are targets for FV, while the largely out-of-cycle normal P-BFU-E are not. In an attempt to shed light on these aspects, we have evaluated the expression of viral cytoplasmic RNA sequences in pools of colonies generated by P-BFU-E and granulocyte-macrophage colony forming units (CFU-GM) from spleen and marrow of polycythemic Friend virus (FVP)-infected mice, as measured by liquid hybridization with FVP- or spleen focus-forming polycythemic virus (SFFVp)-specific DNA probes. Moreover, similar assays were performed on RNAs derived from whole spleen or bone marrow from mice treated with FVP or the anemic strain of Friend virus (FVA). Control studies were performed on corresponding colonies and whole tissues from normal animals. FVP- and SFFVp-specific sequences are more abundant in RNA extracted from infected spleen as compared to marrow by a 10-fold factor. On the other hand, FVP and SFFVp-specific sequences are expressed at a comparable level in both P-BFU-E- and CFU-GM-derived colonies from spleen or marrow of FVP-treated mice. Since in vitro spread of FVP infection was excluded by control studies with addition in culture of antibody to the viral glycoprotein with a molecular weight of 70,000 (gp70) these results indicate that P-BFU-E and CFU-GM are infected in vivo by FVP
DNA fusion gene vaccination mobilizes effective anti-leukemic cytotoxic T lymphocytes from a tolerized repertoire
No full textThe majority of known human tumor-associated antigens derive from non-mutated self proteins. T cell tolerance, essential to prevent autoimmunity, must therefore be cautiously circumvented to generate cytotoxic T cell responses against these targets. Our strategy uses DNA fusion vaccines to activate high levels of peptide-specific CTL. Key foreign sequences from tetanus toxin activate tolerance-breaking CD4+ T cell help. Candidate MHC class Ibinding tumor peptide sequences are fused to the C terminus for optimal processing and presentation. To model performance against a leukemia-associated antigen in a tolerized setting, we constructed a fusion vaccine encoding an immunodominant CTL epitopederived from Friend murine leukemia virus gag protein (FMuLVgag) and vaccinated tolerant FMuLVgag-transgenic (gag-Tg) mice. Vaccination with the construct induced epitopespecificIFN-c-producing CD8+ T cells in normal and gag-Tg mice. The frequency and avidity of activated cells were reduced in gag-Tg mice, and no autoimmune injury resulted. However, these CD8+ T cells did exhibit gag-specific cytotoxicity in vitro and in vivo. Also, epitope-specific CTL killed FBL-3 leukemia cells expressing endogenous FMuLVgag antigen and protected against leukemia challenge in vivo. These results demonstrate a simple strategy to engage anti-microbial T cell help to activate epitope-specific polyclonal CD8+ T cell responses from a residual tolerized repertoire
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Dr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend (photograph)
No full textDr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend
Recommended from our members
Dr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend (photograph)
No full textDr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend
Recommended from our members
Dr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend (photograph)
No full textDr. and Mrs. Hector P. Garcia at wedding of a pharmacist friend
Expression of Friend leukemia virus and spleen focus-forming virus-specific sequences in erythroid bursts and granulocyte-macrophage colonies from spleen and marrow of mice infected with Friend leukemia virus.
No full textA large number of studies have been carried out to identify the Friend leukemia virus (FV) target cell(s). In FV-infected mice, the kinetics of "primitive" erythroid burst-forming units (P-BFU-E) is perturbed, and their proliferative rate is enhanced. These results indirectly suggest, but do not prove, that cycling P-BFU-E may serve as FV target. In vitro infection studies showed that normal erythroid colony forming units (CFU-E) and "mature" erythroid burst-forming units (M-BFU-E) are targets for FV, while the largely out-of-cycle normal P-BFU-E are not. In an attempt to shed light on these aspects, we have evaluated the expression of viral cytoplasmic RNA sequences in pools of colonies generated by P-BFU-E and granulocyte-macrophage colony forming units (CFU-GM) from spleen and marrow of polycythemic Friend virus (FVP)-infected mice, as measured by liquid hybridization with FVP- or spleen focus-forming polycythemic virus (SFFVp)-specific DNA probes. Moreover, similar assays were performed on RNAs derived from whole spleen or bone marrow from mice treated with FVP or the anemic strain of Friend virus (FVA). Control studies were performed on corresponding colonies and whole tissues from normal animals. FVP- and SFFVp-specific sequences are more abundant in RNA extracted from infected spleen as compared to marrow by a 10-fold factor. On the other hand, FVP and SFFVp-specific sequences are expressed at a comparable level in both P-BFU-E- and CFU-GM-derived colonies from spleen or marrow of FVP-treated mice. Since in vitro spread of FVP infection was excluded by control studies with addition in culture of antibody to the viral glycoprotein with a molecular weight of 70,000 (gp70) these results indicate that P-BFU-E and CFU-GM are infected in vivo by FVP
A 760-nW, 180-nm CMOS Fully-Analog Voice Activity Detection System for Domestic Environment
No full text- …
