Tratamiento de agua residual con elevado contenido de nitratos utilizando reactores biomembrana aireados

[ES] Se describe la eliminación conjunta de carbono y nitrógeno de un agua residual, llevada a cabo en reactores biomembrana de laboratorio. El agua residual sintética tuvo una composición similar a la que resultaría de la mezcla, en determinadas proporciones, de agua residual urbana con agua de acuífero rica en nitratos. Se utilizaron dos reactores en paralelo, con igual superficie de soporte pero distinto volumen. Aunque se insufló aire a la biopelícula a través del soporte, el seno del agua permaneció anóxico. La eliminación de nitratos resultó ser una función de la carga orgánica aplicada, estando en un rango de 4 a 6 g N-NO3 elim./(m2•d) para carga aplicada de 120 g DQO/(m2•d), y de 8 a 10 g N-NO3 elim./(m2•d) para carga aplicada de 240 g DQO/(m2•d). La carga orgánica eliminada fue de 87 a 180 g DQO/(m2•d). Se observó que el incremento de nitratos en el agua problema no produjo una mayor desnitrificación, sino una producción y acumulación de nitritos en el reactor. Una sola etapa no permite el máximo aprovechamiento de materia orgánica para desnitrificación, lo cual se podría obtener utilizando dos etapas en serie: una de desnitrificación (para los nitratos del afluente aportados por el agua de acuífero), y la otra de nitrificación-desnitrificación simultáneas (para eliminar el nitrógeno amoniacal afluente aportado por el agua residual urbana). Así, la materia orgánica sería eliminada parcialmente en cada etapa.Lolmede, P.; Jácome, A.; Vidart, T.; Tejero Monzón, I. (2000). Tratamiento de agua residual con elevado contenido de nitratos utilizando reactores biomembrana aireados. Ingeniería del Agua. 7(3):243-254. https://doi.org/10.4995/ia.2000.284724325473Abdel-Warith A.S., Williamson K.J., Strand S.E. (1990). Substratum aerated biofilm reactor. Proceedings of the Environmental Engineering 1990 Specialty Conference (ASCE), Airlington, Virginia on July 8-11. pp. 360-365.Amieva J.J. (1987). 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Membrane vesicles containing matrix metalloproteinase-9 and fibroblast growth factor-2 are released into the extracellular space from mouse mesoangioblast Sstem cells

Certain proteins, including fibroblast growth factor-2 (FGF-2) and matrix metalloproteinase-9 (MMP-9), have proved very effective in increasing the efficacy of mesoangioblast stem cell therapy in repairing damaged tissue. We provide the first evidence that mouse mesoangioblast stem cells release FGF-2 and MMP-9 in their active form through the production of membrane vesicles. These vesicles are produced and turned over continuously, but are stable for some time in the extracellular milieu. Mesoangioblasts shed membrane vesicles even under oxygen tensions that are lower than those typically used for cell culture and more like those of mouse tissues. These findings suggest that mesoangioblasts may themselves secrete paracrine signals and factors that make damaged tissues more amenable to cell therapy through the release of membrane vesicles

Eccentric Exercise Facilitates Mesenchymal Stem Cell Appearance in Skeletal Muscle

Eccentric, or lengthening, contractions result in injury and subsequently stimulate the activation and proliferation of satellite stem cells which are important for skeletal muscle regeneration. The discovery of alternative myogenic progenitors in skeletal muscle raises the question as to whether stem cells other than satellite cells accumulate in muscle in response to exercise and contribute to post-exercise repair and/or growth. In this study, stem cell antigen-1 (Sca-1) positive, non-hematopoetic (CD45-) cells were evaluated in wild type (WT) and α7 integrin transgenic (α7Tg) mouse muscle, which is resistant to injury yet liable to strain, 24 hr following a single bout of eccentric exercise. Sca-1+CD45− stem cells were increased 2-fold in WT muscle post-exercise. The α7 integrin regulated the presence of Sca-1+ cells, with expansion occurring in α7Tg muscle and minimal cells present in muscle lacking the α7 integrin. Sca-1+CD45− cells isolated from α7Tg muscle following exercise were characterized as mesenchymal-like stem cells (mMSCs), predominantly pericytes. In vitro multiaxial strain upregulated mMSC stem cells markers in the presence of laminin, but not gelatin, identifying a potential mechanistic basis for the accumulation of these cells in muscle following exercise. Transplantation of DiI-labeled mMSCs into WT muscle increased Pax7+ cells and facilitated formation of eMHC+DiI− fibers. This study provides the first demonstration that mMSCs rapidly appear in skeletal muscle in an α7 integrin dependent manner post-exercise, revealing an early event that may be necessary for effective repair and/or growth following exercise. The results from this study also support a role for the α7 integrin and/or mMSCs in molecular- and cellular-based therapeutic strategies that can effectively combat disuse muscle atrophy

Macrophage-dependent nitric oxide expression regulates tumor cell detachment and metastasis after IL-2/anti-CD40 immunotherapy

Immunotherapy with IL-2 and anti-CD40 induces the expression of NOS2 in tumor-associated macrophages, and its expression is required for the inhibition of tumor metastasis

Autoimmunity to HSP60 during diet induced obesity in mice

Adaptive immunity has been implicated in adipose tissue inflammation, obesity and its adverse metabolic consequences. No obesity-related autoantigen has yet been identified, although heat shock protein 60 (HSP60) has been implicated in other autoimmune diseases. We investigated whether feeding a high-fat diet to C57BL/6J mice would cause autoimmunity to HSP60 and whether immunomodulation with peptides from HSP60 would reverse the resulting obesity or metabolic dysfunction. Obese mice had higher circulating levels of HSP60 associated with increased T-lymphocyte proliferation responses and the emergence of circulating IgG1 and IgG2c antibody levels against HSP60. Treatment with escalating doses of a mixture of three proven immunomodulatory HSP60 peptides did not reduce weight but completely reversed the increase in VLDL/LDL levels and partially reversed the glucose intolerance in obese mice. Obese mice mount an autoimmune response to HSP60, which partly underlies the resulting metabolic disturbances

Septicaemia models using Streptococcus pneumoniae and Listeria monocytogenes: understanding the role of complement properdin

Streptococcus pneumoniae and Listeria monocytogenes, pathogens which can cause severe infectious disease in human, were used to infect properdin-deficient and wildtype mice. The aim was to deduce a role for properdin, positive regulator of the alternative pathway of complement activation, by comparing and contrasting the immune response of the two genotypes in vivo. We show that properdin-deficient and wildtype mice mounted antipneumococcal serotype-specific IgM antibodies, which were protective. Properdin-deficient mice, however, had increased survival in the model of streptococcal pneumonia and sepsis. Low activity of the classical pathway of complement and modulation of FcγR2b expression appear to be pathogenically involved. In listeriosis, however, properdin-deficient mice had reduced survival and a dendritic cell population that was impaired in maturation and activity. In vitro analyses of splenocytes and bone marrow-derived myeloid cells support the view that the opposing outcomes of properdin-deficient and wildtype mice in these two infection models is likely to be due to a skewing of macrophage activity to an M2 phenotype in the properdin-deficient mice. The phenotypes observed thus appear to reflect the extent to which M2- or M1-polarised macrophages are involved in the immune responses to S. pneumoniae and L. monocytogenes. We conclude that properdin controls the strength of immune responses by affecting humoral as well as cellular phenotypes during acute bacterial infection and ensuing inflammation