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ABSTRACT The largest proportion of greenhouse gas (GHG) emissions in the Agriculture sector of the Brazilian national GHG inventory is derived from the large (>200 million head) herd of cattle. The greatest contribution to these emissions comes from the enteric methane from cattle, but the direct and indirect emissions of nitrous oxide (N2O) from cattle excreta and N fertilizer are responsible for approximately 9 % of all national anthropogenic GHG emissions. Ammonia (NH3) can be volatilized from N fertilizer and cattle excreta and deposited in sites remote from the source, constituting an indirect source of N2O. This study aimed to determine whether direct N2O emissions and NH3 volatilization from N-fertilized pastures were greater than those derived from a mixed grass-legume pasture without N fertilizer addition. Emissions of N2O and NH3 from excreta and N fertilizer from a Palisade grass (Urochloa brizantha cv. Marandu) monoculture fertilized with 2 × 60 kg N ha-1 yr-1 urea were compared to those from a mixed Palisade grass-forage peanut (Arachis pintoi) pasture. Dung and urine were collected from these cattle, and NH3 losses and N2O emissions from the excreta and from N fertilizer were monitored using static chamber techniques. Volatilization of NH3 and N2O emissions were found to be greater from urine than from dung. Ammonia losses from excreta and urea fertilizer were low, not exceeding 6.8, 1.1, and 4.7 % of the N applied as urine, dung, and fertilizer, respectively. The N2O emissions showed a tendency to be greater for the urine from the N-fertilized compared to the mixed grass-legume pasture, and the N2O emissions from the urine of the N-fertilized pasture ranged from 0.08 to 0.94 % of applied urine N. The N2O emission from the N fertilizer was at maximum 0.46 % of the applied N. The direct N2O emissions and the loss of NH3 by volatilization (indirect N2O emission) from the excreta of cattle grazing the mixed grass-legume pasture were similar to, or lower than, the grazed grass monoculture fertilized with 120 kg N ha-1 yr-1. As the mixed pasture received no N fertilizer and hence no GHG emission from its manufacture or application, introducing forage peanut to the Urochloa brizantha pastures shows potential to be responsible for lower GHG emissions than the N fertilized grass pasture.

E. Lahner [1] C. Grossi [1] P. Caruana [2] R. Negrini [3] G. Capurso [1] C. Bordi [2] G. Delle Fave [1] B. Annibale [1] [7/17] Does Positive Serology indicate [...]

C. Grossi [1] R. Negrini [2] E. Lahner [1] G. Capurso [1] P. Caruana [3] C. Bordi [3] G. Delle Fave [1] B. Annibale [1] [7/10] [*] Relationship between Atrophic [...]

This work considers the crystallisation mechanisms of the most common and aggressive salts that generate stress in porous building stones as a result of changing ambient conditions. These mechanisms include the salt crystallisation that result from decreasing relative humidity and changes in temperature and, in hydrated salts, the dissolution of the lower hydrated form and the subsequent precipitation of the hydrated salt. We propose a new methodology for thermodynamic calculations using PHREEQC that includes these crystallisation mechanisms. This approach permits the calculation of the equilibrium relative humidity and the parameterization of the critical relative humidity and crystallisation pressures for the dissolution-precipitation transitions. The influence of other salts on the effectives of salt crystallisation and chemical weathering is also assessed. We review the sodium and magnesium sulphate and sodium chloride systems, in both single and multicomponent solutions, and they are compared to the sodium carbonate and calcium carbonate systems. The variation of crystallisation pressure, the formation of new minerals and the chemical dissolution by the presence of other salts is also evaluated. Results for hydrated salt systems show that high crystallisation pressures are possible as lower hydrated salts dissolve and more hydrated salts precipitate. High stresses may be also produced by decreasing temperature, although it requires that porous materials are wet for long periods of time. The presence of other salts changes the temperature and relative humidity of salt transitions that generates stress rather than reducing the pressure of crystallisation, if any salt has previously precipitated. Several practical conclusions derive from proposed methodology and provide conservators and architects with information on the potential weathering activity of soluble salts. Furthermore, the model calculations might be coupled with projections of future climate to give as improved understanding of the likely changes in the frequency of phase transitions in salts within porous stone. [ABSTRACT FROM AUTHOR]

Abstract: 222Rn concentration time series at 10 m and at 100 m have been measured hourly for one year at the meteorological station, El Arenosillo, on the Spanish southwest coast. A 222Rn flux characterization was also done. A seasonal analysis of atmospheric 222Rn concentration was performed and results for each season present evidence associated with the origin of air masses reaching the El Arenosillo station. An increase in 222Rn concentration was observed when the wind came from Morocco, the Sierra Morena and the Guadalquivir valley areas. On the other hand, a net 222Rn concentration decrease was found when the wind came from the Atlantic Ocean and the South of Portugal. Low 222Rn flux of 4 Bq m−2 h−1 was measured. This result makes this station a useful site for studies related to remote 222Rn source contributions because of low local 222Rn background. The measured annual average concentration of 222Rn gas at the El Arenosillo station is 3.51 ± 0.05 Bq m−3 at 10 m and 2.61 ± 0.05 Bq m−3 at 100 m. [Copyright &y& Elsevier]

The anti-phospholipid syndrome (APS) is a systemic autoimmune disease characterized by an adaptive immune response against self phospholipid (PL)--binding proteins. Although APS is considered as an autoantibody-mediated disease, there is now evidence that anti-phospholipid antibodies (aPL) are necessary but not sufficient to trigger some of the clinical manifestations of the syndrome. For example, mediators of the innate immunity are recognized to be additional second hits able to induce the thrombotic events in the presence of aPL. Finally, environmental agents - in particular infectious ones - were reported to act as triggers for the production of autoantibodies cross-reacting with PL-binding proteins as well as inflammatory stimuli that potentiate the aPL thrombogenic effect. Altogether, these findings suggest a role for the innate immunity in APS pathogenesis. Toll-like receptors (TLR) are receptors that induce prompt inflammatory responses and mediate functional activation in immune effector cells. There is evidence that aPL, and in particular anti-β2 glycoprotein I (β2GPI) antibodies, may activate endothelial cells and monocytes through TLR-4-dependent signalling. Whether or not TLR may behave as surface receptors for β2GPI is still matter of research. Drugs or molecules able to interfere with TLR involvement may represent new therapeutic approaches for APS. [ABSTRACT FROM AUTHOR]

Two patients with classic rheumatoid arthritis developed severe neutropenia and increased numbers of large granular lymphocytes in the blood and bone marrow. These lymphocytes exhibited homogeneous surface membrane immunophenotypes of Leu5+, Leu11-, Leu4+, Leu3-, Leu2-, Leu7+ and Leu5+, Leu11+, Leu4+, Leu3-, Leu2+, Leu7-, respectively. In both patients, neutropenia was initially corrected with corticosteroid therapy; long-term improvement followed low-dose oral cyclophosphamide and methotrexate therapies. In these 2 patients and 12 previous patients with rheumatoid arthritis associated with expanded populations of immunophenotypically homogeneous large granular lymphocytes, neutropenia occurred in all 14, thrombocytopenia in 6, anemia in 7, and mild or moderate splenomegaly in 12. In contrast to Felty's syndrome, granular lymphocyte expansions in rheumatoid arthritis usually occur in older patients, may appear simultaneously with arthritis, and are usually associated with normal or elevated blood leukocyte counts. Mild hemocytopenias in these patients can often be managed with observation. Therapy with corticosteroids or immunosuppressive-cytotoxic drugs may be beneficial in more severe cases, but splenectomy is not recommended. [ABSTRACT FROM AUTHOR]

We have examinied the frequencies of Tγδ cells in blood, synovial fluids, and synovial membrances of patients with rheumatoid arthritis (RA) and in blood from age-matched controls. Immunocyto-chemical and immunohistochemical techniques were used with monoclonal antibodies BB3 and A13 to define a major and minor blood subset of Tγδ cells respectively. Together, these antibodies identify the majority (if not all) of the peripheral blood Tγδ cells [ABSTRACT FROM AUTHOR]

A minor population of T cells expresses a heterodimeric antigen receptor composed of γ and &delta chain (TcR-1). In blood from adults, two subsets pf Tγ&delta cells can be identified by the monoclonal antibodies (MoAb) BB3 and A13. Little is known about the distribution and markers of these subsets early in life. We have therefore examined both the frequencies of these cells in cord blood and their expression of the cytotoxicity-associated marker serine esterase (SE), using immunocytochemical techniques. Our data show lower percentages of TcR-1+ cells in the blood of newborns compared with that in adults. However, the ratio of the A13+/BB3+ cells was significantly higher in cord than in adult blood. Whereas virtually all the adult TcR-1+ cells in blood were SE-positive, only a small proportion of the cord blood cells carried this enzyme. This was restricted to the BB3+ Tγδ-cells subset in the cord. Our data suggest different characteristic of the TcR-1+ cells in blood from newborns compared with adult blood, and study of the functions of the different subsets, e.g. cytotoxicity, will be important in understanding their particular role in immunity. [ABSTRACT FROM AUTHOR]

Human peripheral blood large granular lymphocytes (LGL)--that is, cells with intracytoplasmic azurophilic (electron-dense) granules, with a positivity for the cytochemical localization of certain acid hydrolases, and with avid surface receptors for the Fc portion of IgG--have been purified on Percoll density gradients. Approximately 30% of these cells expressed receptors for the third complement component (C3R). They were separated into C3R-positive and C3R-negative cells. C3R+ cells had a significantly greater natural killer (NK) activity against K562 target cells than C3R+ cells. This difference was unrelated to the presence in the C3R+ cells of a contaminant cell type incapable of NK activity, since cytochemical and ultrastructural analysis revealed that C3R+ and C3R- fractions contained comparable LGL numbers. Agarose cytotoxicity assays at the single-cell level demonstrated that C3R+ LGL contained a large number of cells that bound to but did not lyse the target. The remaining fully cytotoxic C3R+ LGL had, however, the same killing and recycling properties as the cells from the C3R- fraction. Electron microscopy and cytochemical studies showed that C3R+ cells had fewer electron-dense granules than C3R- cells and stained more faintly for the localization of alpha-naphtyl acetate esterase. In contrast to C3R- cells, C3R+ LGL displayed morphological features suggesting that an active process of granule formation was taking place. Taken together, the data indicate that C3R+ cells represent a discrete subset or a maturational stage of LGL. [ABSTRACT FROM AUTHOR]

Chromatin fractions (DNA, histones and nonhistone chromosomal proteins NHCP) have been isolated from human peripheral B and T lymphocytes using different methods and analyzed in order to identify their lipid content. While DNA and histone fractions do not reveal the presence of lipids, a 2% of phospholipids is present in the NHCP fraction. The phospholipids associated with NHCP present a constant relative ratio among sphingomyelin, phosphatidyl-choline and phosphatidyl-ethanolamine both in B and T lymphocytes, whichever are the extraction procedures employed. These findings are related to the possible derepressive role of phospholipids on DNA-dependent RNA synthesis. [ABSTRACT FROM AUTHOR]

The CD44 cell surface proteoglycan participates in a variety of functions including lymphohematopoiesis, lymphocyte homing and tumor metastasis. In addition to the standard form (CD44st), a large family of variant isoforms (CD44v) is generated by alternative splicing of a single gene. Certain CD44v (v5 and V6) are upregulated in the course of neoplastic progression and reflect the metastatic potential of tumor cells. CD44 v6 is expressed in high-grade non-Hodgkin's lymphoma cells and is released in the serum, thus providing a soluble marker that reflects tumor burden, disease progression and treatment response. Here we show that serum CD44st is elevated in approximately half of B-CLL patients. In contrast, CD44v5 and v6 are detected at normal levels in the large majority of the cases. CD44st serum levels correlate significantly with the number of circulating leukemic B cells and with the levels of another soluble B-CLL marker, beta2-microglobulin. Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band (82 kDa) detected in B-CLL cell lysates. Elevated serum CD44st associates with a number of unfavorable prognostic factors such as high peripheral blood lymphocytosis, splenomegaly, advanced disease stage and therapy requirement. A follow-up study indicates that serum levels of CD44st are related to disease status, thus reinforcing our veiw that this molecule may represent a reliable tumor marker in B-CLL. [ABSTRACT FROM AUTHOR]

International standards for anti-beta2 glycoprotein I (anti-β2GPI) testing are needed. We evaluated the suitability of polyclonal/monoclonal candidate reference materials (RM) for the assay. IgG/IgM anti-β2GPI were affinity-purified (AP) from high-positive antiphospholipid syndrome sera and IgG from HCAL clone supernatant. Igs were tested for purity by SDS-PAGE, pooled, concentrated, sterile-filtered and the protein concentration determined. One unit was defined as the binding activity of 1 µg/ml of AP anti-β2GPI Ig. IgG/IgM RM were each assigned a unit value using the respective AP material as a calibrator. Polyclonal/monoclonal RM and 30 samples were evaluated for linearity, unit equivalency and commutability. Polyclonal AP material was assigned a value of 100 U IgG and 15 U IgM anti-β2GPI, respectively. IgG-RM had a value of 270 IgG and the IgM-RM of 220.3 IgM anti-β2GPI U. The linearity (R2) of each RM curve for the various assays ranged from 0.96 to 0.99. Commutability samples fit very well within 95% prediction intervals and had excellent correlation when comparing assays. IgG and IgM polyclonal and IgG monoclonal RM displayed excellent linearity and commutability, being good candidates for better standardization of anti-β2GPI immunoassays. [ABSTRACT FROM PUBLISHER]

Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombotic events and/or pregnancy morbidity in the persistent presence of antiphospholipid antibodies (aPL). aPL targeting β2 glycoprotein I (anti-β2GPI Abs) provide the main pathogenic autoantibody subset. In monocytes, platelets and endothelial cells (ECs), the interaction of circulating aPL with membrane-bound β2GPI results in cell activation, and EC perturbation provides an important player in clotting. Several receptors have been suggested to mediate β2GPI/EC binding. AnnexinA2 provides a high-affinity binding site for β2GPI but, since it does not span the cell membrane, an adaptor protein is required to trigger signal. Consistent evidence supports the role of Toll-like receptor (TLR) 4 as co-receptor for β2GPI on ECs. β2GPI was recently reported to behave as lipopolysaccharide (LPS) scavenger. In monocytes, TLR4 activation was shown to be apparent, due to LPS/β2GPI complexes. Conversely, our findings in ECs demonstrate that β2GPI interacts directly with TLR4, and that such interaction may contribute to β2GPI-dependent aPL-mediated EC activation. LPS enhanced anti-β2GPI Ab binding to EC only at cell-activating concentrations, able to up-regulate TLR4. This in vitro model may explain why LPS behaves as a second hit increasing the expression of β2GPI in vascular tissues and triggering aPL-mediated thrombosis in vivo. [ABSTRACT FROM PUBLISHER]