Ambient particulate matter source apportionment using receptor modelling in European and Central Asia urban areas.

This work presents the results of a PM2.5 source apportionment study conducted in urban background sites from 16 European and Asian countries. For some Eastern Europe and Central Asia cities this was the first time that quantitative information on pollution source contributions to ambient particulate matter (PM) has been performed. More than 2200 filters were sampled and analyzed by X-Ray Fluorescence (XRF), Particle-Induced X-Ray Emission (PIXE), and Inductively Coupled Plasma Mass Spectrometry (ICP-MS) to measure the concentrations of chemical elements in fine particles. Samples were also analyzed for the contents of black carbon, elemental carbon, organic carbon, and water-soluble ions. The Positive Matrix Factorization receptor model (EPA PMF 5.0) was used to characterize similarities and heterogeneities in PM2.5 sources and respective contributions in the cities that the number of collected samples exceeded 75. At the end source apportionment was performed in 11 out of the 16 participating cities. Nine major sources were identified to have contributed to PM2.5: biomass burning, secondary sulfates, traffic, fuel oil combustion, industry, coal combustion, soil, salt and "other sources". From the averages of sources contributions, considering 11 cities 16% of PM2.5 was attributed to biomass burning, 15% to secondary sulfates, 13% to traffic, 12% to soil, 8.0% to fuel oil combustion, 5.5% to coal combustion, 1.9% to salt, 0.8% to industry emissions, 5.1% to "other sources" and 23% to unaccounted mass. Characteristic seasonal patterns were identified for each PM2.5 source. Biomass burning in all cities, coal combustion in Krakow/POL, and oil combustion in Belgrade/SRB and Banja Luka/BIH increased in Winter due to the impact of domestic heating, whereas in most cities secondary sulfates reached higher levels in Summer as a consequence of the enhanced photochemical activity. During high pollution days the largest sources of fine particles were biomass burning, traffic and secondary sulfates.

Sources and geographic origin of particulate matter in urban areas of the Danube macro-region: The cases of Zagreb (Croatia), Budapest (Hungary) and Sofia (Bulgaria).

The contribution of main PM pollution sources and their geographic origin in three urban sites of the Danube macro-region (Zagreb, Budapest and Sofia) were determined by combining receptor and Lagrangian models. The source contribution estimates were obtained with the Positive Matrix Factorization (PMF) receptor model and the results were further examined using local wind data and backward trajectories obtained with FLEXPART. Potential Source Contribution Function (PSCF) analysis was applied to identify the geographical source areas for the PM sources subject to long-range transport. Gas-to-particle transformation processes and primary emissions from biomass burning are the most important contributors to PM in the studied sites followed by re-suspension of soil (crustal material) and traffic. These four sources can be considered typical of the Danube macro-region because they were identified in all the studied locations. Long-range transport was observed of: a) sulphate-enriched aged aerosols, deriving from SO2 emissions in combustion processes in the Balkans and Eastern Europe and b) dust from the Saharan and Karakum deserts. The study highlights that PM pollution in the studied urban areas of the Danube macro-region is the result of both local sources and long-range transport from both EU and no-EU areas.

Adhesion molecules of syncytiotrophoblast microvillous membranes inhibit proliferation of human umbilical vein endothelial cells.

It has been shown previously that syncytiotrophoblast microvillous membranes (STBM), isolated from normal or pre-eclampsia placentae, specifically inhibit the proliferation of cultured human umbilical vein endothelial cells (HUVEC) and disrupt the cell monolayer without causing cell death. We have previously shown that this anti-proliferative activity resides in a self-aggregating complex in which eight proteins, namely integrins alpha(5)(CD49e) and alpha(V)(CD51), dipeptidyl peptidase IV (DPP IV, CD26), alpha-actinin, transferrin receptor (TfR, CD71), transferrin, placental alkaline phosphatase (PLAP) and monoamine oxidase A (MAO-A) were identified. In the present study, we investigated which of these components causes the anti-proliferative activity of STBM. Antibodies against integrin alpha(5)and alpha(V)and DPP IV all reduced the STBM-induced inhibition of proliferation of HUVEC, which was also reversed by added fibronectin. A preparation of PLAP inhibited endothelial proliferation, but this was not due to enzymatic activity. The preparation was shown to be impure with more than 12 bands present on Coomassie blue stained SDS-PAGE gels. These included integrins alpha(5)and alpha(V), which could account, at least in part, for the inhibitory activity. We could not exclude, however, the possibility of other unidentified factors being involved. We conclude that adhesion molecules account for a major part of the anti-proliferative activity of STBM; these appear to compete for ligands in the extracellular matrix or serum with the appropriate receptors on HUVEC.

Purification and characterization of a complex from placental syncytiotrophoblast microvillous membranes which inhibits the proliferation of human umbilical vein endothelial cells.

The signs of pre-eclampsia are thought to arise from maternal endothelial dysfunction caused by circulating factors of placental origin. Syncytiotrophoblast microvillous membranes (STBM) cause endothelial disruption and inhibit proliferation in vitro. Significantly increased amounts of STBM can be detected in blood from pre-eclamptic women and could contribute to endothelial dysfunction in vivo. This study purified a complex from STBM which inhibits the proliferation of cultured human endothelial cells. Integral membrane proteins were solubilized with sucrose monolaurate. Anion exchange chromatography yielded two peaks of anti-proliferative activity. Only the second peak was specific to STBM and was subjected to further separation by Sephacryl S-200 gel filtration chromatography (GFC). A single peak of specific activity eluted close to the void volume, at a position unaltered by added denaturing agents, guanidium chloride or urea. On Sephacryl S-300 GFC, two peaks were obtained of 410 and 820 kDa, with similar anti-proliferative activity and protein components (by SDS-polyacrylamide gel electrophoresis). The major protein bands were as integrins alpha5 and alpha v, dipeptidyl peptidase IV, alpha-actinin, transferrin, transferrin receptor, placental alkaline phosphatase and monoamine oxidase A.

Characterization of binding of human beta 2-glycoprotein I to cardiolipin.

beta 2-Glycoprotein I-cardiolipin complexes are reported to be a target antigen for the binding of a subset of anti-phospholipid antibodies. The characteristics of binding of beta 2-glycoprotein I to cardiolipin are reported in this paper. Binding at neutral pH is specific, saturable, dependent on ionic strength and independent of bivalent cation. Binding at low pH is qualitatively different from that at neutral pH, and is not dependent on ionic strength. Denaturation of beta 2-glycoprotein I by heat inactivation and reduction/alkylation indicates that beta 2-glycoprotein I-cardiolipin interaction does not require the native three-dimensional structure of beta 2-glycoprotein I, implying that a linear sequence motif may be responsible. Modification of amino acid residues by KCNO treatment completely destroys binding capacity, indicating crucial involvement of lysine residues in binding of beta 2-glycoprotein I to cardiolipin. Complement factor H, which has some similar highly charged linear sequence motifs to beta 2-glycoprotein I and is composed of the same type of protein module, was found to bind to cardiolipin and inhibit the binding of beta 2-glycoprotein I to cardiolipin. Three different lysine-rich segments of the fifth domain of beta 2-glycoprotein I may be involved in binding to cardiolipin.

Red-cell bound anti-A is more efficient than anti-B in competition for fluid phase complement.

Lysis of group A and B erythrocytes by human complement was studied by an anti-A (BRIC.131) and an anti-B (BRIC.30) IgM monoclonal antibody in a 51Cr-release assay. The relative concentration of membrane-bound immunoglobulins was detected by flow cytometric analysis, and the amount of C1q and C3 bound to the sensitized red cells was measured by using purified, 125I-labelled molecules. The direct haemolysis was identical with both reagents in the presence of excess and suboptimal complement over a wide range of antibody concentration (between 50 and 7000 ng/ml). The indirect effect of membrane-bound antibody, i.e. its influence on complement binding by sensitized bystander cells, was examined in a cold target competition assay in which sensitized, non-labelled cells are present when complement is incubated with sensitized labelled cells. We have found that the competitive capacity of sensitized erythrocytes correlated with the amount of membrane-bound immunoglobulins. In accordance with our earlier findings, an equal level of target and competitor cell lysis was obtained only if the fluid phase anti-B antibody concentration was 2 to 4 times higher than that of the anti-A antibodies. We demonstrate in this paper that the different competitive activity of IgM anti-A and anti-B monoclonal antibodies might be accounted for by differences in their C1q and C3 binding capacities.

Interactions in the complement-mediated lysis of blood group AB erythrocytes sensitized simultaneously with anti-A and anti-B monoclonal antibodies.

The lysis of group AB erythrocytes by human complement was studied by different anti-A and anti-B IgM monoclonal antibodies (mabs) in a 51Cr-release assay. The concentration of membrane-bound immunoglobulin was detected by ELISA, and the amount of C1q and C3 bound to sensitized red cells was measured by using purified, 125I-labelled molecules. We have demonstrated that there is an exponential relationship between the concentration of the sensitizing IgM mabs and C1q binding to the sensitized AB cell. The efficiency of binding was related to the number of antibodies bound; thus, anti-A sensitized cells bound 3-6 times more C1q than anti-B sensitized cells did. AB cells, on the other hand, bound similar amounts of C3 whether anti-A or anti-B was present. The lytic efficiencies of the various IgM mabs during short incubation times were different, suggesting that the complement activation rates vary widely with different antibodies on the AB cell membrane. The binding of C1q to an antibody-sensitized target activates a cascade, whose components may migrate away from the sensitizing antibody; interactions between the activation processes generated by the anti-A and anti-B antibodies may thus occur. Choosing appropriate pairs of anti-A and anti-B mabs for the simultaneous sensitization of AB cells has indeed resulted in stimulation in some and inhibition in other combinations of mabs. It is suggested that stimulation is observed when the activated intermediates are produced in excess, whereas inhibition occurs when a shortage of activated intermediates prevents mutual utilization.

Antioxidant properties of di- and polyamines.

1. One diamine, putrescine and two polyamines, spermidine and spermine (PAs) of different concentrations, were processed through antioxidant systems in order to study their antioxidant effects. The systems investigated were as follows. 2. "Oxidative stress" was induced in RBCs to investigate filtration parameters, the effect of reduced glutathione (GSH) and the change in lipid peroxidation (LP) superoxide dismutase (SOD) activities. 3. Initiated LP-decreasing characteristics of the substances were studied in pig brain homogenate. 4. The LP-decreasing effect of these PAs were studied in guinea-pig heart tissue homogenate perfused with Tyrode solution, stimulated, and then perfused by the Langendorff method. 5. In all three tests, the antioxidant characteristics of PAs were unambiguously proved.

Activity, disulphide mapping and structural modelling of the fifth domain of human beta 2-glycoprotein I.

Complexes formed by the interaction of negatively charged phospholipids and beta 2-glycoprotein I (beta 2-I) are the target of autoantibodies in systemic lupus erythematosus. The highly positively charged fifth (C-terminal) domain of human beta 2-I was produced as a fusion protein in an Escherichia coli expression system and was shown to bind to the negatively charged phospholipid, cardiolipin, almost as well as the intact protein. In an attempt to define the 3D structure of this domain, the disulphide linkage pattern was determined and shown to be Cys 1-4, Cys 2-5 and Cys 3-6 in contradiction to an earlier report. In the light of this information, the sequence of the fifth domain of beta 2 I (beta 2-I-5) is readily aligned with that of the 16th repeat of factor H, of which the 3D structure is known, and a model of beta 2I-5 has been built by homology. On the basis of the model we suggest residues that might be the target of profitable site-directed mutagenesis in structure-function studies.

Cytochemical effect of a stable PGI2 analog iloprost on guinea-pig heart in calcium-free and calcium paradox conditions.

Morphological and cytochemical effects of stable prostacyclin analog, iloprost were studied on isolated and perfused guinea-pig hearts according to Langendorff in Ca-free and Ca paradox conditions. Samples from the papillary muscles and left ventricular wall-muscles were examined. For calcium cytochemistry lead acetate and potassium pyroantimonate, and for nickel cytochemistry dimethylglyoxime (DMG) techniques were used. Electron microscopic studies showed that during Ca-free perfusion (for 15 min) and the following Ca repletion (for 15 min) disruption of the sarcolemma, damages in the sarcotubular system and in the mitochondria and gradual separation of intercalated discs were observed. Treatment with iloprost (1 microM) prevented those alterations in Ca-free and Ca paradox conditions. Iloprost caused a change in the intracellular distribution of Ca2+, decreased the cytochemically-demonstrated calcium in the cytoplasma, and inhibited the formation of calcium phosphate granules in mitochondria. Iloprost did not modify the number of nickel-DMG complexes either in Ca-free or in Ca paradox conditions. This study indicates that iloprost prevents the morphological damages caused by Ca paradox. The study also suggests that iloprost has an effect on the intracellular handling of calcium.