437 research outputs found
Re-evaluation of thin layer chromatography as an alternative method for the quantification of prostaglandins from rat Kupffer cells
No full textIn contrast to conventionally used inummoassays, thin layer chromatography (TLC)-by prelabeling of cells with radioactive arachidonic acid (AA)-allows to differentiate between cellularly built and added prostanoids and thus to investigate feedback effects of prostanoids on their own release. PGD(2), TXB2 and PGE(2) released from zymosan-stimulated Kupffer cells were separated with distinct R-F-values, corresponding to those of the pure substances. Quantification of PGD(2) and PGE(2) gave comparable results with TLC and immunoassays, but measurement in the presence of added prostanoids was only possible with TLC. Moreover TLC was superior to immunoassays in having a longer linear range while being comparably sensitive. Cellularly built TXB2 in its radioactively labeled form was not detectable by TLC. Inhibition of TXB2 release by externally added AA or technical artifacts were excluded, suggesting that the cellular AA-pools used for prostaglandin and thromboxane synthesis differ in their accessibility for added AA. Thus, TLC is a simple, sensitive and precise method for the quantification of cellularly built prostaglandins but not of thromboxane even in the presence of added prostanoids. (c) 2004 Elsevier Inc. All rights reserved
Inhibition of prostaglandin D-2 clearance in rat hepatocytes by the thromboxane receptor antagonists daltroban and ifetroban and the thromboxane synthase inhibitor furegrelate
No full textProstanoids, i.e. prostaglandins and thromboxane, regulate liver-specific functions both in homeostasis and during defense reactions. For example, prostanoids are released from Kupffer cells, the resident liver macrophages, in response to the inflammatory mediator anaphylatoxin C5a, and mediate an enhanced glucose output from hepatocytes as energy supply. In perfused rat livers, the thromboxane receptor antagonist daltroban enhanced C5a-induced prostanoid overflow and reduced glucose output. It was the aim of this study to elucidate whether daltroban interfered with prostanoid release from Kupffer cells or prostanoid clearance by hepatocytes, and/or whether it directly influenced prostanoid-dependent glucose metabolism in these cells. In perfused rat livers, daltroban enhanced prostaglandin (PG)D, overflow not only after infusion of C5a (15-fold), but also after PGD(2) (10-fold). Neither daltroban nor another receptor antagonist, ifetroban, or the thromboxane synthase inhibitor furegrelate enhanced prostanoid release from Kupffer cells. In contrast, all inhibitors reduced clearance, i.e. uptake and degradation, of PGD2 by hepatocytes: within 5 min uptake of 1 nmol/L PGD(2) was reduced from 43 +/- 5 fmol (controls) to 22 +/- 6 fmol (daltroban), 24 +/- 6 fmol (ifetroban) and 21 +/- 6 fmol (furegrelate). PGD(2) in the medium was reduced to 39 +/- 7% in the controls, but remained at 93 +/- 9%, 93 +/- 11% and 60 +/- 3% in the presence of the inhibitors. PGD(2)-dependent glucose output in the perfused liver or activation of glycogen phosphorylase in isolated hepatocytes remained unaffected by daltroban. These data clearly demonstrate that the thromboxane-inhibitors reduced PGD(2) clearance by hepatocytes, presumably by inhibition of prostanoid transport into the cells. In contrast, they did not interfere with PGD(2)-dependent glucose metabolism, suggesting an independent mechanism for the inhibition of glucose output from the liver. (C) 2003 Elsevier Inc. All rights reserved
Inhibition by prostaglandin E-2 of anaphylatoxin C5a - but not zymosan-induced prostanoid release from rat Kupffer cells
No full textThe proinflammatory anaphylatoxin C5a induces the release of prostanoids, le, prostaglandins (PG) and thromboxane (TX), from the resident liver macrophages (Kupffer cells [KC]). Because KC themselves express prostanoid receptors, prostanoids-besides having paracrine functions-might regulate their own release in an autocrine loop. So far, such a possible feedback regulation has not been investigated systematically, probably because of methodological difficulties to measure newly synthesized prostanoids in the presence of added prostanoids. Here, after prelabeling of phospholipids with [C-14]arachidonate, cellularly formed [C-14] prostanoids were determined in the presence of added unlabelled prostanoids by thin layer chromatography. In cultured KC, recombinant rat C5a (rrC5a) rapidly increased PGD(2), PGE(2), and TXA(2) release, which was strongly reduced by PGE(2), but neither by PGD(2) nor by the TXA(2) analog U46619. The inhibitory effect of PGE(2) was mimicked by cAMP, indicating that the G(s)-coupled PGE(2) receptors type 2 or 4 were involved. Zymosan also enhanced prostanoid release from KC, but with slightly slower kinetics; this action was neither inhibited by PGE2 nor by cAMP. Also in perfused rat livers, rrC5a enhanced prostanoid release from KC as shown by prostanoid overflow and thereby indirectly increased glucose output from hepatocytes. Again, PGE(2), but not PGD(2), inhibited rrC5a-elicited prostanoid overflow. This resulted in a complete inhibition of rrC5a-incluced, prostanoid-mediated glucose output. Thus, PGE2 can inhibit specifically the C5a-induced prostanoid release from KC via a feedback mechanism and thereby limit prostanoid-mediated hepatocellular defense reactions, eg, glucose release
Inhibition by prostaglandin E-2 of anaphylatoxin C5a - but not zymosan-induced prostanoid release from rat Kupffer cells
No full textThe proinflammatory anaphylatoxin C5a induces the release of prostanoids, le, prostaglandins (PG) and thromboxane (TX), from the resident liver macrophages (Kupffer cells [KC]). Because KC themselves express prostanoid receptors, prostanoids-besides having paracrine functions-might regulate their own release in an autocrine loop. So far, such a possible feedback regulation has not been investigated systematically, probably because of methodological difficulties to measure newly synthesized prostanoids in the presence of added prostanoids. Here, after prelabeling of phospholipids with [C-14]arachidonate, cellularly formed [C-14] prostanoids were determined in the presence of added unlabelled prostanoids by thin layer chromatography. In cultured KC, recombinant rat C5a (rrC5a) rapidly increased PGD(2), PGE(2), and TXA(2) release, which was strongly reduced by PGE(2), but neither by PGD(2) nor by the TXA(2) analog U46619. The inhibitory effect of PGE(2) was mimicked by cAMP, indicating that the G(s)-coupled PGE(2) receptors type 2 or 4 were involved. Zymosan also enhanced prostanoid release from KC, but with slightly slower kinetics; this action was neither inhibited by PGE2 nor by cAMP. Also in perfused rat livers, rrC5a enhanced prostanoid release from KC as shown by prostanoid overflow and thereby indirectly increased glucose output from hepatocytes. Again, PGE(2), but not PGD(2), inhibited rrC5a-elicited prostanoid overflow. This resulted in a complete inhibition of rrC5a-incluced, prostanoid-mediated glucose output. Thus, PGE2 can inhibit specifically the C5a-induced prostanoid release from KC via a feedback mechanism and thereby limit prostanoid-mediated hepatocellular defense reactions, eg, glucose release
Determinação da relação entre o carbono e o nitrogênio ideal para inibição da produção de sulfeto em um consórcio microbiano enriquecido a partir de água de produção de um reservatório de óleo offshore
No full textDissertação (mestrado) - Universidade Federal de Santa Catarina, Centro Tecnológico, Programa de Pós-Graduação em Engenharia Química, Florianópolis, 2015.Um dos maiores problemas nos poços maduros de petróleo é a presença de acidez biogênica (souring), gerada principalmente pela produção biológica de sulfeto na recuperação secundária do petróleo em plataformas offshore. Uma das estratégias para o controle do souring em reservatórios consiste na injeção de nitrato, o qual é utilizado preferencialmente como aceptor de elétron, limitando desta forma a produção de sulfeto. O objetivo do presente estudo foi investigar a relação entre o carbono e o nitrogênio (Relação C:N) necessária para inibição da produção de sulfeto num consórcio microbiano enriquecido a partir de água de produção de um reservatório de óleo offshore. Foi realizado primeiramente um ensaio em batelada com acetato e propionato (ácidos graxos de fácil degradação) para avaliar o melhor doador de elétrons utilizado pelas bactérias redutoras de sulfato (BRS) para produção de sulfeto. A partir do ensaio concluiu-se que o consórcio de bactérias utiliza propionato para produzir acetato e CO2, Com isso, para subseqüentes ensaios, foi utilizado propionato como aceptor de elétrons. Dois ensaios mais foram feitos, a fim, de avaliar a relação C:N inibitória da produção de sulfeto: o primeiro, mudando a concentração de carbono e a concentração de nitrogênio; o segundo, mantendo a concentração de carbono constante e variando a concentração de nitrogênio. No primeiro, evidenciou-se que, nas condições onde a concentração de nitrogênio, expressada em nitrato (N-NO3?), foi superior à concentração de carbono orgânico, expressada em propionato ( ). A produção de sulfeto ficou inibida, possivelmente, pela indisponibilidade de carbono, ou então pelo favorecimento de processos de desnitrificação autotrófica, que resultariam na remoção de algum sulfeto formado. Já, nas condições onde a concentração de nitrato foi inferior à de carbono orgânico houve formação de sulfeto, a partir do ponto de término do nitrito, não havendo uma influência da concentração residual de matéria orgânica no sistema. Os resultados da segunda série de ensaios foi concordante com a primeira, evidenciando que a relação C:N propriamente dita não é um fator que resulte em inibição ou estimulação das BRS num ponto especifico de injeção, mas sim, a presença ou ausência de nitrato ou nitrito, de forma independente da concentração de matéria orgânica. Um ensaio adicional foi realizado para determinação da presença ativa de bactérias autotróficas redutoras de nitrato e oxidadoras de sulfeto (BRN-OS); os resultados mostram presença ativa de BRN-OS.Abstract : A major problem in oil wells is the presence of biogenic acid (Souring) generated mainly by the production of sulfide in secondary recovery of oil at offshore platforms. The control of souring in reservoirs can be done through nitrate injection, which is preferably used as the electron acceptor, limiting the production of sulphide. The objective of this study was to investigate the carbon-nitrogen ratio required (C:N) for inhibition of sulfide production in an enriched microbial consortia coming from a production water from an offshore oil reservoir. It was first performed a batch assay with acetate and propionate (easily degradable fatty acids) to evaluate the best electron donor used by sulphate reducing bacteria (SBR) to produce sulfide. It was concluded from this assay that the bacteria consortia has a greater affinity to propionate. Two more assays were made with the objective to evaluate the C:N ratio that inhibit sulfide production: the first, it was maintained constant carbon concentration and varying nitrogen concentration; the second, it was maintained nitrogen concentration constant and varying carbon concentration. The first assay showed that, under the conditions where the concentration of nitrate expressed as nitrogen (N- NO3?) was greater than the concentration of organic carbon ( ), sulfide production was possibly inhibited by the lack of organic matter, or it was favored by autotrophic denitrification processes, that contributes to remove of some sulfide formed. When nitrate concentration was lower than organic carbon, sulfide was formed immediately after nitrogen species were totally consumed. There was no influence of residual concentration of organic matter in the system. The second assay results corroborate with the previous one, indicating that the C:N ratio is not a factor that results in SBR inhibition or stimulation, but, what matter is the nitrate, or nitrite, presence or absence, independently of the organic matter concentration. An additional test was performed to determine the presence active of sulfide-oxidizing, nitrate reducing bacteria (NBR - OS)
Search for B0(S) - anti-B0(S) oscillations in DELPHI using high-P(T) leptons.
No full textOscillations in the B-s(0)- [(B-s(0))over bar] system were studied in events selected from about 4.3 million hadronic Z(0) decays registered by DELPHI between 1992 and 2000. This paper presents updates of two published analyses ([11, 12]). The first analysis, which utilizes leptons emitted with large momentum transverse to a jet, was improved by means of a better algorithm for the vertex reconstuction and a new algorithm for flavour-tagging at production time. The second analysis, which utilizes D-s-lepton events, was improved by optimizing the treatment of proper time resolution. No signal of B-s(0) oscillations was observed and limits on the mass difference between the physical B-s(0) states were obtained to be: Deltam(s) gt 8.0 ps-1 at the 95% C.L. with a sensitivity of Deltam(s)= 9.1 ps(-1) in the high p(t) lepton analysis and Deltam(s) gt 4.9 ps(-1) at the 95% C.L. with a sensitivity of Deltam(s)=8.6 ps(-1) in the D-s-lepton analysis. Previously published results on these analyses are superseded. The combination of these results with those obtained in other independent analyses previously performed in DELPHI (D-s- hadron, exclusive B-s(0), inclusive vertex) gives: Deltam(s) gt 8.5 ps(-1) at the 95% C.L. with a sensitivity of Deltam(s)=12.0 ps(-1
Measurement of the mass and width of the W boson in e+e- collisions at s√= 161–209 GeV
No full textAbdallah, J., Abreu, P., Adam, W., Adzic, P., Albrecht, T., Alemany-Fernandez, R., Allmendinger, T., Allport, P.P., Amaldi, U., Amapane, N., Amato, S., Anashkin, E., Andreazza, A., Andringa, S., Anjos, N., Antilogus, P., Apel, W.-D., Arnoud, Y., Ask, S., Asman, B., Augustin, J.E., Augustinus, A., Baillon, P., Ballestrero, A., Bambade, P., Barbier, R., Bardin, D., Barker, G.J., Baroncelli, A., Battaglia, M., Baubillier, M., Becks, K.-H., Begalli, M., Behrmann, A., Ben-Haim, E., Benekos, N., Benvenuti, A., Berat, C., Berggren, M., Bertrand, D., Besancon, M., Besson, N., Bloch, D., Blom, M., Bluj, M., Bonesini, M., Boonekamp, M., Booth, P.S.L., Borisov, G., Botner, O., Bouquet, B., Bowcock, T.J.V., Boyko, I., Bracko, M., Brenner, R., Brodet, E., Bruckman, P., Brunet, J.M., Buschbeck, B., Buschmann, P., Calvi, M., Camporesi, T., Canale, V., Carena, F., Castro, N., Cavallo, F., Chapkin, M., Charpentier, Ph., Checchia, P., Chierici, R., Chliapnikov, P., Chudoba, J., Chung, S.U., Cieslik, K., Collins, P., Contri, R., Cosme, G., Cossutti, F., Costa, M.J., Crennell, D., Cuevas, J., D'Hondt, J., Da Silva, T., Da Silva, W., Della Ricca, G., De Angelis, A., De Boer, W., De Clercq, C., De Lotto, B., De Maria, N., De Min, A., De Paula, L., Di Ciaccio, L., Di Simone, A., Doroba, K., Drees, J., Duperrin, A., Eigen, G., Ekelof, T., Ellert, M., Elsing, M., Espirito Santo, M.C., Fanourakis, G., Fassouliotis, D., Feindt, M., Fernandez, J., Ferrer, A., Ferro, F., Flagmeyer, U., Foeth, H., Fokitis, E., Fulda-Quenzer, F., Fuster, J., Gandelman, M., Garcia, C., Gavillet, Ph., Gazis, E., Gokieli, R., Golob, B., Gomez-Ceballos, G., Goncalves, P., Graziani, E., Grosdidier, G., Grzelak, K., Guy, J., Haag, C., Hallgren, A., Hamacher, K., Hamilton, K., Haug, S., Hauler, F., Hedberg, V., Hennecke, M., Hoffman, J., Holmgren, S.-O., Holt, P.J., Houlden, M.A., Jackson, J.N., Jarlskog, G., Jarry, P., Jeans, D., Johansson, E.K., Jonsson, P., Joram, C., Jungermann, L., Kapusta, F., Katsanevas, S., Katsoufis, E., Kernel, G., Kersevan, B.P., Kerzel, U., King, B.T., Kjaer, N.J., Kluit, P., Kokkinias, P., Kourkoumelis, C., Kouznetsov, O., Krumstein, Z., Kucharczyk, M., Lamsa, J., Leder, G., Ledroit, F., Leinonen, L., Leitner, R., Lemonne, J., Lepeltier, V., Lesiak, T., Liebig, W., Liko, D., Lipniacka, A., Lopes, J.H., Lopez, J.M., Loukas, D., Lutz, P., Lyons, L., MacNaughton, J., Malek, A., Maltezos, S., Mandl, F., Marco, J., Marco, R., Marechal, B., Margoni, M., Marin, J.-C., Mariotti, C., Markou, A., Martinez-Rivero, C., Masik, J., Mastroyiannopoulos, N., Matorras, F., Matteuzzi, C., Mazzucato, F., Mazzucato, M., Mc Nulty, R., Meroni, C., Migliore, E., Mitaroff, W., Mjoernmark, U., Moa, T., Moch, M., Moenig, K., Monge, R., Montenegro, J., Moraes, D., Moreno, S., Morettini, P., Mueller, U., Muenich, K., Mulders, M., Mundim, L., Murray, W., Muryn, B., Myatt, G., Myklebust, T., Nassiakou, M., Navarria, F., Nawrocki, K., Nicolaidou, R., Nikolenko, M., Oblakowska-Mucha, A., Obraztsov, V., Olshevski, A., Onofre, A., Orava, R., Osterberg, K., Ouraou, A., Oyanguren, A., Paganoni, M., Paiano, S., Palacios, J.P., Palka, H., Papadopoulou, Th.D., Pape, L., Parkes, C., Parodi, F., Parzefall, U., Passeri, A., Passon, O., Peralta, L., Perepelitsa, V., Perrotta, A., Petrolini, A., Piedra, J., Pieri, L., Pierre, F., Pimenta, M., Piotto, E., Podobnik, T., Poireau, V., Pol, M.E., Polok, G., Pozdniakov, V., Pukhaeva, N., Pullia, A., Radojicic, D., Rames, J., Read, A., Rebecchi, P., Rehn, J., Reid, D., Reinhardt, R., Renton, P., Richard, F., Ridky, J., Rivero, M., Rodriguez, D., Romero, A., Ronchese, P., Roudeau, P., Rovelli, T., Ruhlmann-Kleider, V., Ryabtchikov, D., Sadovsky, A., Salmi, L., Salt, J., Sander, C., Savoy-Navarro, A., Schwickerath, U., Sekulin, R., Siebel, M., Simard, L., Sisakian, A., Smadja, G., Smirnova, O., Sokolov, A., Sopczak, A., Sosnowski, R., Spassov, T., Stanitzki, M., Stocchi, A., Strauss, J., Stugu, B., Szczekowski, M., Szeptycka, M., Szumlak, T., Tabarelli, T., Tegenfeldt, F., Thomas, J., Timmermans, J., Tkatchev, L., Tobin, M., Todorovova, S., Tome, B., Tonazzo, A., Tortosa, P., Travnicek, P., Treille, D., Tristram, G., Trochimczuk, M., Troncon, C., Turluer, M.-L., Tyapkin, I.A., Tyapkin, P., Tzamarias, S., Uvarov, V., Valenti, G., Van Dam, P., Van Eldik, J., Van Remortel, N., Van Vulpen, I., Vegni, G., Veloso, F., Venus, W., Verdier, P., Verzi, V., Vilanova, D., Vitale, L., Vrba, V., Wahlen, H., Washbrook, A.J., Weiser, C., Wicke, D., Wickens, J., Wilkinson, G., Winter, M., Witek, M., Yushchenko, O., Zalewska, A., Zalewski, P., Zavrtanik, D., Zhuravlov, V., Zimin, N.I., Zintchenko, A., Zupan, M
Recent advancements in the development of radiation hard semiconductor detectors for S-LHC.
No full textThe proposed luminosity upgrade of the Large Hadron Collider (S-LHC) at CERN will demand the innermost layers of the vertex detectors to sustain fluences of about 1016 hadrons/cm2. Due to the high multiplicity of tracks, the required spatial resolution and the extremely harsh radiation field new detector concepts and semiconductor materials have to be explored for a possible solution of this challenge. The CERN RD50 collaboration “Development of Radiation Hard Semiconductor Devices for Very High Luminosity Colliders” has started in 2002 an R&D program for the development of detector technologies that will fulfill the requirements of the S-LHC. Different strategies are followed by RD50 to improve the radiation tolerance. These include the development of defect engineered silicon like Czochralski, epitaxial and oxygen-enriched silicon and of other semiconductor materials like SiC and GaN as well as extensive studies of the microscopic defects responsible for the degradation of irradiated sensors. Further, with 3D, Semi-3D and thin devices new detector concepts have been evaluated. These and other recent advancements of the RD50 collaboration are presented and discussed
Charge collection efficiency and resolution of an irradiated double sided silicon microstrip detector operated at cryogenic temperatures
No full textIrradiated silicon detectors operated at cryogenic temperatures: the Lazarus effect
No full textAn increasing interest in the behaviour of silicon detectors at cryogenic temperatures has been awakened by the discovery of the so-called Lazarus effect, namely the recovery of charge collection efficiency (CCE) by means of cryogenic cooling. We measured the CCEs of three single diodes previously irradiated with different neutron fluences. The current-voltage characteristic were measured at 300 and 77 K, showing that the low-temperature operation considerably decreases the steady- state current. This is also the case when a forward voltage bias is applied, which then becomes a suitable option. At 77 K, in the case of samples irradiated with 5 x 10(14) neutrons cm(- 2), the CCE is completely recovered. A third sample irradiated with 2 x 10(15) neutrons cm(-2) shows a 60% CCE at 250 V forward bias
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