Academic literature on the topic 'Inhibition par produit'
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Journal articles on the topic "Inhibition par produit"
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Hamdaoui, O., M. Ouchefoun, and M. Zerdaoui. "Inhibition de la corrosion d'un acier au carbone par le Kemazur 1620." Revue des sciences de l'eau 13, no. 1 (April 12, 2005): 47–54. http://dx.doi.org/10.7202/705380ar.
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Dans cette étude, des mesures électrochimiques ont été utilisées pour caractériser l'efficacité inhibitrice du produit commercial Kemazur 1620, employé pour le traitement des eaux des circuits de refroidissement. L'influence de la concentration de ce composé ainsi que l'effet de la température du milieu ont été étudiés.Les courbes de polarisation ont été obtenues à l'aide d'un montage à trois électrodes. La méthode électrochimique a permis de déterminer la vitesse de corrosion en l'absence et en présence d'inhibiteur et par conséquent, le taux de protection. Ainsi, le Kemazur 1620 présente une très bonne efficacité pour une concentration de 2000 ppm. Entre 1000 et 2000 ppm, l'efficacité inhibitrice augmente de 56 à 91 %. En outre, l'efficacité inhibitrice du composé a été comparée à celle du nitrite de sodium.
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Peings, Vanessa, Albéric Andrin, Mickael Le Bechec, Sylvie Lacombe, Jérôme Frayret, and Thierry Pigot. "Couplage photocatalyse-oxydation par le ferrate (VI) pour le traitement du colorant rhodamine 6G." Revue des sciences de l’eau 30, no. 1 (June 8, 2017): 35–39. http://dx.doi.org/10.7202/1040061ar.
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Un facteur limitant de l’oxydation photocatalytique du dioxyde de titane (TiO2) sous irradiation UV est la recombinaison des électrons de la bande de conduction (e-cb) avec les trous d’électron (h+vb) à la surface de TiO2. Le couplage du ferrate(VI), Fe(VI), connu comme un oxydant respectueux de l’environnement, avec la photocatalyse UV/TiO2 pourrait conduire à une synergie oxydative de par le piégeage de e-cb par Fe(VI) et la consécutive formation de l’espèce hautement réactive Fe(V). Cette étude décrit les résultats du couplage TiO2 commercial P25 avec Fe(VI) sous forme pure ou sous forme d’une matière synthétisée dans notre laboratoire (produit solide nommé Fe(VI) matter) pour l’abattement du colorant rhodamine 6G (R6G). Les cinétiques de transformation de R6G ([R6G]0 = 10‑5 M; pH = 8,00 ± 0,05), en présence de TiO2 ([P25] = 0,1 g∙L‑1) illuminé sous UV et/ou de Fe(VI) ([Fe(VI)]0 = 10‑4 M) sont suivies par spectrophotométrie. Une synergie est mise en évidence lors du traitement de R6G par UV/TiO2/Fe(VI) pur, conduisant à une accélération de la transformation de R6G et à une minéralisation plus importante. Cependant, cet abattement n’est pas atteint lors du couplage UV/TiO2/Fe(VI) matter. Une étude de l’impact de sels inorganiques présents dans Fe(VI) matter sur l’activité photocatalytique est présentée. Le sulfate, SO42‑, et le Fe(OH)3 en particulier mènent à une forte inhibition de l’activité de TiO2. Le suivi de la production des radicaux hydroxyles (OH•) montre une inhibition physique de leur production due à la formation d’une couche de sels inorganiques à la surface de TiO2 et au piégeage de radicaux OH• dans la solution.
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Blache, Denis, Laurence Gesquière, Nadine Loreau, and Phillipe Durand. "Oxidant stress: the role of nutrients in cell-lipoprotein interactions." Proceedings of the Nutrition Society 58, no. 3 (August 1999): 559–63. http://dx.doi.org/10.1017/s0029665199000737.
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Oxidant stress is increasingly becoming an important hypothesis to explain the genesis of several pathologies, including cancer, atherosclerosis and also ageing. Beside a few rare genetic defects, dietary factors are thought to play a key role in the regulation of the production of reactive oxygenated species. An imbalance between nutrients, and in particular those involved in antioxidant status, could explain the onset of an enhanced production of free radicals. We will briefly review information concerning oxidation of lipids and lipoproteins which lead to atherothrombosis. We also present new findings supporting a role for blood platelets in generating oxidant species. New data are also described concerning the role of oxygenated derivatives of cholesterol, oxysterols, in cellular cholesterol efflux and NO production. Also, new developments relating to the influence of direct effects of free radicals on cellular cholesterol homeostasis are presented. Finally, the in vitro effects of butyrate, a natural short-chain fatty acid produced by bacterial fermentation, in the protection against free radical-mediated cytotoxicity are discussed. These data provide information on the mechanisms of dietary antioxidants in preventing oxidant stress.Résumé Au côté des rares cas d’origine génétique, les facteurs nutritionnels (déséquilibres alimentaires, déficience en nutriments antioxydants) jouent des rôles cruciaux dans la modulation de la production d’espèces actives de l’oxygène, conduisant à l’établissement d’un stress oxydant, situation métabolique de plus en plus reconnue comme susceptible d’être à l’origine de nombreuses pathologies comme les cancers, l’athérosclérose et également le vieillissement. Après avoir brièvement rappelé les données concernant l’oxydation des lipides et des lipoprotéines susceptibles de conduire au développement de l’athéro-thrombogenèse, nous présentons des données récentes et originales indiquant que les plaquettes sont en fait capables à l’instar d’autres cellules, de produire des formes actives de l’oxygène susceptibles de modifier les LDL. Des résultats originaux sont également exposés concernant l’effets des oxystérols, produits d’oxydation du cholestérol générés au cours de l’oxydation des LDL ou présents dans l’alimentation, sur deux paramètres importants comme l’efflux du cholestérol cellulaire et la production de monoxyde d’azote. De plus, des données nouvelles relatives à l’effets du stress oxydant et son inhibition par des antioxydants d’origine nutritionnelle sont exposées sur l’homéostasie du cholestérol cellulaire. Enfin, dans ce contexte, les effets potentiellement antiathérogènes d’un acide gras à courte chaîne produit par la fermentation bactérienne, le butyrate, sont décrits sur la protection de cellules en culture vis-à-vis d’un stress oxydant in vitro. Ces éléments contribuent à apporter de nouvelles informations renforçant la notion de fonctionnalité des nutriments dans la protection du stress oxydant en relation avec la pathogenèse.
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Baila, Stefano, Christian Furlan Freguia, Nicholas Iacobelli, Danielle Dunn, Joerg Schuettrumpf, Federico Mingozzi, Patricia Andrade-Gordon, and Valder R. Arruda. "Protease−Activated Receptor 2 (PAR−2) as a Novel Target To Prevent Inhibitor Formation to FIX." Blood 108, no. 11 (November 16, 2006): 763. http://dx.doi.org/10.1182/blood.v108.11.763.763.
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Abstract Direct intramuscular injection (IM) of adeno−associated viral (AAV) serotype 2 in humans with hemophilia B (HB) is a promising therapeutic strategy since muscle biopsies obtained >3 years after vector injection demonstrated stable local gene expression. However to achieve therapeutic FIX levels using AAV−2 would required hundreds IM injections. The use of alternate AAV serotypes is an attractive strategy since AAV−1 or AAV−6, resulted in a >10−fold increase in transgene levels compared to AAV−2 in large animals, but the immune response to the transgene product has been consistently demonstrated as a major limitation of this strategy. There is growing evidence that blood proteases play an important role in modulating inflammatory and immune responses through activation of PARs. Mice lacking PAR−1(−/−) or PAR−2(−/−) alleles presented amelioration of immune− or infection−mediated diseases. Here we sought to determine whether inhibition of PARs could be used as a strategy to prevent immune responses to the FIX following AAV−mediated gene transfer to skeletal muscle. We used PAR−1 and PAR−2 knockout mice on C57Bl/6 background and littermate mice received IM injection of AAV1−CMV−hFIX. At dose 5x1011vg/kg, PAR−2 (−/−) mice (n=5) exhibited circulating FIX levels of 500± 99ng/ml (8–10%) which remained stable for the duration of the experiment (10 weeks), and no antibodies for FIX were detected (n=5). In contrast, all PAR−2 (+/+) mice (n=4) developed antibodies to FIX which inhibits FIX clotting activity, as determined by Bethesda assay (2.1± 0.6 BU). However, when similar vector doses were delivered to PAR−1(−/−) or PAR−1(+/+) (n=4/genotype) mice, antibodies to FIX developed in all animals. We next tested a higher vector dose in PAR−2 models. At dose 1x1012vg/kg, PAR−2(−/−) mice(n=7) resulted in FIX levels of 1,500±353ng/ml, and again no antibodies for FIX were detected. At the same dose, 6 out of 10 mice of PAR−2 (+/+)/(+/−) developed inhibitory antibodies (1.8± 0.7 BU). Further increase in the vector dose to 5 x 1012 vg/kg resulted in the development of inhibitor to FIX in both PAR−2 (−/−) (4/11 mice, 36%) and PAR−2(+/+)/(+/−) (10/17 mice, 60%). This suggests a threshold value in the protective effect in the PAR−2 (−/−) model. We sought to assay for FIX−specific T−cell by ELISPOT assay to quantify IFN−γ secretion from splenocytes of PAR−2 (−/−) and PAR−2 (+/+) mice injected at 5x1011 or 1x1012vg/kg. No difference in IFN−γ secretion was observed between PAR−2 (−/−) and their controls. Moreover, upon repeated challenges with FIX protein following vector injection antibody to FIX was detected in only 1/4 PAR−2 (+/+) mouse and none of 5 PAR−2 (−/−). Thus, PAR−2 inhibition does not compromise the tolerance to FIX. In a different model, intravenous injection of FIX protein into normal mice upon simultaneous activation of PAR−2 by using specific agonist peptide the rates of FIX antibody formation were comparable with those of a control peptide group. Thus, PAR−2−mediating antibody formation to FIX may differ among distinct immunologic challenges. Together, these data suggest that PARs play a role in the immune response to FIX and that inhibition of PAR−2 (but not PAR−1) could be a novel target in preventing inhibitor formation in hemophilia gene therapy and potentially for protein−based therapy.
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Deans, N. L., R. D. Allison, and D. L. Purich. "Steady-state kinetic mechanism of bovine brain tubulin: tyrosine ligase." Biochemical Journal 286, no. 1 (August 15, 1992): 243–51. http://dx.doi.org/10.1042/bj2860243.
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The ATP-dependent resynthesis of tubulin from tyrosine and untyrosinated tubulin was examined to establish the most probable steady-state kinetic mechanism of the tubulin: tyrosine ligase (ADP-forming). Three pair-wise sets of initial rate experiments, involving variation of two substrates pair-wise with the third substrate held at a high (but non-saturating) level, yielded convergent-line data, a behaviour that is diagnostic for sequential mechanisms. Michaelis constants were 14 microM, 1.9 microM and 17 microM for ATP, untyrosinated tubulin and L-tyrosine respectively, and the maximal velocity was 0.2 microM/min. AMP was a competitive inhibitor with respect to ATP, and a non-competitive inhibitor versus either tubulin or tyrosine. Likewise, L-dihydroxyphenylalanine acted competitively relative to tyrosine and non-competitively with respect to either ATP or tubulin. These findings directly support a random sequential mechanism. Product inhibition patterns with ADP were also consistent with this assignment; however, inhibition studies were not practical with either orthophosphate or tyrosinated tubulin because both were very weak inhibitors. Substrate protection of the enzyme against alkylation by N-ethylmaleimide and thermal inactivation, along with evidence of enzyme binding to ATP-Sepharose and tubulin-Sepharose, also supports the idea that this three-substrate enzyme reaction exhibits a random substrate addition pathway.
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Ohtsuki, M., and J. Massagué. "Evidence for the involvement of protein kinase activity in transforming growth factor-beta signal transduction." Molecular and Cellular Biology 12, no. 1 (January 1992): 261–65. http://dx.doi.org/10.1128/mcb.12.1.261.
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Transforming growth factor-beta 1 (TGF-beta 1) rapidly increases the expression of junB transcription factor and plasminogen activator inhibitor-1 (PAI-1) and prevents the cell cycle-dependent phosphorylation of the RB retinoblastoma susceptibility gene product during late G1 phase in Mv1Lu lung epithelial cells. These responses are shown in this report to be blocked by the potent serine/threonine protein kinase inhibitor, H7, added with TGF-beta 1. Added alone, H7 does not alter the basal junB or PAI-1 mRNA levels, the deposition of PAI-1 into the extracellular matrix, or the phosphorylation of RB in late G1 phase, suggesting that this inhibitor does not have a general nonspecific effect on the cell. The analogs H8 and H9, which are preferential inhibitors of cyclic nucleotide-dependent protein kinases, are fivefold less potent than H7 as inhibitors of the TGF-beta response. The PAI-1 response to TGF-beta 1 is not affected by the simultaneous addition of staurosporine, which is a protein kinase C inhibitor, or by the prolonged preincubation of cells with phorbol 12-myristate 13-acetate, which down-regulates protein kinase C. The results suggest the possibility that H7 and its analogs block various early TGF-beta responses by inhibiting a protein serine/threonine kinase(s).
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Ohtsuki, M., and J. Massagué. "Evidence for the involvement of protein kinase activity in transforming growth factor-beta signal transduction." Molecular and Cellular Biology 12, no. 1 (January 1992): 261–65. http://dx.doi.org/10.1128/mcb.12.1.261-265.1992.
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Transforming growth factor-beta 1 (TGF-beta 1) rapidly increases the expression of junB transcription factor and plasminogen activator inhibitor-1 (PAI-1) and prevents the cell cycle-dependent phosphorylation of the RB retinoblastoma susceptibility gene product during late G1 phase in Mv1Lu lung epithelial cells. These responses are shown in this report to be blocked by the potent serine/threonine protein kinase inhibitor, H7, added with TGF-beta 1. Added alone, H7 does not alter the basal junB or PAI-1 mRNA levels, the deposition of PAI-1 into the extracellular matrix, or the phosphorylation of RB in late G1 phase, suggesting that this inhibitor does not have a general nonspecific effect on the cell. The analogs H8 and H9, which are preferential inhibitors of cyclic nucleotide-dependent protein kinases, are fivefold less potent than H7 as inhibitors of the TGF-beta response. The PAI-1 response to TGF-beta 1 is not affected by the simultaneous addition of staurosporine, which is a protein kinase C inhibitor, or by the prolonged preincubation of cells with phorbol 12-myristate 13-acetate, which down-regulates protein kinase C. The results suggest the possibility that H7 and its analogs block various early TGF-beta responses by inhibiting a protein serine/threonine kinase(s).
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Zhang, Wenlin, Gongwei Li, Fei Jin, Yu Huo, Tengfei Sun, and Chunli Li. "Synthesis and characterization of an ionic liquid–carboxylic acid copolymer scale inhibitor and its scale inhibition performance." Water Supply 19, no. 5 (January 22, 2019): 1463–72. http://dx.doi.org/10.2166/ws.2019.011.
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Abstract A phosphorus-free scale inhibitor (ionic liquid–carboxylic acid copolymer) was successfully synthesized by the reaction of 1-sulfobutyl-3-vinylimidazolium hydrogen sulfate (SVIS) and acrylic acid (AA). The structure of the product was characterized by Fourier transform infrared spectroscopy (FTIR), hydrogen nuclear magnetic resonance (1H NMR) and carbon-13 nuclear magnetic resonance (13C NMR). Then the scale inhibition efficiency of 1-sulfobutyl-3-vinylimidazolium hydrogen sulfate-acrylic acid (SVIS-AA) copolymer against CaCO3 and CaSO4 was determined. The results indicated that SVIS-AA copolymer showed better scale inhibition efficiency than poly (acrylic acid) (PAA). After that, the effects of temperature and Ca2+ concentration on the scale inhibition efficiency against CaCO3 were studied. Results showed that when the temperature reached 90 °C, the scale inhibition efficiency could still remain 91% at a concentration of 18 mg L−1. When the concentration of Ca2+ reached 1,200 mg L−1, the scale inhibition efficiency could remain 70% at a concentration of 20 mg L−1. At last, the effect of SVIS-AA copolymer on the morphologies of CaCO3 and CaSO4 scale was studied by scanning electron microscopy (SEM) and X-ray diffraction (XRD).
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Xiao, Guang-Hui, Ryan Gallagher, Justin Shetler, Kristine Skele, Deborah A. Altomare, Richard G. Pestell, Suresh Jhanwar, and Joseph R. Testa. "The NF2 Tumor Suppressor Gene Product, Merlin, Inhibits Cell Proliferation and Cell Cycle Progression by Repressing Cyclin D1 Expression." Molecular and Cellular Biology 25, no. 6 (March 15, 2005): 2384–94. http://dx.doi.org/10.1128/mcb.25.6.2384-2394.2005.
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ABSTRACT Inactivation of the NF2 tumor suppressor gene has been observed in certain benign and malignant tumors. Recent studies have demonstrated that merlin, the product of the NF2 gene, is regulated by Rac/PAK signaling. However, the mechanism by which merlin acts as a tumor suppressor has remained obscure. In this report, we show that adenovirus-mediated expression of merlin in NF2-deficient tumor cells inhibits cell proliferation and arrests cells at G1 phase, concomitant with decreased expression of cyclin D1, inhibition of CDK4 activity, and dephosphorylation of pRB. The effect of merlin on cell cycle progression was partially overridden by ectopic expression of cyclin D1. RNA interference experiments showed that silencing of the endogenous NF2 gene results in upregulation of cyclin D1 and S-phase entry. Furthermore, PAK1-stimulated cyclin D1 promoter activity was repressed by cotransfection of NF2, and PAK activity was inhibited by expression of merlin. Interestingly, the S518A mutant form of merlin, which is refractory to phosphorylation by PAK, was more efficient than the wild-type protein in inhibiting cell cycle progression and in repressing cyclin D1 promoter activity. Collectively, our data indicate that merlin exerts its antiproliferative effect, at least in part, via repression of PAK-induced cyclin D1 expression, suggesting a unifying mechanism by which merlin inactivation might contribute to the overgrowth seen in both noninvasive and malignant tumors.
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Benallaoua, S., P. Nguyen Van, M. P. De Meo, J. Coulon, G. Dumenil, and R. Bonaly. "Recherches sur le mode d'action d'un antifongique non polyénique (désertomycine) produit par une souche de Streptomyces spectabilis." Canadian Journal of Microbiology 36, no. 9 (September 1, 1990): 609–16. http://dx.doi.org/10.1139/m90-106.
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A metabolite with antifungal activity, of non polyenic macrolide structure, was extracted and purified from the culture supernatant of a soil-isolated Streptomyces spectabilis strain, BT 352. This product was found to be related to (or being) desertomycin. Six yeast and five filamentous fungus strains were used to determine minimum concentration of the metabolite that inhibits growth by 80% (IMC); it was established at 50 μg/mL for the fungi and at 100 μg/mL or more for the yeasts tested. Short-term genotoxicity tests showed no antifungal effect on the bacterial genome, and desertomycin at concentration levels of 100 μg/mL or more affected protein synthesis. The antifungal metabolite had no immediate inhibiting effect upon yeast respiration, even at high concentrations; however, the respiration activity of cells grown in the presence of subinhibiting doses and collected during their growth phase was reduced by as much as 40%. Saccharomyces uvarum spheroplast regeneration in a liquid medium containing desertomycin was inhibited at doses fivefold weaker than the IMC determined with intact cells. Contrary to amphotericin B, desertomycin subinhibiting doses do not modify, and if so lightly, the yeast latent phase or the spheroplast wall regeneration phase, thus indicating a fungicidal action. Moreover, following a 30-min contact with desertomycin subinhibiting and inhibiting doses, yeasts liberated potassium in large amounts, indicating that plasma membranes were affected. Key words: Streptomyces spectabilis, desertomycin, antifungal activity, genotoxicity, yeast. [Translated by the journal]
Dissertations / Theses on the topic "Inhibition par produit"
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Blanc, Philippe. "Contribution à l'étude de la production d'acide propionique par voie microbienne : modélisation-effets des fortes concentrations cellulaires." Toulouse, INSA, 1986. http://www.theses.fr/1986ISAT0047.
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L'étude de la production d'acide propionique par voie fermentaire est réalisée sur des substrats : les hydrolysats d'ordures ménagères et le lactósérum. Des productions maximales dd'acide propionique égales à 35,6 g/l sont obtenues. L'inhibition de la croissance de la bactérie par l'acide propionique produit est plus marquée que celle de sa biosynthèse. Celle-ci est ingibée suivant un processus linéaire entre 0 et 16 g/l d'acide propionique et reste constante quelle que soit la concentration en acide entre 16 g/l et 35,6 g/l. Le couplage fermentation-ultrafiltration a permis de réaliser des cultures continues et prolongées. Les fortes concentrations en biomasse (112 g/l MS) acquises ont permis d'atteindre des productivités en acide propionique de 2,14 g/l. H soit 6 fois plus fort que les valeurs couramment admises et d'analyser l'effet inhibiteur des cellules sur la propre croissance et excrétion.
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Christen, Pierre. "Faisabilite d'un procede a membrane liquide pour l'extraction continue de l'ethanol produit par fermentation." Paris, ENMP, 1987. http://www.theses.fr/1987ENMP0055.
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Une membrane liquide composee d'un support poreux hydrophobe impregne d'un solvant organique a ete mise au point; l'isotridecanol s'est avere etre biocompatible, impermeable aux sels et au glucose et autorise un flux d'ethanol important (35 g/h. M**(2)). Cette membrane liquide mise en oeuvre avec une phase receptrice aqueuse a permis, par l'extraction de l'ethanol inhibiteur, une detoxification significative d'un mout de fermentation en activite: amelioration de la viabilite des levures et de productivite du fermenteur d'un facteur 2,5. En outre, ce procede d'extraction a permis de mettre en evidence l'activite inhibitrice de metabolites secondaires. Une etape supplementaire de concentration en ligne de l'ethanol extrait peut etre realisee en utilisant le procede a membrane liquide avec une phase receptrice gazeuse et un piege a froid. Enfin, une modelisation mathematique des phenomenes de transfert d'ethanol a travers une membrane liquide a permis de mieux cerner les resistances au transfert et a montre l'importance de parametres lies au support (epaisseur, porosite, tortuosite, des pores) et lies au solvant (coefficient de partage et diffusivite)
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Cans, Pierre. "Contribution a l'identification des dynamiques de production des pristinamycines et a la mise au point de nouvelles procedures de fabrication." Toulouse, INSA, 1987. http://www.theses.fr/1987ISAT0019.
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Un calcul theorique ayant montre que la culture de aspergillus niger sur milieu solide d'amidon de manioc etait limitee par la disponibilite de l'eau dans le substrat, l'introduction de 20% d'un support lignocellulosique a forte capacite de retention d'eau a permis d'augmenter l'activite de l'eau du milieu et, ainsi, d'accelerer et ameliorer le processus fermentatif. L'extension de la notion de support a ensuite conduit a pratiquer des cultures de a. Niger sur un milieu liquide dissous absorbe sur une phase solide. Dans un tel systeme, l'activite de l'eau de la solution d'impregnation, la taille des particules du support et la quantite d'inoculum de spores ont ete les parametres importants de la croissance du champignon. Ce type de culture a permis d'utiliser des milieux liquides glucoses tres concentres (400 g/l) qui sont utilises pour la croissance en 40h. Une etude microcalorimetrique a mis en evidence l'existence d'une phase exothermique situee entre la germination et la croissance exponentielle
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Minier, Michel. "Fermentation acetonobutylique par couplage a des procedes membranaires et fermentation extractive." Toulouse 3, 1987. http://www.theses.fr/1987TOU30290.
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Rohac, Roman. "Etude structurale et fonctionnelle de la protéine à radical SAM Hyde." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV010/document.
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Les protéines à radical S-adénosyl-L-méthionine (SAM) utilisent un centre [Fe4S4] réduit pour initier le clivage réductive homolytique de la SAM et la formation d'une espèce hautement réactive - le radical 5'-déoxyadénosyl ou 5'-dA•. Dans la quasi-totalité de cas ce radical alkyl va arracher un atome d'hydrogène sur le substrat et déclencher ainsi sa conversion en produit. On trouve ces enzymes au niveau d'étapes clé de la synthèse de certaines vitamines, antibiotiques, précurseurs de l'ADN ou encore cofacteurs protéiques où elles sont souvent impliquées dans le clivage ou la formation des liaisons C-C, C-N, C-S ou encore C-P. Les travaux réalisés au cours de cette thèse ont été focalisés sur l'étude structurale et fonctionnelle de la protéine HydE ; une enzyme à radical SAM, qui intervient dans la biosynthèse du site actif organométallique de l'hydrogénase à [FeFe]. L'objectif principal était d'identifier le substrat de HydE et d'étudier les détails du fonctionnement d'une protéine à radical SAM. Nous avons réussi à identifier un groupe de molécules, dérivées de la cystéine, contentant un cycle thiazolidine avec un ou deux groupements carboxylates, qui ont une très bonne affinité pour le site actif de HydE. Certains de ces ligands se sont montrés d’être des substrats non physiologiques de l’enzyme. Grâce à ces substrats nous avons pu mettre en évidence un nouveau mécanisme d’attaque radicalaire dans les protéines à radical SAM. En effet, dans HydE nous avons observé une attaque directe du radical 5'-dA• sur l’atome soufre du thioéther appartenant au cycle thiazolidine. Cette réaction constitue un exemple pas comme les autres d’une insertion d’un atome de soufre (ou de sélénium) catalysée par une enzyme à radical SAM. Il s'agit également d'une première observation d'une réaction radicalaire dans les cristaux protéiques d'une enzyme à radical SAM et également un premier suivi en temps réel par la RMN du 13C et 1H de l'accumulation d'un des produits de la réaction catalysée par ces enzymes. Les résultats de calculs théoriques basés sur nos structures cristallographiques de haute résolution suggèrent que dans le cas de cette superfamille de protéines le radical 5'-dA• serait plutôt un état de transition et donc pas une espèce intermédiaire isolableRadical S-adenosyl-L-methionine (SAM) proteins use a reduced [Fe4S4] cluster to initiate homolytic reductive cleavage of SAM, which leads to the formation of highly reactive 5'-deoxyadenosyl radical species or 5'-dA•. In almost all cases this alkyl radical will abstract a hydrogen atom from the substrate and thus trigger its conversion into product. These enzymes are found in key steps of the synthesis of certain vitamins, antibiotics, DNA precursors or protein cofactors. They are often involved in the cleavage or formation of C-C, C-N, C-S or C-P bonds. The present thesis work has been focused on the structural and functional study of HydE protein; a radical SAM enzyme, involved in the biosynthesis of the organometallic active site of [FeFe]-hydrogenase. The main goal was to identify the substrate of HydE and to study details of how radical SAM proteins control the highly oxidizing 5'-dA• species. We managed to identify a group of molecules, derived from cysteine, containing a thiazolidine ring with one or two carboxylate groups, which have a very good affinity for the active site of HydE. We have demonstrated some of these ligands are non-physiological substrates of the enzyme. With these substrates we could highlight a new radical attack mechanism in radical SAM proteins. Indeed, in HydE we observed a direct attack on the 5'-dA • radical on the sulfur atom of the thioether belonging to the thiazolidine ring. This is an unprecedented reaction that contrasts with sulfur (or selenium) atom insertion reactions catalysed by some radical SAM enzymes. This is also the first observation of a radical reaction in the protein crystal of a radical SAM enzyme and also the first real-time monitoring by 1H- & 13C-NMR spectroscopy of the accumulation of products of the reaction catalysed by these enzymes. Theoretical calculations based on our high-resolution crystal structures suggest that in the case of this protein superfamily the 5'-dA• radical, which triggers the reaction in radical SAM enzymes, is a transition state and therefore not an isolable intermediate species
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Djerdjouri, Nour-Eddine. "Blanchiment et inhibition de la réversion par des produits réducteurs dérivés du phosphore /." Thèse, Trois-Rivières : Université du Québec à Trois-Rivières, 1998. http://www.uqtr.ca/biblio/notice/resume/03-2188260R.html.
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Djerdjouri, Nour-Eddine. "Blanchiment et inhibition de la réversion par des produits réducteurs dérivés du phosphore." Thèse, Université du Québec à Trois-Rivières, 1998. http://depot-e.uqtr.ca/3770/1/000648934.pdf.
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Matta-El-Ammouri, Ghassan. "Fermentation acétonobutylique : Obtention de mutants résistants au butanol, action des acides acétique et butyrique sur la formation de solvants." Nancy 1, 1986. http://www.theses.fr/1986NAN10079.
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Dans la fermentation acétonobutylique, la conversion du sucre en solvants est de l'ordre de 33 % ; le rapport habituel butanol/acétone/éthanol est 6/3/1/ ; la concentration maximale de glucose pouvant être dégradé est de 60 g/1 pour une teneur finale en solvants de 20 g/1. La principale limitation de cette fermentation réside dans une inhibition par les produits, en particulier le butanol, qui perturbe le métabolisme bactérien. Ce travail s'est focalisé sur l'obtention de mutants résistants au butanol, et sur le mécanisme d'action des acides acétique et butyrique dans la formation de solvants. En utilisant différents cribles de mutation, tels que l'alcool allylique, le butyraldéhyde, le pentanol et le butanol, on a pu isoler différentes sortes de mutants. Certains ont perdu leur phase solvantogène, d'autres se sont montrés plus résistants au butanol que la souche sauvage. L'addition des acides acétique et butyrique a montré que le premier augmente la production d'acétone, sans toucher à celle du butanol, tandis que le deuxième augmente la production d'acétone et de butanol, d'une manière équivalente. Par la suite, nous avons proposé un mécanisme d'action de ces deux acides dans la formation de solvants. Dans la dernière partie, nous avons montré que ces deux acides modifiaient l'activité spécifique des enzymes acétate et butyrate kinase, au cours de la première phase de fermentation
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Ndong, Engone Jean Gérard. "Développement de matériaux cimentaires à base de sous-produits bois : mise en forme par extrusion et vibrocompactage." Thesis, Artois, 2015. http://www.theses.fr/2015ARTO0211/document.
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En France, le gisement de déchets bois produits au sein des entreprises de première et seconde transformations est estimé à environ douze millions de tonnes par an. Soixante pourcent de ces déchets proviennent essentiellement des scieries sous forme de sciure, de copeaux de bois. Actuellement, il existe différentes filières de valorisation de ces déchets plus ou moins nocives à l'environnement. Un nouvel enjeu est donc de trouver des voies et moyens permettant une valorisation durable et conséquente de ces déchets. Dans ce contexte, la région Nord-Pas-de-Calais a initié un projet visant à la valorisation de ces déchets en élaborant de nouveaux matériaux de construction à base de sous-produits bois. Les objectifs de ce travail de thèse sont de développer des composites à base de pâte cimentaire et de sciure de bois issus de l'essence de Peuplier. Ces composites sont destinés à être utilisés comme éléments de maçonneries porteuses et sont assujettis à des critères de résistances mécaniques fixés par la norme française. La caractérisation de l'influence de la sciure sur les propriétés mécaniques, rhéologiques et physico-chimiques d'un mortier a été effectuée en substituant le sable par de la sciure à des taux variant de 10 à 100\%. Les résultats obtenus ont montré une perte de résistance mécanique avec l'augmentation du volume de bois dans le mélange due à des phénomènes chimiques et physiques. Néanmoins les résistances obtenues pour des taux de substitutions importants (50 à 60\%) restaient conformes à la norme. Ces résultats ont conduit à l'optimisation d'une formulation de mortier de bois extrudable à l'aide d'une extrudeuse à piston. Afin d'appliquer le développement de ces composites à l'échelle industrielle, la sciure de bois a été introduite dans une formulation de micro-béton servant à la production de blocs de béton industriels mis en forme par vibrocompactage. Les résultats obtenus ont montré que jusqu'à 50 \% de substitution du sable par la sciure, les résistances mécaniques étaient conformes. La caractérisation thermique des blocs a montré une capacité isolant intéressanteIn France, the waste wood deposit product in companies of first and second transformation is estimated at about twelve million tons per year. 60\% of this waste comes mainly from mills in the form of sawdust and wood chips. There are many methods of recovery of such waste, which in turn causes environmental problems through the use of products harmful to the environment. A new challenge is to find ways and means to sustainable and consistent recovery of such waste. A new challenge is to find ways and means to sustainable and consistent recovery of such waste. The recovery of such waste in construction materials could be a sustainable solution. In this context, the Nord-Pas-de-Calais Council initiated a project for the recovery of such wastes by developing new building materials from wood byproducts. This thesis has been intended to develop biocomposites based on cement paste and sawdust resulting from Poplar species. These biocomposites are designed for be used as part-bearing masonry and are subject to mechanical strength criteria set by the French standard. The study of the influence of sawdust on the mechanical, rheological and physico-chemical of a mortar was performed by replacing the sand by sawdust at rates ranging from 10 to 100 \%. The results obtained showed a loss of mechanical strength with increasing volume of wood in the mixture generated by chemical phenomena. However the compressive strength obtained for significant substitution rate (50 to 60\%) were in accordance with the French standard. These results led to the optimization of a wood mortar formulation met can be extruded using a ram extruder. In order to apply the development of these biocomposites in an industrial scale, the sawdust was introduced into a formulation of micro-concrete used in the production of industrial concrete blocks manufactured by vibro-compaction. The results showed that up to 50\% of substitution of sand by the sawdust, the mechanical properties were compliant. The thermal characterization of the blocks showed an interesting insulation capacity
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Reyne, Rinaldi Valérie. "Isolement et caractérisation de glycosidases produites par "Aspergillus Niger" : application à l'hydrolase d'hétérosides terpéniques." Montpellier 2, 1992. http://www.theses.fr/1992MON20148.
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Nous avons entrepris l'isolement et la caracterisation de trois glycosidases produites par aspergillus niger. Apres avoir elimine les sucres presents dans differentes preparations enzymatiques commerciales, nous avons compare l'aptitude de ces enzymes a liberer du rhamnose a partir de rutine, utilise comme modele de substrat. Les activites arabinase, rhamnosidase et glucosidase ont ete isolees d'une preparation pectinase et leurs caracteristiques generales ont ete determinees (ph optimum, temperature optimale, ph#i, masse molaire). Une etude cinetique de la rhamnosidase a permis de connaitre l'effet du glucose, du rhamnose, de la gluconolactone et d'evaluer les variations d'efficacite catalytique en fonction des substrats. D'autre part, les activites glucosidase et rhamnosidase ont ete separees de la preparation hesperidinase et des etudes comparables a celles precedemment effectuees ont ete realisees. La possibilite d'utiliser les trois activites enzymatiques pour hydrolyser les heterosides terpeniques a ete etudiee en utilisant le pool heterosidique isole du vin muscat de frontignan
Book chapters on the topic "Inhibition par produit"
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Polya, Gideon M. "Inhibition of eukaryote signal transduction components by plant defensive secondary metabolites." In Bioactive Natural Products (Part F), 513–64. Elsevier, 2001. http://dx.doi.org/10.1016/s1572-5995(01)80017-x.
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Hase, Koji, Quanbo Xiong, and Shigetoshi Kadota. "Hepatoprotective effect of plant components: Inhibition of tumornecrosis factor-α-dependent inflammatory liver injury." In Bioactive Natural Products (Part F), 459–82. Elsevier, 2001. http://dx.doi.org/10.1016/s1572-5995(01)80015-6.
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Bourdon, Allen K., Greg Villareal, George Perry, and Clyde F. Phelix. "Alzheimer's and Parkinson's Disease Novel Therapeutic Target." In Research Anthology on Diagnosing and Treating Neurocognitive Disorders, 411–26. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-3441-0.ch021.
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Thiazolidinedione (TZD) drugs (Takeda Pharmaceuticals and Metabolic Solutions Development Company) targeting inhibition of the mitochondrial pyruvate carrier (MPC) are currently being tested in clinical trials to prevent progression into mild cognitive impairment of Alzheimer's disease (AD) or in the pipeline to prevent neurodegeneration in Parkinson's disease (PD). These have Ki values in the µM range. This study was focused on identifying candidate drug precursors of the natural cinnamic acid products that might have good bioavailability in the nM ranges forming covalent thiol bonds with targets. In silico protein homology modeling and ligand docking has demonstrated that binding cysteine residues within the transport channel is a key part of the inhibitory mechanism. These are covalent thiohemiacetal bonds with the alpha-carbon, carboxylate group, off a phenol ring. Like the classic MPC inhibitors, these natural derivatives of hydroxycinnamic acid have a conjugated pi-system used to form thiol bonds with the cysteine residue via Michael addition.
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Chou, Tzu-Chuan, Robert G. Dyson, and Philip L. Powell. "Managing Strategic IT Investment Decisions." In Encyclopedia of Information Science and Technology, First Edition, 1875–79. IGI Global, 2005. http://dx.doi.org/10.4018/978-1-59140-553-5.ch331.
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IT can have a significant impact on organizational performance, but it can also be a major inhibitor of change and can be a resource-hungry investment that often disappoints. Organizations can best influence the success of IT projects at the decision stage by rejecting poor ones and accepting beneficial ones. However, little is known about IT decision processes. Research demonstrates the importance of managing strategic IT investment decisions (SITIDs) effectively. SITIDs form part of the wider range of corporate strategic investment decisions (SIDs) that cover all aspects that the organization might wish to invest in. SIDs will then have different degrees of IT intensity that may impact on outcome. IT investment intensity is the degree to which IT is present in an investment decision. Here, IT investment intensity is defined as the ratio of IT spending to total investment. The higher IT investment intensity, the more important IT is to the whole investment. For example, Chou et al. (1997) find IT investment intensity to be negatively associated with SID effectiveness. The concept of IT intensity is similar to, but also somewhat different from, the concept of information intensity. Information intensity may be defined as the degree to which information is present in the product or service of a business (Porter & Millar, 1985).
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Mathews, Jennifer L., and Anne Schweighardt. "The Role of Natriuretic Peptides in the Pathophysiology and Treatment of Heart Failure." In Emerging Applications, Perspectives, and Discoveries in Cardiovascular Research, 1–16. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-2092-4.ch001.
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The pathophysiology of heart failure is due in part to compensatory mechanisms utilized to maintain cardiac output. Neurohormonal responses include activation of the renin-angiotensin-aldosterone and sympathetic nervous systems leading to vasoconstriction, increased blood volume through reabsorption of sodium and water, and increased myocardial contractility and heart rate. Prolonged activation of these systems often results in a maladaptive response and a further reduction in cardiac output (Colucci, 2015). Natriuretic peptides counterbalance the neurohormonal systems by antagonizing the actions of renin-angiotensin-aldosterone, promoting vasodilation and natriuresis. In hypervolemic states atrial myocytes are stretched resulting in the release of atrial natriuretic peptide (ANP). Ventricular cells secrete brain-type natriuretic peptide (BNP) in response to the high ventricular filling pressures (de Sa, 2008). The natriuretic peptides are degraded enzymatically by neprilysin. Plasma concentrations of ANP and BNP can be used as markers for the diagnosis of heart failure (Grewal, 2004). The kidneys also produce a natriuretic peptide, urodilatin, and new studies suggest a role for this peptide in the pathophysiology and treatment of heart failure (Anker, 2015). The natriuretic peptides can be targeted therapeutically for the treatment of heart failure. Nesiritide, a recombinant preparation of human B-type natriuretic peptide (BNP), is FDA approved and has been available for several years for treatment of acute decompensations of heart failure, but has received limited use due to cost and adverse effect profile. Ularatide, a synthetic analog of urodilatin, is currently in phase three clinical trials. In addition, the FDA has recently approved an angiotensin receptor blocker-neprilysin inhibitor that has shown mortality benefit.
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Ojeda, Sergio R. "The Anterior Pituitary and Hypothalamus." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0008.
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The hypothalamic-pituitary complex represents the core of the neuroendocrine system. The hypothalamus is composed of a diversity of neurosecretory cells arranged in groups, which secrete their products either into the portal blood system that connects the hypothalamus to the adenohypophysis (see later) or directly into the general circulation after storage in the neurohypophysis (see Chapter 6). Because of the nature of their actions, the hypothalamic hormones are classified as releasing or inhibiting hormones. The hypothalamic hormones delivered to the portal blood system are transported to the adenohypophysis, where they stimulate or inhibit the synthesis and secretion of different trophic hormones. In turn, these hormones regulate gonadal, thyroid, and adrenal function, in addition to lactation, bodily growth, and somatic development. No attempt will be made in this chapter to cover the actions of the different pituitary trophic hormones on their target glands, because they are discussed in detail in other chapters. An exception to this is growth hormone (GH). Although Chapter 11 considers several aspects of the control and actions of GH, a broader discussion of its physiological actions will be presented here because GH is the only anterior pituitary hormone that does not have a clear-cut target gland. The pituitary gland has two parts: the neurohypophysis, of neural origin (see Chapter 6), and the adenohypophysis, of ectodermal origin. In embryonic development, an evagination from the roof of the pharynx pushes dorsally to reach a ventrally directed evagination from the base of the diencephalon. The dorsally projecting evagination, known as Rathke’s pouch , forms the adenohypophysis, whereas the ventrally directed evagination of neural tissue forms the neurohypophysis. The neurohypophysis has three parts: the median eminence, the infundibular stem, and the neural lobe itself. The median eminence represents the intrahypothalamic portion and lies just ventral to the floor of the third ventricle protruding slightly in the midline. The main part of the neurohypophysis, the neural lobe, is connected to the median eminence by the infundibular stem.
Conference papers on the topic "Inhibition par produit"
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Kiso, U., H. Kaudewitz, A. Henschen, B. Åstedt, E. K. O. Kruithof, and F. Bachmann. "DETERMINATION OF INTERMEDIATES, PRODUCTS AND CLEAVAGE SITE IN THE REACTION BETWEEN PLASMINOGEN ACTIVATOR INHIBITOR 2 (PAI 2) AND UROKINASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642809.
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Several specific inhibitors for both urokinase-type and tissue-type plasminogen activators have in recent years been isolated from various organs and cell lines. The inhibitors isolated from human placenta and from the human histiocytic lymphoma cell line U-937 have been shown to be immunologically related.They are denoted as plasminogen activator inhibitor type 2 (PAI 2). It has earlier been demonstrated by gel electrophoresis that during the inhibition reaction at first complexes are formed between activator and inhibitor and then the inhibitor is cleaved and the complex can be dissociated.In the present study the reactions between urokinase aijd PAI 2 were analysed by means of reversed-phase high-performance liquid chromatography (HPLC) and SDS-polyacrylamide gelelectrophoresis (PAGE). Both high-molecular-weight (54 kDa) and low-molecular weight (33 kDa) urokinase (UK) were used. The PAI 2 was derived from placenta and from U-937 cells. It has a molecular size of L5 kDa. Equimolar amounts of UK and PAI 2 were incubated for 15 min at room temperature. On HPLC and SDS-PAGE analysis new components, corresponding to the UK-PAI 2-complexes, appeared and both UK and PAI 2 disappeared. The apparent sizes of the complexes were approx. 82 kDa and 62 kDa, depending on the type of UK used. The HPLC retention times of the complexes were higher than those of UK or PAI 2. The complexes were stable under the conditions employed for the analyses, but could be completely dissociated by incubation for 1 h at pH 10 and 37°. The released UK behaved identical with the UK starting material. However, the released PAI 2 had decreased in molecular size according to the PAGE analysis, and on HPLC an additional component appeared. As PAI 2 has a blocked N-terminus and the new component shows an N-terminal sequence it must correspond to the C-terminal part of PAI 2. The sequence defines thus the reactive site for the cleavage by the plasminogen activator.
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Makris, P. E., A. Papadopoulos, and D. A. Tsakiris. "LIPOXYGENASE PRODUCTS CHANGES IN ‘IN VITRO’ AND ‘IN VIVO’ ASPIRINISED PLATELETS UNDER THE INFLUENCE OF PAF AND EPINEPHRINE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644829.
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We aimed to investigate the changes of lipoxygenase products in platelets and the simultaneous behaviour of ‘in vivo’ or ‘in vitro’ aspirinised platelets, stimulated by two agonists, PAF and epinephrine (EPI). 12 healthy were included. 6 received 20mg of aspirin (ASA) per os for 7 days (group A), and in 6 (group B) platelets were aspirinised ‘in vitro’ (5 or lOmin incubation at 37°C with ASA 1M). In group A blood was drawn once at the beginning and once at the end of the trial, while in group B just ome. First, platelet aggregation was studied using two agonists simultaneously (0.6 ¼M EPI and 20 nM PAF). We incubated then all platelet samples with 0.5 M of the substance BW755C (kind offer of Dr Moncada) far 3 min at 37°C. Second we measured PL0 products according to Takayama et al (1980), in platelets with or without ASA, and in platelets with ASA and after treatment with BW755C, always after addition of both agonists. Our results showed: a) Irreversible aggregation was slightly enhanced by the simultaneous addition of PAF and EPI in both groups and in non-aspirinised platelets. After ASA treatment, each agonist alone did not induce irreversible aggregation, whereas their combination overcame this inhibition, a fact not noticed under BW755C (a known PLO inhibitor). b) PLO products were measured in nmol TBRS/10 platelets:Our results agree with Cerletti et al (1986) and confirm that the two agonists combined are capable of overcoming the inhibition caused by ASA, possibly by activating the PLO pathway (Cerletti et al, 1986). Respectively the quantitative determination of PLO products (about which we did not notice any other report insofar) confirm the above assumption, since inhibition by BW755C coincides with the steep fall of PLOlevels, which for group A is statisticallysignificant (p≺0.01, paired t-test) and for group B entirely significant (p ≺0.001).
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DUBOR, F., A. M. DOSNE, and L. CHEDID. "Effect of dexamethasone and endothelial cell supernatant on u-PA produced by human promyelocyte cells treated with phorbol myristate acetate (PMA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643191.
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After treatment with PMA the human promyelocytic HL60 cells were induced to differentiate into a monocyte-macrophage population and to produce a high amount of plasminogen activator in the supernatant. This response was detected from 0,5 ng/ml of PMA and culminated at 5 ng. The plasminogen activator appeared of urokinase-type as showed by fibrinenzymographic analysis : the enzymatic profile of cell supernatant showed 2 lysis band (Mr 33.000 and 55.000) corresponding to those of urokinase of low and high mol. weight. Dexamethasone (100 pM) suppressed the production of this macrophage u-PA without evidence of plasminogen activator inhibitor (PAI) generation in the supernatant : free PAI was not detected in urokinase inhibition assays ; complexes of u-PA-PAI were not observed in fibrinoenzymographic studies. Supernatant of human endothelial cells added to HL60 cell supernatant neutralized the two molecular species of macrophage u-PA and gave rise to complexes (Mr 110.000 and 84.000) detected by fibrinoenzymography. These results suggested different possible levels for controlling u-PA of inflammatory macrophages including interaction with endothelial cells secretion since endothelial PAI is increased by some inflammatory monokine and also by dexamethasone, it appears that endothelium could have a regulatory role on inflammatory fibrinolysis.
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Loskutoff, D. J., J. Mimuro, and C. Hekman. "PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644763.
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Plasminogen activation provides an important source of localized proteolytic activity not only during fibrinolysis, but also during ovulation, cell migration, epithelial cell differentiation, tumor invasion and a variety of other physiological processes. Precise regulation of plasminogen activator (PA) activity thus constitutes a critical feature of many biological processes. This control is achieved in large part through the action of specific PA inhibitors (PAIs). Although 4 distinct PAIs have been detected,1the endothelial cellTderived inhibitor (PAI-1) is the only one that efficiently inhibits both urokinase (Kd=2.3×10−13M; Kassoc =1.6×108 M−1s−1) and single-chaintissue-type PA (tPA; Kd=1.3×lO−15 M Kd=3.9×lO7M−1s−1). It also inhibits trypsin (Kassoc=6.8×106M−1 s−1 ) ancl Plasmin (Kassoc=7.6×l05 M−1 s5 Analysis of the effect of PAI-1 on the rate of plasminogen activation revealed a competitive type of inhibition when urokinase was employed but a linear mixed type of inhibition when single chain tPA was employed. These results suggest that the interaction of PAI-1 with tPA, in contrast to its interaction with urokinase, may involve 2 sites on the tPA molecule.PAI-1 has been purified from medium conditioned by cultured bovine aortic endothelial cells and partially characterized. It is a major biosynthetic product of these cells, accounting for as much as 12% of the total protein released by the cells in 24 h. It has an M of 50,000, an isoelectric point of 4.5-5.0, and is immunologically and biochemically related to the rapidly acting inhibitor present in human platelets and in the plasma of some patients at risk to develop thrombotic problems. Although it is relatively stable to conditions which inactivate most protease inhibitors (acid pH, SDS), it is extremely sensitive to oxidants. The molecular cloning of the PAI-1 gene revealed that the mature human protein is 379 amino acids long, contains an NH2-terminal valine, lacks cysteines and has a methionine at the Pi position of it's reactive center. The conversion of this methionine to methionine sulfoxide may be responsible for the rapid inactivation of PAI-1 by oxidants. Human PAI-1 has extensive (30%) homology with α1-antitrypsin and antithrombin III and is thus a member of the serine proteinase inhibitor (serpin) family; a group of related molecules that control the major protease cascades of the blood. The PAI-1 gene is approximately 12.2 kilobase pairs in length and is organized into nine exons and eight introns.The production of PAI-1 by endothelial cells is stimulated by endotoxin, interleukin-1, tumor necrosis factor, and transforming growth factor β(TGFβ). The cells are extremely sensitive to TGFβwith maximal effects (100-fold stimulation) observed with 1-2 ng/ml. These changes were relatively specific for PAI-1, and could be detected at both the protein and the RNA level. Interestingly, TGFgalso stimulated the amount of PAI-1 present in the extracellular matrix (ECM) of BAEs. PAI-1 was one of the primary ECM components of these cells, constituting 10-20% of the ECM proteins detected after SDS-PAGE.One of the most unusual properties of PAI-1 is that it exists in blood and in various cellular samples in both an active and an inactive (latent) form, the ratio depending on the source. The latent form can be converted into the active one by treatment with denaturants like SDS or guanidine-HCl. Although the majority of the cell-associated PAI-1 is active, it rapidly decays (t1/2=3 h) into the latent form once it is released from the cells. In contrast, the half-life of ECM associated PAI-1 was greater than 24 h. These data suggest that PAI-1 is produced by BAEs in an active form, and is then either released into the medium where it is rapidly inactivated, or released into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.
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Altman, R., A. Scazziota, S. Windor, and C. A. Dujovne. "ADDITIVE EFFECT OF DILTIAZEM (DIL) ON THE INHIBITION OF PLATELET AGGREGATION PRODUCED BY ASPIRIN (ASA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643437.
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Platelet activation in vivo occurs by the action of several stimuli. It is generally agreed that actives products of arachidonic acid derived via the cyclooxy-genase pathway can stimulate platelet aggregation. ASA decrease thromboxane A2 generation and thereby inhibit platelet aggregation produced by AA and, partially, by others agonists. Nevertheless, the antiaggregating effect of ASA can be overcome by the conjointly activity of arachidonic acid(AA) and platelet activating factor (PAF). The inhibition of this cooperative aggregating effect can be important in platelet function suppressive therapy. The effect of DIL was tested in this sys tern. DIL was added in vitro to platelet rich plasma oS talned from volunteers before and after ASA(100mg/dayT intake for 7 days. DIL (2ug/ml) inhibited 50% platelet aggregation induced by AA (0.75mM) in non aspiri-nated volunteers. At even lower concentrations of DIL (0.4-lug/ml) an inhibition of aggregation induced by 300nM of PAF was also observed. After ASA, no aggregation by AA, only a first wave followed by disaggregation when PAF (30nM) was used and a full response when this pair of agonists were added together was obtained. DIL (0.lug/ml) added in vitro, produced significant inhibition of the synergism.The effect in vivo of DIL plus low dose of ASA was also explored. In vivo administration of therapeutic dose of DIL (60mg T.I.D.) and low dose of ASA (75-100 mg/day), prevented the synergistic activity of AA plus PAF on platelet aggregation. In conclusion, DIL may enhance the effectiveness of low dose of ASA in the prevention of arterial thromboembolism.
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Risberg, B., G. K. Hansson, E. Eriksson, and B. Wiman. "IMMUNOHISTOCHEMICAL LOCALIZATION OF PLASMINOGEN ACTIVATOR INHIBITOR (PAI) IN TISSUE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644443.
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The origin of tissue plasminogen activator inhibitor (PAI) has not been fully elucidated. Platelets are rich in PAI and endothelial cells (EC) in culture produce the inhibitor (PAI 1), which seems to be a major secretory protein. Another inhibitor (PAI 2) has been demonstrated in the placenta. In the present study we localized PAI 1 in various human tissues using a polyclonal antibody against human PAI 1 and fluorescence technique. Tissue sections were incubated with a polyclonal rabbit-anti-human PAI antibody in various dilutions followed by incubation with biotinylated goat-anti-rabbit IgG and FITC-labelled Avidin. Positive identification using this technique was made in endothelium of liver sinusoids and in hepatocytes. Most vessels in systemic and pulmonary circulation showed positive fluorescence in the endothelial layer. No quantitative evaluation was possible with this technique. Synthesis of PAI in liver could provide an explanation for the efficient inactivation of tissue plasminogen activator (t-PA) during liver passage. Localization of PAI in vascular tissue corroborated studies from EC cultures.
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Laug, Walter E. "HUMAN VASCULAR SMOOTH MUSCLE CELLS (HVSMC) PRODUCE PLASMINOGEN ACTIVATOR INHIBITOR 1 (PAI-1) AND PROTEASE-NEXIN (PN)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642854.
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The arteriosclerotic lesion is characterized by myointimal proliferation. The pathological growth of SMC may alter the biological function of the overlaying endothelial cells.Thus we have found that HVSMC produce large amounts of plasminogen activator inhibitor (PAI) activities, which neutralize the PA activities elaborated by endothelial cells. Most ( 95%) of the PA activities detectable by reverse fibrin autography bind to heparin affigel at low salt concentration (0.05 m NaCl). Two peaks with PAI activities are eluted with a linear NaCl gradient from 0.05 m to 1.0 m. The first peak eluted at NaCl concentrations of 0.05 m to 0.3 m while the second peak was found in the range of 0.5 m to 0.7 m NaCl. Both PAI had an approximate molecular weight of 45,000 to 50,000 as estimated by SDS PAGE followed by either reverse fibrin autography or silver stain. The pooled fractions of the first peak did not bind 125I-thrombin while the protein of the second peak formed SDS resistant complexes with it like PN.The pooled fractions of the first PAI peak were further purified by SDS gel electrophoresis followed by electro-blotting onto glass fiber paper. Partial amino acid microsequencing demonstrated homology with the amino acid sequence of PAI-1. In addition, positive reaction with specific antiserum to PAI-1 was demonstrated in Western blots. Oligonucleotide probes were synthesized from the amino acid sequences obtained and PAI-1 gene probes were isolated from a human placenta cDNA library. Subsequently PAI-1 gene expression in HVSMC was demonstrated with Northern blots.These studies show that PAI-1 binds to heparin affigel at low salt concentrations which facilitates considerably its purification. In addition, the production of PAI-1 and PN by HVSMC may be of importance for the pathogenesis of thrombotic complications in arteriosclerotic vessels.
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Oujdad, S., S. Zafad, H. El Attar, and I. Ben Yahya. "Histiocytose langerhansienne de l’adulte : à propos d’un cas." In 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603013.
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L’histiocytose langerhansienne est une maladie rare causée par la prolifération et l’infiltration d’un ou plusieurs organes, par des cellules dendritiques de type Langerhans. Elle s’exprime par des manifestations cliniques extrêmement polymorphes et peut toucher l’os, la peau, l’hypophyse, les poumons, le système nerveux central, et plus rarement le foie et le système digestif. Elle a été initialement décrite chez les enfants. L’histiocytose langerhansienne de l’adulte présente une entité particulière tant par ses manifestations cliniques que par sa prise en charge. Le cas présenté est celui d’un patient âgé de 53ans, en bon état de santé apparent et non fumeur, qui s’est présenté à la consultation pour des lésions nécrotiques et douloureuses des muqueuses gingivales mandibulaires et maxillaires, associées à des mobilités dentaires sévères. L’examen exobuccal ne révélait aucune asymétrie faciale ni adénopathies. L’examen endobuccal confirmait la présence de lésions nécrotiques gingivales et une parodontite sévère au niveau mandibulaire antérieur et maxillaire postérieur. Le secteur maxillaire antérieur présentait un parodonte sain. L’examen radiologique panoramique et Cone Beam CT , révélaient des lyses osseuses moyennes à terminales s’étendant de la 44 à la 38 et au niveau des molaires maxillaires droites et gauches. Les dents antérieures ne présentaient quant à elles pas de lyse. Par ailleurs des images lacunaires à l’emporte pièce siégeaient au niveau du secteur mandibulaire édenté. Ces manifestations évoquaient un lymphome ou une manifestation orale d’une infection virale type VIH. L’examen biologique révélait une légère hyperleucocytose et une augmentation de la vitesse de sédimentation à la première heure. L’examen anatomopathologique des lésions muqueuses, a rapporté la présence d’éléments histiocytaires se regroupant en nodules, concluant en une histiocytose langerhasienne de l’adulte. Le bilan d’extension ne révélait aucune atteinte associée, concluant en une histiocytose localisée. L’étude moléculaire a montré la présence d’une mutation V600E du gène BRAF (Facchetti et al, European journal of pathology, 471(4); 2017). Ce dernier est situé sur le chromosome 7, et il est impliqué dans l’envoi des signaux qui déterminent la croissance cellulaire. L’évolution et le pronostic de cette maladie sont étroitement liés à l’âge et aux organes atteints. Les régressions spontanées ont été rapportées, et peuvent être induites par un curetage ou par une simple biopsie. (Goncalves et al, Biomedical research notes,9(19); 2016) Pour notre cas, les extractions des dents mobiles avec curetage des lésions ont permis une cicatrisation complète. La thérapeutique médicamenteuse peut comprendre une corticothérapie locale ou systémique, des bisphosphonates, voire même une radiothérapie. Par ailleurs la confirmation de la mutation BRAF permet d’oser un traitement spécifique par inhibition de l’enzyme produite par ce gène. (Martıénez et al, Revisita Odontologica Mexicana, 16(2 ); 2012)
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Sørhaug, E., M. M. M. Jordan, R. A. A. McCartney, R. Stalker, E. J. J. Mackay, and J. Green. "Selection of Scale Control Strategy on a Sub Sea Developed Field in the North Sea and How 6 Different Companies Contributed." In SPE International Oilfield Scale Conference and Exhibition. SPE, 2014. http://dx.doi.org/10.2118/spe-169788-ms.
Full textAbstract:
AbstractThe Blane field is a sub-sea oil and gas production development located in the southern part of the North Sea straddling the UK and Norwegian border. The field is expected to produce inorganic scale (BaSO4) when injection water containing sulphate breaks through in the production wells. This will require scale inhibitor squeezes from an intervention vessel to mitigate scale deposition.The wells were completed with long horizontal sections straddling multiple producing zones. This could potentially result in scale deposition severely reducing productivity if both formation water and injection water were to be produced simultaneously into the wells. Adding to the complexity, the perforation guns were left in the wellbore as part of the completion preventing any access to the perforation area. The distribution of scale inhibitor during a squeeze pumping operation could therefore be uneven leaving parts of the well poorly protected. In addition, the guns prevent physical removal of any type of materials in the well bore like asphaltenes, sand and scale which could plug off the perforations during a pumping operation with a well intervention tool; Wireline, coiled tubing, etc..Injection water supplied from a host platform is used for pressure support of the reservoir. During the field development, the injection water was expected to contain mostly produced water reducing the scale potential considerably as it would have low sulphate content. When water injection started, very little produced water was being produced resulting in mostly seawater being available available for pressure support. Scale deposition in the well and around the well bore could therefore prove to be impossible to control unless reactions in the reservoir would reduce the scale potential or a reliable scale inhibitor squeeze method to mitigate scaling could be identified.This paper describes the joint effort of 6 different companies to identify the risks associated with the inorganic scaling during production and how a scale squeeze strategy was developed. The work included scale inhibitor selection, a geo-chemical study, and reservoir and near well bore simulations, sub-sea deployment selection, deciding on water chemistry and production monitoring and development of an overall management plan.
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Páramo, J. A., R. Arcas, J. Fernández, J. Herreros, R. Llorens, and E. Rocha. "FIBRINOLYSIS AFTER HEART TRANSPLANTATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643114.
Full textAbstract:
Some aspects of the function of the fibrinolytic system were investigated in 12 patients undergoing cardiac transplantation. Plasminogen, euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor activity (PAI),α2-antiplasmin (α2-Ap) and fibrinogen degradation products (FDP) were determined preo-peratively and on postoperative days 1 and 5. Results showed a significant decrease of plasminogen (p <0.005), EFA (p <0.0001) and t-PA (p ^.0.001) on postoperative day 1 as compared to the baseline value, followed by recovery on day 5. There was a significant increase of PAI (p < 0 . 005) , α2-AP (p <0.0001) and FDP (p < 0.02) on postoperative day 1 as compared to the preoperative value. PAI and FDP reached the baseline value on postoperative day 5, but α2AP also increased on postoperative day 5. Our data show that there is an impairment in blood fibrinolytic activity early after cardiac transplantation, mainly related to a decrease of plasminogen and t-PA and a increase of PAI and α2AP. The clinical relevance of these data needs further evaluation.
Reports on the topic "Inhibition par produit"
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Watts, Benjamin E., Danielle E. Kennedy, Ethan W. Thomas, Andrew P. Bernier, and Jared I. Oren. Long-Term Durability of Cold Weather Concrete : Phase II. Engineer Research and Development Center (U.S.), January 2021. http://dx.doi.org/10.21079/11681/39579.
Full textAbstract:
Recent laboratory results confirm that it is possible to protect concrete from freezing solely using chemical admixtures and indicate that the amount of admixture required may be significantly less than previously recommended. Researchers have also verified that admixture-based freeze protection can produce concrete that is durable to winter exposure for a minimum of 20 years, through petrographic examination of core specimens obtained from past field demonstrations. Freeze protection for concrete using chemical admixtures alone has been an area of active research for 3 decades; however, the most recent methodology recommends very high addition rates of accelerating and corrosion inhibiting admixtures, which result in significant challenges, including slump loss, rapid setting, and potentially excessive temperature rise. As part of a laboratory study, researchers systematically varied the dosage of freeze protection admixtures used in concrete cured in a 23 °F environment. Preliminary findings indicate that a 50% reduction in admixture dose maintained adequate freeze protection and resulted in compressive strengths exceeding those of room-temperature controls at 7 and 28 days. The combination of improved handling, reduced cost, and verified durability associated with the use of admixtures for freeze protection makes a compelling case for broader adoption of this technique in winter operations