Literatura académica sobre el tema "Latent inhibition"
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Artículos de revistas sobre el tema "Latent inhibition"
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Reed, Phil. "Blocking latent inhibition". Bulletin of the Psychonomic Society 29, n.º 4 (abril de 1991): 292–94. http://dx.doi.org/10.3758/bf03333922.
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Lubow, R. E., I. Weiner, A. Schlossberg y I. Baruch. "Latent inhibition and schizophrenia". Bulletin of the Psychonomic Society 25, n.º 6 (junio de 1987): 464–67. http://dx.doi.org/10.3758/bf03334742.
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Abramson, Charles I. y M. E. Bitterman. "Latent inhibition in honeybees". Animal Learning & Behavior 14, n.º 2 (junio de 1986): 184–89. http://dx.doi.org/10.3758/bf03200054.
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Rodriguez, Gabriel y Geoffrey Hall. "Potentiation of latent inhibition." Journal of Experimental Psychology: Animal Behavior Processes 34, n.º 3 (2008): 352–60. http://dx.doi.org/10.1037/0097-7403.34.3.352.
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Joseph, M. H. y S. H. Jones. "Latent inhibition and blocking". Behavioural Pharmacology 2, n.º 6 (diciembre de 1991): 521???526. http://dx.doi.org/10.1097/00008877-199112000-00010.
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Swerdlow, Neal R., David L. Braff, Heidi Hartston, William Perry y Mark A. Geyer. "Latent inhibition in schizophrenia". Schizophrenia Research 20, n.º 1-2 (mayo de 1996): 91–103. http://dx.doi.org/10.1016/0920-9964(95)00097-6.
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Gould, Thomas J., Allan C. Collins y Jeanne M. Wehner. "Nicotine enhances latent inhibition and ameliorates ethanol-induced deficits in latent inhibition". Nicotine & Tobacco Research 3, n.º 1 (1 de febrero de 2001): 17–24. http://dx.doi.org/10.1080/14622200020032060.
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J. Gould, Allan C. Collins, Jeanne, Thomas. "Nicotine enhances latent inhibition and ameliorates ethanol-induced deficits in latent inhibition". Nicotine & Tobacco Research 3, n.º 1 (1 de febrero de 2001): 17–24. http://dx.doi.org/10.1080/14622200125450.
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Kraemer, Philipp J. y Christopher K. Randall. "Latent inhibition in preweanling rats". Psychobiology 20, n.º 1 (marzo de 1992): 81–84. http://dx.doi.org/10.3758/bf03327166.
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Weiner, I., I. Hairston, M. Shayit, G. Feldman, D. Joel y J. Feldon. "Strain differences in latent inhibition". Psychobiology 26, n.º 1 (marzo de 1998): 57–64. http://dx.doi.org/10.3758/bf03330592.
Texto completoTesis sobre el tema "Latent inhibition"
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Jakob, Andrea F. (Andrea Frances). "The effects of serotonergic ligands on latent inhibition". Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23401.
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Latent inhibition (LI) is the attenuation in the acquisition of Pavlovian conditioning to a conditioned stimulus (CS) due to prior extensive exposure to that CS. It is assumed that LI is an animal model of attention in that animals learn to ignore the preexposed CS. The present series of experiments investigated the effects of selective serotonergic (5-HT) ligands known to increase 5-HT neurotransmission on LI using a conditioned emotional response (CER) procedure. In experiment 1, rats preexposed (PE) to 40 presentations of a tone CS acquired CER suppression more slowly than vehicle-treated nonpreexposed (NPE) animals, suggesting LI was obtained. Administration of 10 mg/kg fluoxetine (i.p.) did not influence CER acquisition in PE animals, suggesting that LI was not affected by fluoxetine. However, it was assumed that 40 CS presentations exerted a powerful LI effect, which might mask any effect of fluoxetine. Consequently, we assessed the effects of 5-HT ligands on LI following 10, rather than 40, CS preexposures. Under these conditions, both acute fluoxetine (experiment 2), and chronic (14 day) fluoxetine (experiment 3) administration, were found to augment LI. Experiment 4 suggested that acute administration of the 5-HT2 agonist DOI (2.5 mg/kg) also enhances LI. Experiment 5 revealed that 1 mg/kg 8-OH-DPAT did not influence LI, suggesting that postsynaptic 5-HT1a receptors are not involved in LI. These results suggest that enhancement of 5-HT neurotransmission enhance LI and that this effect is mediated, in part, through the 5-HT2 receptor subtype. The results are discussed within the context of the switching model of LI, which suggests that the effects of 5-HT are mediated through the modulation of the mesolimbic dopamine pathway.
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Killcross, Andrew Simon. "Dopaminergic mechanisms and latent inhibition : implications for schizophrenia". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261541.
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Leung, Hiu Tin Psychology Faculty of Science UNSW. "Spontaneous recovery in Pavlovian fear extinction and latent inhibition". Publisher:University of New South Wales. Psychology, 2009. http://handle.unsw.edu.au/1959.4/43701.
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The experiments reported in the present thesis examined the behavioural processes of Pavlovian fear extinction and latent inhibition. The first series of experiments studied the reacquisition of extinguished fear responses following different amounts of extinction training. Rapid reacquisition occurred when rats were reconditioned after moderate extinction, showing that the original learning remained intact across this extinction. In contrast, when reconditioning was given after massive extinction, reconditioned responding was first depressed but then spontaneously recovered over time. This suggests that massive extinction produces a relatively permanent loss of the originally learned responding, while additionally imposes on the extinguished CS a transient latent inhibitory process that prevented the immediate but not the delayed expression of reconditioning. The second series of experiments studied the impact of spontaneous recovery of extinguished fear responses on their additional extinction. These experiments demonstrated that a CS that had time to show spontaneous recovery underwent greater response loss across additional extinction than one lacking recovery. They also showed that an excitor extinguished in compound with a CS showing recovery suffered greater response loss than an excitor extinguished in compound with a CS lacking recovery. Further, extinction of a compound composed of two CSs, one showing recovery and a second lacking recovery, produced greater extinction to the CS that showed recovery. These results show that spontaneous recovery of extinguished responses deepens their extinction through an error-correction mechanism regulated by both common and individual error terms. The third series of experiments studied the spontaneous recovery of latently inhibited and extinguished fear responses in within-subject designs. Using a compound test procedure, a CS that had received extensive preexposure or extensive extinction was found to have undergone greater spontaneous recovery relative to a CS just moderately preexposed or moderately extinguished. A CS given a mixed history of preexposure and extinction also underwent greater recovery relative to a CS just preexposed or just extinguished. These results suggest that both latent inhibition and extinction share a transient depressive process, and that the resulting recovery of responding is proportional to the amount of this depression.
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Tsakanikos, Elias. "Latent inhibition and psychometrically defined schizotypy : an experimental investigation". Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405897.
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Martins, Serra Ana Maria. "Latent inhibition and the Kamin blocking effect in schizophrenia and schizotypy". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307402.
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Gray, Nicola Susan. "The attentional deficit in schizophrenia : a neurobiological account". Thesis, King's College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319152.
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Schmidt-Hansen, Mia. "Evaluation of latent inhibition and learned irrelevance as assays of attentional abnormalities in schizotypy". Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/56176/.
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The claim that the positive symptoms of schizophrenia are associated with attentional abnormalities was investigated by using naturally occurring individual differences in schizotypic characteristics in a normal population of undergraduate students. Attention was measured using a variety of novel procedures that assessed latent inhibition (Chapters 2 and 3), learned irrelevance (Chapters 4 and 5) and stimulus detection (Chapter 6). The results provide restricted support for the claim that attentional processes are aberrant in groups of participants with high schizotypy scores (in particular high levels of unusual experiences on the Oxford-Liverpool Inventory of Feelings and Experiences).
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Quinn, Veronica Frances. "Sources of learning and their role in the experience of placebo nausea". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15541.
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The purpose of the project was to better understand sources of learning that lead to placebo nausea, with the aim of developing interventions with clinical utility. After introducing theory regarding placebo effects and nausea in Chapter 1, Chapter 2 systematically reviewed studies that had previously attempted to manipulate nausea via the placebo effect. This review revealed that there were some features of interventions associated with success, but that results were often conflicting and a better paradigm to model placebo nausea in healthy participants was required. Chapter 3 introduced such a paradigm, illustrating how Galvanic Vestibular Stimulation (GVS) could be used to administer both placebo and nauseating stimulation under the guise of an experiment looking at the effects of GVS on spatial ability. Chapter 4 presented a study that used this paradigm to explore the development of placebo-induced relief from nausea through instruction, conditioning, and their combination. Both sources of learning reduced nausea on test relative to controls. Chapter 5 refocused on the problem of nausea that is incidentally conditioned in the treatment context. A model of conditioned nausea was tested, and it appeared that conditioning had developed and had also generalized perfectly well to a new test context. This finding was taken as evidence that the GVS device had overshadowed any context-nausea learning, and was used to inform the development of a new latent inhibition paradigm tested in Chapters 6 and 7. Chapter 6 pre-exposed these GVS-related reactive cues in the form of placebo stimulation in an attempt to retard conditioning through latent inhibition. Here, pre-exposure reduced conditioned nausea to the placebo on test relative to a group who did not receive pre-exposure, and had reduced nausea to the level of a control group who received no conditioning. Given that the applicability of any such intervention to applied settings rests on its ethicality, in a novel extension, Chapter 7 tested whether this latent inhibition effect required deception. This study replicated the effect of pre-exposure observed in Chapter 6, as well as finding that latent inhibition occurred to the same extent in a group fully informed as to the nature of the pre-exposure phase. Together, these findings suggest that placebo effects can occur after both instruction and conditioning, and that taking advantage of placebo effects in the clinic could offer an important method of intervening to reduce nausea.
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Gracey, David J. "An investigation of some CCK ligands as potential antipsychotic compounds using latent inhibition in rats". Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388091.
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Lawrence, Natalia Sophie. "The role of ventral pallidal GABA transmission in latent inhibition : a behavioural and neurochemical study". Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251870.
Texto completoLibros sobre el tema "Latent inhibition"
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Lubow, R. E. y Ina Weiner, eds. Latent Inhibition. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511730184.
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Latent inhibition and conditioned attention theory. Cambridge [England]: Cambridge University Press, 1989.
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Schmajuk, Nestor A. Latent inhibition and its neural substrates. Boston: Kluwer Academic Pub., 2002.
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Latent inhibition and its neural substrates. Boston: Kluwer Academic Pub., 2002.
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Schmajuk, Nestor A. Latent Inhibition and Its Neural Substrates. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0841-0.
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Weiner, Ina y Robert E. Lubow. Latent inhibition: Cognition, neuroscience, and applications to schizophrenia. Cambridge: Cambridge University Press, 2010.
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Wellman, N. A. Latent inhibition, negative priming and neuroleptics in schizophrenic patients and matched controls. [Guildford]: University of Surrey, 1994.
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Schmajuk, Nestor. Latent Inhibition and Its Neural Substrates. Springer, 2012.
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Schmajuk, Nestor. Latent Inhibition and Its Neural Substrates. Springer, 2002.
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Lubow, R. E. Latent Inhibition and Conditioned Attention Theory. Cambridge University Press, 2011.
Buscar texto completoCapítulos de libros sobre el tema "Latent inhibition"
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Fischer, Gabriele, Annemarie Unger, W. Wolfgang Fleischhacker, Cécile Viollet, Jacques Epelbaum, Daniel Hoyer, Ina Weiner et al. "Latent Inhibition". En Encyclopedia of Psychopharmacology, 686–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_344.
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Weiner, Ina y Segev Barak. "Latent Inhibition". En Encyclopedia of Psychopharmacology, 877–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_344.
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Lubow, Robert E. "Latent Inhibition". En Encyclopedia of the Sciences of Learning, 1727–29. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4419-1428-6_1010.
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Ramírez, Simón, Gonzalo Miguez, Vanetza E. Quezada-Scholz, Felipe Parrado, Rocío Angulo y Mario A. Laborda. "Latent Inhibition". En Encyclopedia of Animal Cognition and Behavior, 1–3. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-47829-6_745-1.
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Weiner, Ina y Segev Barak. "Latent Inhibition". En Encyclopedia of Psychopharmacology, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-27772-6_344-2.
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Ramírez, Simón, Gonzalo Miguez, Vanetza E. Quezada-Scholz, Felipe Parrado, Rocío Angulo y Mario A. Laborda. "Latent Inhibition". En Encyclopedia of Animal Cognition and Behavior, 3885–87. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_745.
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Schmajuk, Nestor A. "Theories of latent inhibition". En Latent Inhibition and Its Neural Substrates, 1–10. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0841-0_1.
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Schmajuk, Nestor A. "Latent inhibition and schizophrenia". En Latent Inhibition and Its Neural Substrates, 167–78. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0841-0_8.
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Schmajuk, Nestor A. "Behavioral properties of latent inhibition". En Latent Inhibition and Its Neural Substrates, 23–65. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0841-0_3.
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Schmajuk, Nestor A. "Dopaminergic involvement in latent inhibition". En Latent Inhibition and Its Neural Substrates, 79–105. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0841-0_5.
Texto completoActas de conferencias sobre el tema "Latent inhibition"
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Lambers, J. W. J., M. Cammenga, B. Konig, H. Pannekoek y J. A. van Mourik. "ACTIVATION OF HUMAN ENDOTHELIAL TYPE PLASMINOGEN ACTIVATOR INHIBITOR (PAI-1) BY NEGATIVELY CHARGED PHOSPHOLIPIDS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642807.
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The endothelial cell type plasminogen activator inhibitor (PAI-1) may exist in an active, latent form that can be converted into an active form upon exposure to denaturants such as sodium dodecyl sulphate (SDS), guanidine-HCl or urea. Here we show that latent PAI-1 can be activated with lipid vesicles, consisting of the negatively charged phospholipids phosphatidylserine (PS) or phosphatidylinositol (PI). The presence of a net negative charge on the phospholipid headgroup is essential for activation. Incubation with lipid vesicles, consisting of the zwitterionic phospholipids phosphatidylcholine (PC) and phosphatidylethanol-amine (PE), does not result in activation of the inhibitor. In the presence of PS vesicles, the capacity of PAI-1 to inhibit tissue type plasminogen activator (t-PA) is 50-fold higher than that of the untreated protein. For comparison, the activity of PAI-1 was enhanced 25-fold by treatment of the protein with SDS. PS induces activation of the inhibitor at much lower concentrations than SDS. For example, to achieve 50% inhibition of t-PA with a more than 100-fold excess of PAI-1, 0.25 nmoles of PS are required, whereas L.60 nmoles of SDS are necessary to reach half maximal inactivation of t-PA. Activation of PAI-1 by PS can be reversed by the addition of Ca2+-ions, suggesting that Ca2+-ions interfere with the interaction of PAI-1 with the negatively charged lipid surface, thus preventing its activation. The lipid-induced activation of PAI-1 points to a possibly important role of phospholipids in fibrinolysis; regulation of the fibrinolytic activity in blood plasma may ultimately be determined by the extent to which these phospholipids activate the inhibitor of t-PA.This study was supported by the Netherlands Thrombosis Foundation.
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Loskutoff, D. J., J. Mimuro y C. Hekman. "PLASMINOGEN ACTIVATOR INHIBITOR". En 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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Kuo, Be-Sheng, Maciej Dryjski y Thorir D. Bjornsson. "EFFECTS OF NICOTINE AND COTININE ON THE SYNTHESIS AND RELEASE OF PLASMINOGEN ACTIVATOR FROM BOVINE AORTIC ENDOTHELIAL CELLS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644657.
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While cigarette smoking has beenimplicated in the development of cardiovascular diseases, it has been reported to increase fibrinolytic activity in vivo. However, no data is available regarding the underlying mechanism of action. The present investigation was carried out to evaluate the effects of nicotine and its major metabolite, cotinine, on the seretion of plasminogen activator (PA) and PA inhibitor (PAI) by cultured bovine aortic endothelial cells. PA activity was determined by the fibrin plate method, and individual molecular species with PA and PAI activities were separated and visualized using SDS-PAGE with zymography and reverse fibrin autography. Both nicotine and cotinine increased PA secretion in a time- and dose-dependent manner. A maximum stimulation in PA secretion after 24-hour incubation was observed for nicotine at 10-8 M and for cotinine at 10-7> M, which corresponded to 2.5- and 2.7-foldincreases over control, respectively. These concentrations are in the range observed after cigarette smoking. The pharmacological stimulation of PA activity required both RNA and protein synthesis, as evidencedby its inhibition by cycloheximide and actinomycin D. Both control cells and cells treated with nicotine and cotinine produced multiple forms of PA and a single form of PAI. The PAI was mainly of the latent form as no quenching effect was observed on standard tissue plasminogen activator (tPA) and urokinase (UK) after they were mixed with the conditioned culture medium. The PAs werefound to consist of both tPA and UK,and the corresponding complexes with PAI, however, the UK bands were wider than the tPA bands. Both species were enhanced by nicotine and cotinine. Although activities of all species of PA were enhanced by nicotine and cotinine, these compounds had no apparent quantitative or qualitative effects on the release ofPAI. These results thus suggest that the mechanism underlying the enhanced fibrinolytic activity after cigarette smoking may be due to nicotine- and cotinine-induced stimulation of PA synthesis and subsequent release.
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Beteta, Alan, Lorraine Boak, Katherine McIver, Myles Jordan y Robin Shields. "Mechanistic Understanding of the Impact of EOR Polymer on the Inhibition Mechanism and Performance of Phosphonate Scale Inhibitors". En SPE International Conference on Oilfield Chemistry. SPE, 2021. http://dx.doi.org/10.2118/204383-ms.
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Abstract With the current trend for application of Enhanced Oil Recovery (EOR) technologies, there has been much research into the possible upsets to production, from the nature of the produced fluids to changes in the scaling regime. The key question being addressed in this publication is the influence of EOR chemicals, such as hydrolyzed polyacrylamide (HPAM), on scale inhibitor (SI) squeeze lifetime for barium sulphate and calcium carbonate scale risk. Squeeze lifetime is defined as the duration of time (or produced water volume) before the minimum inhibitor concentration (MIC) is reached. This is controlled by the adsorption, and later release, of the inhibitor onto the reservoir rock and the MIC of the inhibitor selected for the produced brine. This paper builds on earlier published work investigating potential changes to inhibitor adsorption caused by polymer EOR produced and moves to the evaluation of the changes in MIC due to the presence of EOR chemical. In the static inhibitor performance bottle tests, the EOR polymer alone appeared to show some degree of inhibition performance against BaSO4, but below a level required for effective scale management. However, in combination with the inhibitor (DETPMP) at near MIC levels, the inhibition efficiency was negatively impacted by the presence of degraded HPAM EOR polymer. During dynamic tube blocking tests, the inclusion of even low levels of HPAM (2.5 ppm) were shown to reduce the differential pressure build up suggesting barite scale inhibition or reduced adhesion to the coil. Furthermore, the scale morphology produced in these tests, examined under a scanning electron microscope, was clearly impacted in the presence of HPAM. For the CaCO3 system there appears to be increasing positive impact from HPAM on CaCO3 morphology with HPAM concentration and, as observed for BaSO4, an improved performance in dynamic efficiency experiments. However, at higher HPAM concentrations (500 ppm) the precipitate was amorphous and only a minor pressure rise was observed during the tube blocking experiments. From these observations, it is clear that HPAM can impact the way both calcite and barite scale grow, especially at lower inhibitor concentrations (<MIC) and hence impacts the mechanism by which DETPMP can function to prevent scale nucleation and growth. This study represents a comprehensive review of both inhibition performance in the presence of an EOR polymer and with these findings the implication to field treatment lifetimes and associated costs of scale management via scale squeeze in a field under HPAM flooding.
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Liu, Keshun y Mike Woolman. "Developing an optimized method for measuring chymotrypsin inhibitor activity in protein products". En 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/yucc6741.
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Protease inhibitors of protein nature, such as trypsin inhibitors and chymotrypsin inhibitors, are rich in seeds of legume crops. Soybeans contain Kunitz inhibitor and Bowman-Birk inhibitor. The former mainly inhibits trypsin, while the latter inhibits both trypsin and chymotrypsin. Other legumes contain similar types. Historically, trypsin inhibitor activity in legume products has been of primary interest for measurement due to its antinutritional implication. However, Bowman-Birk inhibitor has been shown therapeutic. It is also more resistant to heat than Kunitz inhibitor. As increasing volumes of plant proteins are being used for food or feed in recent years, there is a growing interest in monitoring chymotrypsin inhibitor activity (CIA) in these products as well. Yet, reported methods for CIA assay vary greatly, with no standard method being available. Three years ago, at our USDA lab, we developed an improved method for measuring trypsin inhibitor activity, which was later adopted as AOCS Official Method, Ba 12a-2020. This presentation reports our new effort in developing a method for measuring CIA, using N-benzoyl-L-tyrosine p-nitroanilide (BTpNA) as a substrate. Unlike the substrate for measuring trypsin inhibitor activity, BTpNA is not water soluble, an organic solvent that is miscible with water must be present. Therefore, the assay system for measuring CIA was much more complicated than that for measuring trypsin inhibitor activity. This made the method development more difficult than originally thought. After investigating effects of many assay parameters, such as organic solvent, the sequence of adding reagents, % chymotrypsin inhibition, etc., an optimized method for CIA measurement was finally developed. It featured dimethylformamide as the organic solvent, the enzyme-last sequence, 5 mL total assay volume, and calculation of the inhibitor activity based on % chymotrypsin inhibition. The proposed method was reliable and robust and could be standardized for measuring CIA in various protein products.
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Booth, N. A., A. Reith y B. Bennett. "A PLASMINOGEN ACTIVATOR INHIBITOR (PAI-2) CIRCULATES IN TWO HIGH MOLECULAR WEIGHT FORMS IN PREGNANCY". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644459.
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Normal vascular endothelium and platelet α-granules contain an inhibitor of plasminogen activator (PAI-1) of about 48000 molecular weight, which is released by stimuli such as thrombin. An immunologically distinct inhibitor (PAI-2) of about 47000 molecular weight has been purified from placenta and from a histiocytic cell line U-937. The level of PA-inhibition in plasma is raised in late pregnancy and this may be due to increases in PAI-1 or in PAI-2 or in both.Using SDS-PAGE and zymography on fibrin/plasminogen /u-PA detector gels, we have found that normal plasma contains a band of inhibition of apparent molecular weight 40000, which can be neutralised by antiserum raised against PAI-1. Pregnancy plasma contained this band as well as additional inhibitor bands of apparent molecular weights 75000 and 130000. The novel high molecular weight PA-inhibitors were detectable by zymography at about 12 weeks gestation. They were specific for plasminogen activator and did not inhibit plasmin. They were inhibited by antiserum raised against PAI-2 from U-937 cells (a gift from Dr EKO Kruithof) and thus are immunologically related to PAI-2. They may represent circulating complexes of PAI-2 with another protein or aggregates of PAI-2, which retain inhibitory activity after SDS-PAGE. PAI-2 appears to represent a pregnancy associated protein that circulates in a number of different molecular weight forms.
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McCabe, P. J., L. E. Stratton, E. J. Hornby y M. Foster. "INHIBITION OF GUINEA-PIG PLATELET FUNCTION IN VIVO AND EX VIVO USING THE THROMBOXANE A2 ANTAGONISTS, AH23848 AND GR32191". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643468.
Texto completoResumen
The thromboxane A2 antagonist, GR32191 (Lumley et al., this meeting) was tested as an inhibitor of platelet aggregation in the guinea-pig and compared with another Tx-antagonist, AH23848 (Brittain et al, 1985). Guinea-pigs were dosed with AH23848 or GR32191 at 0.01-1.0mg/kg. At intervals, blood was taken and PRP was prepared for ex vivo aggregation studies. Collagen concentrations causing half maximal aggregation (IC50) were calculated for test and vehicle-dosed groups. Inhibition was expressed as a concentration ratio (IC50 test/IC50 vehicle). For in vivo studies, 111In-labelled platelets (12μCi, 200μl) were injected into anaesthetised guinea-pigs and 24 hrs later oral doses of AH23848 or GR32191 (0.01-1.0mg/kg) or indomethacin (5mg/kg) were given. After one hour, blood was taken for platelet and radioactivity counting. The carotid artery was exposed under anaesthesia and a current of 2mA was applied for 60 sec. After 90 min, 1cm of the damaged and contralateral carotid vessels were removed for gamma-counting. Inhibition of accumulation of platelets on the injured artery was measured by comparison with the undamaged contralateral artery. Numbers of platelets deposited were calculated from the radioactivity of each section of artery and the radioactivity and platelet count in the blood. Oral doses of AH23848 or GR32191 inhibited ex vivo platelet aggregation induced by collagen. Maximum inhibition occurred one hour after dosing, and was still present at 6 hours for AH23848 (l.Omg/kg) and GR32191 (0.3mg/kg). GR32191 and AH23848 were active in vivo causing inhibition of platelet deposition at doses of 0.01-lmg/kg. The maximum inhibition of deposition was 58% for AH23848 (0.1mg/kg) and 63% for GR32191 (0.1mg/kg), with 50% inhibition at 0.02mg/kg for both. Indomethacin (5mg/kg p.o.) caused maximum inhibition of 58% at 5mg/kg p.o. suggesting that this represents the total thromboxane involvement in platelet deposition. GR32191 and AH23848 are thromboxane A2 antagonists with antithrombotic activity after oral dosing to guinea-pigs.Brittain R.T. et al Circulation, 72, 1208-1218, 1985.
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Avello, A. Garcia, R. A. Fernandez Trejo, L. J. Garcia Frade, A. Pardo Vigo, J. Cesar y J. L. Navarro. "A METHOD FOR DETERMINATION OF FUNCTIONAL α-2 ANTIPLASMIN LEVELS IN PLASMA: THE CIRCULAR LYSIS INHIBITION OF AGAROSE-FIBRIN PLATE". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644841.
Texto completoResumen
A new, simple and reliable technique .has been developed for the determination of functional α-2 Antiplasmin in plasma; It is based on the circular inhibition of lysis produced by a-2 Antiplasmin from a hole punched out in an agarose-fibrin plate in which Urokinase has been previously dissolved.Briefly: An Agarose-Fibrin plate is made with Agarose>(l%), Fibrinogen (0.5%) and Urokinase (0.5 U/ml). The components are mixed at 422 C and thrombinCO.25 U/ml is used to coagulate Fibrinogen. The mixture is poured on a horizontal glass, plate and left at room temperature. 30 min later a series of holes are punched out in the plate and the samples and controls are seeded in the holes.The plate is incubated during 18 hours at 37° C in a humid chamber. After that time, all the plate has been lysed by plasmin produced by Urokinase except a circular area around the holes where α-2 Antiplasmin has migrated from the border: A round opaque circle can be seen around the holes and the diameters are proportional in a log-log scale with the aα-2 Antiplasmin levels of the sample.A standard curve is constructed with a pool of plasmas and the diameters of each sample are referred to it in a log-log scale, determining in this way the levels of functional α-2 Antiplasmin as a percentage.The lysis inhibition circle is entirely due_ to α-2 Antiplasmin and not to any other Fibrinolysis inhibitor: This has been demonstrated incubating previosusly the samples with antibodies directed to α-2 Macroglobulin, α-1 antitrypsin and C-l Esterase Inhibitor with no change in the circle. But when samples were incubated with an antibody to α-2 Antiplasmin, the opaque lysis inhibition circle disapeared.This method presents a very good correlation with other functional methods (cromogenic substrate s-2251 Kabi:r=0.92 p(0.01) and is comparatively simpler.the sensibility of the method is 0.5 % and the reproductibility is 3% day by day and 1% in a same day.
9
Rocca, Emmanuel, Pierre Steinmetz y Michel Moliere. "Revisiting the Inhibition of Vanadium-Induced Hot Corrosion in Gas Turbines". En ASME Turbo Expo 2001: Power for Land, Sea, and Air. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/2001-gt-0005.
Texto completoResumen
Since the 70’s, nothing substantially new has been published in the Gas Turbine Community about the hot corrosion by vanadium and its inhibition, after the “inhibition orthodoxy” based on the formation of magnesium vanadate, was established. However, the experience acquired since the late 80’s with Heavy Duty Gas Turbines burning ash-forming fuels in Southern China, shows that the combustion of very contaminated fuels does not entail corrosion nor abundant ash-deposit on gas turbines buckets. Analyses of deposits collected from gas turbines fired with these crude oils showed that the ash-deposit contains a large amount of nickel. These new facts led to revisit the role played by nickel and envisage its possible inhibiting action against the vanadium-induced hot corrosion. A thorough review of the literature on the vanadium-induced corrosion have been carried out, and the study of the nickel effects with respect to magnesium effects on the ash deposit have been performed Results show that nickel presents an interesting way to substitute magnesium for the inhibition of vanadium-induced hot corrosion. The advantages of nickel with respect to magnesium are to be efficient at a low Ni/V ratio, to produce less abundant, less adherent ash and to act, to some extent, as a self-cleaning agent for the blades of the turbine.
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SIMON, M. F., H. CHAP y L. DOUSTE-BLAZY. "EFFECTS OF SIN 1 ON PLATELET ACTIVATION INDUCED BY THROMBIN IN HUMAN PLATELETS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643423.
Texto completoResumen
The mechanism of platelet activation is well known. The interaction of agonist such as thrombin, on specific membrane receptor induces phosphatidylinositol-specific phospholipase C activation, with a concomitant formation of two second messengers (from PIP2): inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 is able to induce a rapid discharge of Ca2+ from internal stores and Ca2+ influx through plasma membrane by unidentified Ca2+ channels linked to receptor activation. The increase of cytoplasmic free calcium concentration leads to the activation of the calcium calmodulin dependent myosine light chain kinase which phosphoryla-tes 20 kD proteins (myosine light chain). DAG is a potent activator of protein kinase C, which phosphorylates 40 kD proteins. These different pathways act in synergism.Sin 1 is a platelet aggregating inhibitor. This compound is an active metabolite of molsidomine, which activates platelet guany-late cyclase, inducing a rapid rise in cyclic GMP level. The precise role of cyclic GMP in platelet activation is not yet known. In order to study the mechanism of action of this drug, we tried to determine the effect of Sin 1 on the different steps described above. We measured Ca2+ fluxes and phospholipase C activation in thrombin (0,5 U/ml) stimulated platelets in the presence of different doses of Sin 1 (10™7-10™3M). Serotonin secretion was inhibited by 30 % with Sin 1 (10™4M-10™5m). A parallel inhibition of phospholipase C was detected by measurement of [32P)-PA level. Platelets loaded with Quin 2 and stimulated by thrombin showed a 70 % inhibition of external Ca2+ influx as soon as a concentration of 10™7M of Sin 1 was added. A study on platelet loaded with [45Ca2+) and Quin 2 confirmed these results. On the contrary, discharge of internal Ca2+ store seemed to be unaffected.In conclusion, the major effect of Sin 1 on platelet phospholipase C pathway is an inhibition of Ca2+ influx through plasma membrane. Some further experiments are necessary to shown whether this inhibition is correlated with cyclic GMP formation (the major effect of Sin 1) and try to establish a relation between this inhibition and that exerted on phospholipase C.Sin 1 was a generous gift of Hoechst.
Informes sobre el tema "Latent inhibition"
1
Friedman, Haya, Chris Watkins, Susan Lurie y Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, diciembre de 2009. http://dx.doi.org/10.32747/2009.7613883.bard.
Texto completoResumen
Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.
2
Moran, Nava, Richard Crain y Wolf-Dieter Reiter. Regulation by Light of Plant Potassium Uptake through K Channels: Biochemical, Physiological and Biophysical Study. United States Department of Agriculture, septiembre de 1995. http://dx.doi.org/10.32747/1995.7571356.bard.
Texto completoResumen
The swelling of plant motor cells is regulated by various signals with almost unknown mediators. One of the obligatory steps in the signaling cascade is the activation of K+-influx channels -K+ channels activated by hyperpolarization (KH channels). We thus explored the regulation of these channels in our model system, motor cell protoplasts from Samanea saman, using patch-clamp in the "whole cell" configuration. (a) The most novel finding was that the activity of KH channels in situ varied with the time of the day, in positive correlation with cell swelling: in Extensor cells KH channels were active in the earlier part of the day, while in Flexor cells only during the later part of the day; (b) High internal pH promoted the activity of these channels in Extensor cells, opposite to the behavior of the equivalent channels in guard cells, but in conformity with the predicted behavior of the putative KH channel, cloned from S. saman recently; (c) HIgh external K+ concentration increased (KH channel currents in Flexor cells. BL depolarized the Flexor cells, as detected in cell-attached patch-clamp recording, using KD channels (the K+-efflux channels) as "voltage-sensing devices". Subsequent Red-Light (RL) pulse followed by Darkness, hyperpolarized the cell. We attribute these changes to the inhibition of the H+-pump by BL and its reactivation by RL, as they were abolished by an H+-pump inhibitor. BL increased also the activity KD channels, in a voltage-independent manner - in all probability by an independent signaling pathway. Blue-Light (BL), which stimulates shrinking of Flexor cells, evoked the IP3 signaling cascade (detected directly by IP3 binding assay), known to mobilize cytosolic Ca2+. Nevertheless, cytosolic Ca2+ . did not activate the KD channel in excised, inside-out patches. In this study we established a close functional similarity of the KD channels between Flexor and Extensior cells. Thus the differences in their responses must stem from different links to signaling in both cell types.
3
Blumwald, Eduardo y Avi Sadka. Sugar and Acid Homeostasis in Citrus Fruit. United States Department of Agriculture, enero de 2012. http://dx.doi.org/10.32747/2012.7697109.bard.
Texto completoResumen
Citrus fruit quality standards have been determined empirically, depending on species and on the particular growing regions. In general, the TSS (total soluble solids) to total acidity (TA) ratio determines whether citrus fruit can be marketed. Soluble sugars account for most of the TSS during harvest while TA is determined almost solely by the citric acid content, which reaches levels of 1-5% by weight in many cultivated varieties. Acid and sugar homeostasis in the fruit is critical for the management of existing cultivars, the development of new cultivars, the improvement of pre- and post-harvest strategies and the control of fruit quality and disorders. The current proposal (a continuation of a previous proposal) aimed at: (1) completing the citrus fruit proteome and metabolome, and establish a citrus fruit functional database, (2) further characterization of the control of fruit acidity by studying the regulation of key steps affecting citrate metabolism, and determine the fate of citrate during acid decline stage, and (3) Studying acid and sugar homeostasis in citrus fruits by characterizing transport mechanisms across membranes. These aims were completed as the following: (1) Our initial efforts were aimed at the characterization and identification of citric acid transporters in citrus juice cells. The identification of citrate transporters at the vacuole of the citrus juice cell indicated that the steady-state citrate cytosolic concentration and the action of the cytosolic aconitase were key elements in establishing the pH homeostat in the cell that regulates the metabolic shift towards carbon usage in the fruit during the later stages of fruit development. We focused on the action of aconitase, the enzyme mediating the metabolic use of citric acid in the cells, and identified processes that control carbon fluxes in developing citrus fruits that control the fruit acid load; (2) The regulation of aconitase, catalyzing a key step in citrate metabolism, was further characterized by using two inhibitors, citramalte and oxalomalte. These compounds significantly increased citrate content and reduced the enzyme’s activity. Metabolite profiling and changes of amino-acid metabolizing enzymes in oxalomalate- treated cells suggested that the increase in citrate, caused by aconitase inhibition, induces amino acid synthesis and the GABA shunt, in accordance with the suggested fate of citrate during the acid decline stage in citrus fruit. (3) We have placed a considerable amount of time on the development of a citrus fruit proteome that will serve to identify all of the proteins in the juice cells and will also serve as an aid to the genomics efforts of the citrus research community (validating the annotation of the fruit genes and the different ESTs). Initially, we identified more than 2,500 specific fruit proteins and were able to assign a function to more than 2,100 proteins (Katz et al., 2007). We have now developed a novel Differential Quantitative LC-MS/MS Proteomics Methodology for the identification and quantitation of key biochemical pathways in fruits (Katz et al., 2010) and applied this methodology to identify determinants of key traits for fruit quality (Katz et al., 2011). We built “biosynthesis maps” that will aid in defining key pathways associated with the development of key fruit quality traits. In addition, we constructed iCitrus (http://wiki.bioinformatics.ucdavis.edu/index.php/ICitrus), a “functional database” that is essentially a web interface to a look-up table that allows users to use functional annotations in the web to identify poorly annotated citrus proteins. This resource will serve as a tool for growers and field extension specialists.
4
Splitter, Gary, Zeev Trainin y Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, julio de 1995. http://dx.doi.org/10.32747/1995.7570556.bard.
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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
5
Perl-Treves, Rafael, Rebecca Grumet, Nurit Katzir y Jack E. Staub. Ethylene Mediated Regulation of Sex Expression in Cucumis. United States Department of Agriculture, enero de 2005. http://dx.doi.org/10.32747/2005.7586536.bard.
Texto completoResumen
Monoecious species such as melon and cucumber develop separate male and female (or bisexual) flowers on the same plant individual. They display complex genetic and hormonal regulation of sex patterns along the plant. Ethylene is known to play an important role in promoting femaleness and inhibiting male development, but many questions regarding critical sites of ethylene production versus perception, the relationship between ethylene and the sex determining loci, and the possible differences between melon and cucumber in this respect are still open. The general goal of the project was to elucidate the role of ethylene in determining flower sex in Cucumis species, melon and cucumber. The specific Objectives were: 1. Clone and characterize expression patterns of cucumber genes involved in ethylene biosynthesis and perception. 2. Genetic mapping of cloned genes and markers with respect to sex loci in melon and cucumber. 3. Produce and analyze transgenic melons altered in ethylene production or perception. In the course of the project, some modifications/adjustments were made: under Objective 2 (genetic mapping) a set of new mapping populations had to be developed, to allow better detection of polymorphism. Under Objective 3, cucumber transformation systems became available to us and we included this second model species in our plan. The main findings of our study support the pivotal role of ethylene in cucumber and melon sex determination and later stages of reproductive development. Modifying ethylene production resulted in profound alteration of sex patterns in melon: femaleness increased, and also flower maturation and fruit set were enhanced, resulting in earlier, more concentrated fruit yield in the field. Such effect was previously unknown and could have agronomic value. Our results also demonstrate the great importance of ethylene sensitivity in sex expression. Ethylene perception genes are expressed in sex-related patterns, e.g., gynoecious lines express higher levels of receptor-transcripts, and copper treatments that activate the receptor can increase femaleness. Transgenic cucumbers with increased expression of an ethylene receptor showed enhanced femaleness. Melons that expressed a defective receptor produced fewer hermaphrodite flowers and were insensitive to exogenous ethylene. When the expression of defective receptor was restricted to specific floral whorls, we saw that pistils were not inhibited by the blocked perception at the fourth whorl. Such unexpected findings suggest an indirect effect of ethylene on the affected whorl; it also points at interesting differences between melon and cucumber regarding the mode of action of ethylene. Such effects will require further study. Finally, our project also generated and tested a set of novel genetic tools for finer identification of sex determining genes in the two species and for efficient breeding for these characters. Populations that will allow easier linkage analysis of candidate genes with each sex locus were developed. Moreover, effects of modifier genes on the major femaleness trait were resolved. QTL analysis of femaleness and related developmental traits was conducted, and a comprehensive set of Near Isogenic Lines that differ in specific QTLs were prepared and made available for the private and public research. Marker assisted selection (MAS) of femaleness and fruit yield components was directly compared with phenotypic selection in field trials, and the relative efficiency of MAS was demonstrated. Such level of genetic resolution and such advanced tools were not used before to study these traits, that act as primary yield components to determine economic yields of cucurbits. In addition, this project resulted in the establishment of workable transformation procedures in our laboratories and these can be further utilized to study the function of sex-related genes in detail.
6
Blumwald, Eduardo y Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, octubre de 2007. http://dx.doi.org/10.32747/2007.7587732.bard.
Texto completoResumen
Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.
7
Meir, Shimon, Michael Reid, Cai-Zhong Jiang, Amnon Lers y Sonia Philosoph-Hadas. Molecular Studies of Postharvest Leaf and Flower Abscission. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696523.bard.
Texto completoResumen
Original objectives: Understanding the regulation of abscission competence by exploring the nature and function of auxin-related gene expression changes in the leaf and pedicelAZs of tomato (as a model system), was the main goal of the previously submitted proposal. We proposed to achieve this goal by using microarray GeneChip analysis, to identify potential target genes for functional analysis by virus-induced gene silencing (VIGS). To increase the potential of accomplishing the objectives of the previously submitted proposal, we were asked by BARD to show feasibility for the use of these two modern techniques in our abscission system. Thus, the following new objectives were outlined for the one-year feasibility study: 1.to demonstrate the feasibility of the VIGS system in tomato to perform functional analysis of known abscission-related genes; 2. to demonstrate that by using microarray analysis we can identify target genes for further VIGS functional analysis. Background to the topic: It is a generally accepted model that auxin flux through the abscission zone (AZ) prevents organ abscission by rendering the AZ insensitive to ethylene. However, the molecular mechanisms responsible for acquisition of abscission competence and the way in which the auxin gradient modulates it are still unknown. Understanding this basic stage of the abscission process may provide us with future tools to control abscission for agricultural applications. Based on our previous study, performed to investigate the molecular changes occurring in leaf and stem AZs of MirabillisJalapaL., we have expanded our research to tomato, using genomic approaches that include modern techniques for gene discovery and functional gene characterization. In our one-year feasibility study, the US team has established a useful system for VIGS in tomato, using vectors based on the tobacco rattle virus (TRV), a Lcreporter gene for silencing (involved in regulation of anthocyanin biosynthesis), and the gene of interest. In parallel, the Israeli team has used the newly released Affymetrix Tomato GeneChip to measure gene expression in AZ and non-AZ tissues at various time points after flower removal, when increased sensitivity to ethylene is acquired prior to abscission (at 0-8 h), and during pedicelabscission (at 14 h). In addition, gene expression was measured in the pedicel AZ pretreated with the ethylene action inhibitor, 1-methylcyclopropene (1-MCP) before flower removal, to block any direct effects of ethylene. Major conclusions, solutions and achievements: 1) The feasibility study unequivocally established that VIGS is an ideal tool for testing the function of genes with putative roles in abscission; 2) The newly released Affymetrix Tomato GeneChip was found to be an excellent tool to identify AZ genes possibly involved in regulation and execution of abscission. The VIGS-based study allowed us to show that TAPG, a polygalacturonase specifically associated with the tomato AZ, is a key enzyme in the abscission process. Using the newly released Affymetrix Tomato GeneChip we have identified potential abscission regulatory genes as well as new AZ-specific genes, the expression of which was modified after flower removal. These include: members of the Aux/IAAgene family, ethylene signal transduction-related genes, early and late expressed transcription factors, genes which encode post-translational regulators whose expression was modified specifically in the AZ, and many additional novel AZ-specific genes which were previously not associated with abscission. This microarray analysis allowed us to select an initial set of target genes for further functional analysis by VIGS. Implications: Our success in achieving the two objectives of this feasibility study provides us with a solid basis for further research outlined in the original proposal. This will significantly increase the probability of success of a full 3-year project. Additionally, our feasibility study yielded highly innovative results, as they represent the first direct demonstration of the functional involvement of a TAPG in abscission, and the first microarray analysis of the abscission process. Using these approaches we could identify a large number of genes involved in abscission regulation, initiation and execution, and in auxin-ethylene cross-talk, which are of great importance, and could enable their potential functional analysis by VIGS.
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Meidan, Rina y Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, marzo de 1995. http://dx.doi.org/10.32747/1995.7604935.bard.
Texto completoResumen
The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.