Relevant bibliographies by topics / Platelet activating factor

Academic literature on the topic 'Platelet activating factor'

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Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Platelet activating factor"

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Perry, Seth W., Jason A. Hamilton, Larry W. Tjoelker, Ghassan Dbaibo, Kirk A. Dzenko, Leon G. Epstein, Yusuf Hannun, J. Steven Whittaker, Stephen Dewhurst, and Harris A. Gelbard. "Platelet-activating Factor Receptor Activation." Journal of Biological Chemistry 273, no. 28 (July 10, 1998): 17660–64. http://dx.doi.org/10.1074/jbc.273.28.17660.

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Zhou, W., M. A. Javors, and M. S. Olson. "Platelet-activating factor as an intercellular signal in neutrophil-dependent platelet activation." Journal of Immunology 149, no. 5 (September 1, 1992): 1763–69. http://dx.doi.org/10.4049/jimmunol.149.5.1763.

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Abstract The role of platelet-activating factor (PAF) in heterotypic cell to cell interactions in a rabbit neutrophil-platelet mixture model was investigated. Platelets were exposed to each of three chemotactic agonists: PAF, leukotriene B4 (LTB4), or FMLP. Only PAF stimulated aggregation, [3H]serotonin secretion, and cytosolic Ca2+ mobilization in platelets alone. However, platelets were stimulated by LTB4 and FMLP in the presence of neutrophils. This neutrophil-dependent platelet activation was blocked by pretreatment of platelets with PAF receptor antagonists, and was prevented by desensitization of platelets to PAF. Furthermore, the time-course of platelet activation showed a positive correlation with PAF production by neutrophils stimulated with either LTB4 or FMLP. The PAF-mediated neutrophil-platelet interaction was dependent on direct cell to cell contact, as demonstrated by experiments in which the majority of newly formed PAF was neutrophil associated (rather than released). Platelet activation did not occur when the neutrophil-platelet mixture was not stirred, minimizing cell to cell contact, or when platelets were challenged with a cell-free supernatant prepared from neutrophils activated with LTB4 or FMLP. Finally, the neutrophil-platelet interaction was abolished by SC-49992, a peptidomimetic of the fibrinogen binding sequence Arg-Gly-Asp-Phe, indicating a Arg-Gly-Asp-specific recognition mechanism. Our results demonstrate that neutrophil-generated PAF plays a crucial role in neutrophil-dependent platelet activation in this model system. This type of intercellular signaling event may be important in certain inflammatory or thrombotic processes.
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KAWASAKI, Tomio, and Jun-ichi KAMBAYASHI. "Platelet-activating Factor." Japanese Journal of Thrombosis and Hemostasis 2, no. 4 (1991): 274–85. http://dx.doi.org/10.2491/jjsth.2.274.

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Kingsnorth, A. N. "Platelet-Activating Factor." Scandinavian Journal of Gastroenterology 31, sup219 (January 1996): 28–31. http://dx.doi.org/10.3109/00365529609104996.

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McCORMACK, DAVID G., PETER J. BARNES, and TIMOTHY W. EVANS. "Platelet-activating factor." Critical Care Medicine 18, no. 12 (December 1990): 1398–402. http://dx.doi.org/10.1097/00003246-199012000-00018.

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Martin, John. "PLATELET-ACTIVATING FACTOR." Lancet 332, no. 8626-8627 (December 1988): 1486. http://dx.doi.org/10.1016/s0140-6736(88)90956-7.

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Humphreys, Randy F. "PLATELET ACTIVATING FACTOR." Southern Medical Journal 83, Supplement (September 1990): 2S—2. http://dx.doi.org/10.1097/00007611-199009001-00004.

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Prescott, S. M., G. A. Zimmerman, and T. M. McIntyre. "Platelet-activating factor." Journal of Biological Chemistry 265, no. 29 (October 1990): 17381–84. http://dx.doi.org/10.1016/s0021-9258(18)38167-5.

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Welch, Emily J., Ram P. Naikawadi, Zhenyu Li, Phoebe Lin, Satoshi Ishii, Takao Shimizu, Chinnaswamy Tiruppathi, Xiaoping Du, Papasani V. Subbaiah, and Richard D. Ye. "Opposing Effects of Platelet-Activating Factor and Lyso-Platelet-Activating Factor on Neutrophil and Platelet Activation." Molecular Pharmacology 75, no. 1 (October 17, 2008): 227–34. http://dx.doi.org/10.1124/mol.108.051003.

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Lomazova, K. D., A. M. Polyakova, O. S. Astrina, and D. B. Tsukerman. "Platelet activating factor and endotoxin-induced platelet activation." Bulletin of Experimental Biology and Medicine 107, no. 5 (May 1989): 611–14. http://dx.doi.org/10.1007/bf00841762.

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Dissertations / Theses on the topic "Platelet activating factor"

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Scarlett, Julie Anne. "Platelet activating factor in the horse." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387750.

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Murphy, Christine Therese. "Mechanisms of stimulus-response coupling in platelet-activating factor stimulated platelets." Thesis, University of Bath, 1992. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304999.

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DENTAN, CHRISTINE. "Platelet-activating factor (paf), acetylhydrolase et atherosclerose." Paris 6, 1996. http://www.theses.fr/1996PA066772.

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L'atherosclerose est une pathologie des vaisseaux, multifactorielle, qui a un caractere immuno-inflammatoire chronique. Or, de plus en plus de donnees argumentent le role pro-atherogene et pro-thrombogene d'un puissant mediateur glycerophospholipidique, le platelet-activating factor (paf), qui est degrade specifiquement par l'acetylhydrolase. Cette hypothese est etayee par nos travaux qui ont mis en evidence la formation du paf dans un modele de cellules spumeuses, riches en esters de cholesterol, stimulees par phagocytose. Ces cellules, qui representent la principale composante cellulaire du noyau lipidique des plaques d'atherome, pourraient donc constituer in vivo une source importante de paf. Nous avons montre egalement que l'acetylhydrolase regule la quantite du paf present dans ces cellules activees. Par la suite, nous avons focalise nos etudes sur cette enzyme. Nous avons d'abord caracterise un nouvel inhibiteur de l'acetylhydrolase : le 4-2-aminoethyl benzenesulfonyl fluoride (pefabloc) qui se fixe sur le groupement serine du site actif enzymatique. Nous avons ensuite mis en evidence, chez des sujets normolipidemiques, une heterogeneite de la distribution de l'activite acetylhydrolase au sein des lipoproteines plasmatiques. En effet, parmi les lipoproteines de faible et haute densite (ldl et hdl), les particules les plus denses et les plus petites (ldl-5 et vhdl-1) possedent une grande proportion de l'activite acetylhydrolase plasmatique au sein desquelles celle-ci presente des proprietes catalytiques distinctes. De plus, les ldl denses seraient notamment le vecteur principal de l'acetylhydrolase secretee par les monocytes humains adherents. Ainsi, puisque l'entree des lipoproteines plasmatiques dans l'espace sous-endothelial serait inversement proportionnelle a la taille des particules, les ldl denses et les vhdl-1 pourraient jouer un role-cle anti-inflammatoire au sein de l'intima arterielle. Cependant, par la suite, nos travaux ont montre que l'acetylhydrolase associee aux ldl est totalement inactivee lorsque les particules sont oxydees. De meme, l'activite anti-coagulante de l'inhibiteur du facteur tissulaire (tfpi) est inhibee dans les ldl oxydees. Nous avons donc demontre une nouvelle propriete atherogene des ldl oxydees qui, in vivo au sein des lesions atherosclerotiques, ne seraient notamment plus capables d'inhiber les effets atherogenes du paf ainsi que ceux des phosphatidylcholines oxydees, egalement substrats et presentes dans les ldl oxydees. Ces travaux apportent des donnees nouvelles sur le metabolisme du paf ; ce dernier interviendrait certainement dans la constitution et l'evolution des lesions atherosclerotiques ainsi que dans les evenements menant a la rupture de la plaque et a la thrombose. L'acetylhydrolase jouerait un role-cle dans la regulation des effets inflammatoires du paf et les etudes a venir devront preciser les fonctions de cette enzyme in vivo au sein de l'intima arterielle.
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Bonin, Fanny. "Cytoprotective effects of intracellular platelet activating factor acetylhydrolases." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26529.

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Platelet activating factor (PAF) is a biologically active phospholipid implicated in the developmental brain disorder Miller-Dieker Syndrome (MDS) and purported to be a primary mediator of cell death in HIV-dementia, ischemia, and epilepsy. As part of my honour's thesis, I demonstrated that PAF can elicit cell death independently of its G-protein coupled receptor (PAFR) in PC12 cells. In my M.Sc. research, I have sought to identify how PAF-mediated cell death is regulated in PC12 cells. PAF is inactivated in brain by two intracellular PAF-acetylhydrolases (PAF-AHs): PAF-AH I and PAF-AH II. PAF-AH I is a trimeric complex composed of two catalytic subunits (alpha1 and alpha2) and one regulatory subunit (beta). Mutations in the Lis1 gene, coding for the beta subunit of PAF-AH I, are the genetic determinant of MDS. However, it is not clear whether these mutations impact on PAF-AH I enzymatic activity in MDS. Furthermore, it is not known whether cytosolic PAF-AH activity regulates the kinetics of neuronal loss following pathophysiological challenge. To begin to address these questions, I sought to identify an in vitro model system suitable for study of PAF-AH activity.* (Abstract shortened by UMI.) *This dissertation is a compound document (contains both a paper copy and a CD as part of the dissertation). The CD requires the following system requirements: QuickTime.
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Gomez, Jorge. "Characterization and regulation of platelet activating factor receptors." Diss., The University of Arizona, 1990. http://hdl.handle.net/10150/185248.

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Platelet activating factor (PAF) is a potent mediator in a variety of inflammatory events. Determining whether PAF participates in the bronchial hyperresponsiveness characteristic of asthma is the long term obj ecti ve for which the studies described here represent an initial step. PAF is a potent agonist that causes contraction of guinea pig peripheral lung strips. To determine if specific receptor sites for PAF could be demonstrated in guinea pig lung membranes (GPLM), direct radioligand binding studies were performed with [³H]C₁₆-PAF (l-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) and the PAF antagonists [³H]WEB 2086 and [³H]RP52770. Binding parameters were compared to those from rabbit platelet membranes (RPM). These studies demonstrated specific binding sites for [³H] C₁₆-PAF of high affinity in GPLM with a Kd of 3 nM,• and in RPM with a K(d) of 1 nM. [³H]C₁₆-PAF identified receptor densities in GPLM of 200 fmol/mg protein and in RPM of 1922 fmol/mg protein. In both tissue preparations binding of inhibited to the same maximum degree by C₁₆-PAF, C₁₈-PAF, WEB 2086, and RP52770, all with pseudo-Hill coefficients of unity. The PAF antagonist [³H]WEB 2086 identified a receptor density similar to that of [³H]C₁₆-PAF. The binding of [³H]WEB 2086 was inhibited to the same degree by C₁₆-PAF, C₁₈-PAF, WEB 2086 and RP52770, indicating WEB 2086 and PAF interact at the same receptor sites in both GPLM and RPM. Although inhibition curves for antagonists yielded pseudo-Hill coefficients of unity, inhibition by agonists yielded shallow inhibition curves suggesting two types or states for the PAF receptor. The PAF antagonist [³H]RP52770 was found to be an unsuitable ligand because it labeled a much larger density of binding sites (1200 fmol/mg protein in GPLM, and 10105 fmol/mg protein in RPM) and was inhibited to little or no extent by C₁₆-PAF, C₁₈-PAF, WEB 2086 or lyso-C₁₆-PAF . studies of signal transduction suggest that the binding affinity of the agonists C₁₆-PAF and C₁₈-PAF (but not for the antagonist WEB 2086) is regulated by GTPgamroa- S and Na⁺, providing indirect evidence that the PAF receptor in both tissue preparations is coupled to a guanine nucleotide regulatory protein. However, agonist binding retained shallow inhibition curves indicating heterogeneity of sites with respect to this regulation. Binding affinity for the agonists was not affected by cholera toxin or pertussis toxin. These results indicate PAF receptors in lung tissue could not be distinguished from those in RPM, however, both tissues appear to show heterogeneity of binding indicating the existence of receptor subtypes or states.
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Vanags, Daina M. "Adrenergic and serotonergic potentiation of platelet aggregation /." Title page, summary and contents only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phv217.pdf.

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Kabbani, Nazir. "Chemical-genetic profiling of platelet-activating factor in yeast." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28189.

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The basic biological processes between the yeast Saccharomyces cerevisiae and mammals are highly conserved. Yeast posses many genes that are implicated in human diseases and have been successfully used as a model for the study of neurodegeneration. Platelet-Activating Factor (C16:0 PAF) causes neuronal cell death independent of its receptor and has been implicated in Alzheimer's disease. I hypothesized that yeast could be used as a model system for deciphering PAF receptor-independent signalling and have utilized genome-wide chemical genomic screening in yeast to further characterize the molecular mechanism of PAF toxicity. Two complementary screens implicate PAF in many cellular processes, some of which parallel results obtained in mammalian studies. I have found that PAF challenge is cytotoxic, delays cell cycle progression, and affects actin stability leading to spindle misorientation and bi-nucleate mother cells.
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Rowe, Anna-Louise. "The role of platelet-activating factor in necrotising enterocolitis." Thesis, University of Birmingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434713.

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Göggel, Rolf. "The mechanisms of platelet activating factor induced alterations in lung functions /." Konstanz : Hartung-Gorre, 2002. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=009757517&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Bosnic, Anthony Martin. "Human antibody responses to a chlamydia-secreted protease factor : a thesis /." San Antonio : UTHSC, 2005. http://learningobjects.library.uthscsa.edu/cdm4/item%5Fviewer.php?CISOROOT=/theses&CISOPTR=14&REC=5.

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Books on the topic "Platelet activating factor"

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Fred, Snyder, ed. Platelet-activating factor and related lipid mediators. New York: Plenum Press, 1987.

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M, Winslow C., and Lee M. L, eds. New horizons in platelet activating factor research. Chichester [West Sussex]: Wiley, 1987.

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Snyder, Fred, ed. Platelet-Activating Factor and Related Lipid Mediators. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5284-6.

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Nigam, Santosh, Gert Kunkel, and Stephen M. Prescott, eds. Platelet-Activating Factor and Related Lipid Mediators 2. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8.

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S, Authi Kalwant, Watson Steve P, Kakkar V. V, and International Symposium on Mechanisms of Platelet Activation and Control, (1992 : London, England), eds. Mechanisms of platelet activation and control. New York: Plenum Press, 1993.

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Pharmacy), Symposium on Problems on PAF (11th 1987 Tohoku College of. Trends in pharmacological research on platelet activating factor (PAF) in Japan: Proceedings of the Symposium on Problems on PAF held at the Tohoku College of Pharmacy, Sendai, Japan, September 19th, 1987. Tokyo: Ishiyaku EuroAmerica, 1988.

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Kucey, Daryl Stanton. Modulation of macrophage procoagulant activity by platelet activating factor. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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1943-, O'Flaherty Joseph T., Ramwell Peter W, and International Business Communications Inc, eds. PAF antagonists: New developments for clinical application. Woodlands, Tex: Portfolio Pub. Co., 1990.

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1946-, Stute W., and Seminar on Empirical Processes (1985 : Düsseldorf, Germany), eds. Seminar on Empirical Processes. Basel: Birkhäuser Verlag, 1987.

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Fondation IPSEN pour la recherche thérapeutique. Meeting. The role of platelet-activating factor in immune disorders: Proceedings of the Meeting of the "Fondation IPSEN pour la recherche thérapeutique", Paris, June 25-26, 1987 (part II). Edited by Braquet P. Basel: Karger, 1988.

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Book chapters on the topic "Platelet activating factor"

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Dent, Gordon. "Platelet-Activating Factor." In Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction, 227–70. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7504-2_7.

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Schwab, Manfred. "Platelet-Activating-Factor." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4609-2.

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Lopes-Martins, Rodrigo A. B., Claudia V. Araújo, Vanessa Estato, Sheila Moreira, Renato S. B. Cordeiro, and Eduardo V. Tibiriçá. "Platelet-Activating Factor." In Advances in Experimental Medicine and Biology, 223–30. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_36.

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Salajegheh, Ali. "Platelet-Activating Factor." In Angiogenesis in Health, Disease and Malignancy, 253–60. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_39.

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Poeze, M., W. A. Buurman, G. Ramsay, and J. W. M. Greve. "Platelet-Activating Factor." In Multiple Organ Failure, 204–13. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4612-1222-5_22.

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Shukla, Shivendra D. "Platelet Activating Factor and Platelets." In Handbook of Platelet Physiology and Pharmacology, 120–41. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5049-5_6.

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Shimizu, Takao, Hiroyuki Mutoh, and Shigeaki Kato. "Platelet-Activating Factor Receptor." In Advances in Experimental Medicine and Biology, 79–84. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_14.

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Marrache, A. Marilise, Fernand Gobeil, Sylvie G. Bernier, Jana Stankova, Marek Rola-Pleszezynski, Sanaa Choufani, Ghassan Bkaily, et al. "Platelet Activating Factor Receptors." In Advances in Experimental Medicine and Biology, 161–64. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_33.

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Marathe, Gopal Kedihithlu, Shancy Petsel Jacob, Mosale Seetharam Sumanth, Chikkamenahalli Lakshminarayana Lakshmikanth, Kandahalli Venkataranganayaka Abhilash, and Vyala Hanumanthareddy Chaithra. "Platelet-Activating Factor Acetylhydrolase (Pafah)." In Encyclopedia of Signaling Molecules, 4069–77. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101737.

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Benveniste, J. "Paf-acether (Platelet-activating Factor)." In New Trends in Allergy II, 117–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71316-3_13.

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Conference papers on the topic "Platelet activating factor"

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Struk, A., A. Prins, M. C. L. Schaap, J. W. ten Cate, and H. van den Bosch. "SYNTHESIS OF PLATELET ACTIVATING FACTOR BY HUMAN BLOOD PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643486.

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Synthesis of platelet activating factor (PAF) by human blood platelets is a controversial issue. Whereas some groups have reported the synthesis, induced by thrombin, collagen or Ca2--ionophore Azsio?, others were unable to obtain for instance the thrombin-induced PAF synthesis. Also, synthesis of only up to 6 pMoles PAF/10 platelets has been reported, but leucocytes may synthesize up to 6000 pMoles PAF/10 cells. Only an 0.1% leucocyte contamination would thereby explain the “ platelet PAF synthesis” . We therefore optimized the PAF synthesis by human blood platelets and leucocytes, induced by thrombin and A23i07. As platelets have been reported to show an increased PAF synthesis upon treatment with phenylmethylsulfonylfluoride (PMSF), this was also investigated.Leucocytes were optimally stimulated with 10 uM Azale? (mean ± SD 4678 ± 2033, range 1698-7058 pMoles PAF/10 cells, n=6), but could not be stimulated by thrombin. PMSF treatment itself induced PAF synthesis by these cells, but this was not influenced by thrombin or A23ia7.Platelet suspensions, with <0.005% leucocyte contamination as determined by light microscopy after Jenner-Giemsa staining, could synthesize PAF when treated with PMSF and stimulated with 2.5 IU/ml thrombin (mean ± SD 0.6 ± 0.3, range 0.3-1.0 pMoles PAF/10 platelets, n=6), but in these suspensions A23io7-induced synthesis could not be demonstrated.The results indicate that synthesis of PAF by human blood platelets is not due to contaminating leucocytes, if thrombin is used as the stimulus. These results were confirmed by 3H-acetate uptake experiments.
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Del Maschio, A., M. Albors, F. Bucchi, M. Tomasiak, V. Bertele, C. Cerletti, and G. de Gaetano. "HUMAN POLYMORPHONUCLEAR LEUKOCYTE ACTIVATION INDUCED BY PLATELET ACTIVATING FACTOR (PAF)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643482.

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Human polymorphonuclear leukocytes (PMNs) loaded with the photoprotein Aequorin, were exposed to PAF in the presence of extracellular Ca2+ (1 mM). PMNs aggregation measured In the “Platelet Ionized Calcium Aggregometer” (P.I.C.A.) was dependent on the concentration of the stimulus. Ca2+ cytoplasmatic increase was monitored in parallel at concentrations of PAF which did not modify cellular integrity (10-7-10-5M). The intracellular Ca2+ flux (up to 19±3 µM) triggered by PAF was also concentration-dependent. In order to establish the role played by this intracellular messenger, we studied some cellular responses possibly related to Ca2+ mobilization: enzymatic release, oxygen radicals production, and arachidonic acid metabolism. PAF induced release of both lysozyme , and β-glucuronldase (15% to 20% of the total enzyme content at the maximal concentration). However PAF (10-712-10“Vl) stimulated the production of only small amounts of oxygen radicals as compared to Phorbol Myristate Acetate (PMA). Leukotriene B4 (LTB4), the main arachidonic acid metabolite in PMNs and the products of its catabolism (20-OH and 20-C00H LTBO were assayed by two different technics (HPLC and RIA) in the same cellular suspensions. PAF (10-4 M)-stimulated PMNs (0.5-2xl07 cells/ml) did not produce any detectable amount of these arachidonic acid metabolites. In contrast, calcium ionophore A 23187 (2 μM)-stimulated PMNs (in the same range of cellular concentration) produce up to 170 ng/ml of LTB4. In conclusion, cytoplasmatic Ca2+ increase in PAF-stimulated PMNs was not accompanied either by oxygen radicals production or by activation of arachidonic acid metabolism catalyzed by 5-1 ipoxygenase.
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Matsuno, K., F. Katabami, M. Koyama, K. Abe, K. Sakurada, T. Miyazaki, S. Ozasa, H. Saitoh, I. Maekawa, and H. Matsumiya. "PLATELET-ACTIVATING FACTOR (PAF)-INDUCED INTRACELLULAR Ca MOBILIZATION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643483.

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PAF-induced intracellular Ca2+ mobilization and platelet aggregation were investigated in human platelets. Cytosolic free Ca2+ concentration ([Ca2+]cyt) was measured by using fluorescent 45Ca2+ probe quin2 and fura-2, and photoprotein aequorin. Ca2+ uptake was measured after stimulation by PAF. Platelet aggregation was studied by recording the change in light transmission with platelet rich plasma (PRP) or washed platelet suspension (WPS).These three Ca2+ -indicators could determine the elevation of [Ca2+ ]cyt that was stimulated by PAF in the presence of extra- cellular Ca2+ (quin2 method: 98.2nM to 289.7nM; fura-2 method: 102.OnM to 351.4nM; aequorin method: 4.1μM to 8.2μM). In the absence of extracellular Ca2+ , however, little elevation of [Ca2+ ]cyt was detected after stimulation by PAF. PAF could evoke the transient Ca2+ uptake.New PAF specific antagonist, ONO-6240 inhibited PAF-induced platelet aggregation at a concentration from lμM dose-dependently, whereas it didn’t inhibit collagen- and thrombin-induced platelet aggregation at a concentration of lOOyM. ONO-6240 inhibited PAF- induced increase in [Ca2+ ]cyt in a dose-dependent manner as deter mined by these Ca2+ -indicators, as well as platelet aggregation.These results suggest the increase in [Ca2+ ]cyt is responsible for platelet aggregation induced by PAF, and the increased Ca2+ is derived from external Ca2+ influx chiefly.
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Muntean, W., and B. Leschnik. "FACTOR VIII MEDIATES BINDING OF FACTOR IX TO STIMULATED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644074.

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In previous work we have shown that factor VII! binds to phospholipids of the membrane of stimulated platelets and that von Willebrand factor is not required for binding of factor VIII to platelets. Since factor VIII is a cofactor in the activation of factor X by factor IX, we investigated whether factor VIII enhances binding of factor IX to the platelet surface.Factor VIII and factor IX were purified by immunoadsorbent chromatography using specific rabbit antibodies. Washed human platelets (250/nl final concentration) stimulated by human thrombin and collagen were incubated with barbiturate buffer, or with purified factor IX (1 U/ml final concentration), or with factor IX (1 U/ml) in the presence of factor VIII (1 U/ml). Washed and stimulated platelets were also incubated with factor VIII and IX as above in the presence of different amounts of CaCl2. Platelets were then washed again and lysed by sonication. Factor VIII:Ag (immunoradiometric assay) and factor IX:Ag (ELISA) were measured in the platelet lysate prior to and after incubation of the lysate with phospholipase C.Platelet bound IX:Ag was significantly higher after incubation of stimulated platelets with factor IX in the presence of factor VIII than after incubation of platelets with buffer or with factor IX alone. CaCl2 proved to be essential for binding of factor IX to platelets even in the presence of factor VIII, but CaCl2 was not required for binding of factor VIII to platelets. Measurable VIII :Ag and IX:Ag increased significantly after incubation of the platelet lysate with phospholipase C.Our data suggest that factor VIII mediates binding of factor IX to phospholipids or receptors containing phospholipids on the membrane of stimulated platelets and thereby contributes to the assembly of the factor X activating complex on the platelet surface.
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Sturk, A., M. C. L. Schaap, A. Prins Heymans, J. W. ten Cate, R. J. A. Wanders, H. S. A. Heymans, R. B. H. Schutgens, and H. van den Bosch. "SEVERELY IMPAIRED SYNTHESIS OF PLATELET ACTIVATING FACTOR IN CHONDRO DYSPLASIA PUNCTATA RHIZOMELIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642883.

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The first steps of the de novo synthesis of alkoxyether lipids, like plasmalogens and platelet activating factor (PAF) are localized in the peroxisome. We have previously reported the severely impaired PAF synthesis in Zellweger patients. These patients lack cytochemically detectable peroxisomes, and have a severely impaired alkoxyether lipid synthesis. However, chondro dysplasia punctata (CDP) patients have also been shown to have an impaired alkoxyether lipid synthesis. We therefore investigated PAF synthesis in CDP patients.Platelets and leucocytes were isolated from 3 CDP patients. Leucocytes from normal controls produced 4678 ± 2033 pMoles PAF/10 cells (n=6, range 1698-7058) when optimally stimulated with Ca2+-ionophore A23187. Normal control platelets produced 0.6 ± 0.3 pMoles PAF/10 cells (n=6, range 0.3-1.0) when optimally stimulated with thrombin. PAF synthesis by the leucocytes of the patients was severely reduced, but detectable. Leucocytes from patient 1, 2 and 3 synthesized 9, 660 and 325 pMoles PAF/10 cells respectively. Platelets from the patients 1, 2 and 3 synthesized 0.1, 0.2 and 0.2 pMoles PAF/10 cells respectively.Platelet aggregation, induced by ADP, PAF, or thrombin (also in the presence of inhibitors of the first and second pathway of platelet activation) was normal.We conclude that PAF synthesis is severely impaired in leucocytes and reduced in platelets from CDP patients. The residual platelet PAF synthesis may suffice to warrant normal platelet functioning.
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Chung, Chi-Li, Mei-Chuan Chen, Jie-Heng Tsai, and Cheng-Ying Hsieh. "Profibrotic implication of platelet-activating factor in tuberculous pleural effusion." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3356.

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7

Miyashita, L., G. Foley, N. M. Liu, E. McCamlie, M. Idris, J. M. Grigg, and A. On behalf of the Breathing Together. "Airway Platelet-Activating Factor Receptor Expression Is Increased in Neonates." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1893.

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COEFFIER, e., D. Delautier, J.-P. Le Couedic, M. Chinqnard, and J. Benveniste. "ACTIVATED HUMAN PLATELETS AND NEUTROPHILS COOPERATE FOR THE FORMATION OF PAF-ACETHER (PLATELET-ACTIVATING FACTOR)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642881.

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Interactions between platelets and neutrophils have been reported for the production of several mediators of inflammation such as hydrogen peroxides or leukotrienes. Another potential mediator of thrombosis and inflammation is paf-acether which is synthesized by activated platelets and neutrophils.Since platelets form and release large amounts of the paf-acether precursor lyso paf-acether, platelets and neutrophils cooperation for paf-acether biosynthesis was investigated. Purified human neutrophils (4 × 106 /ml) stimulated by opsonized zymosan (ZC, 1 mg/ml) formed 4.5 ± 2.5 ng/ml paf-acether. Human washed platelets (3 × 108 /ml) stimulated with thrombin (l IU/ml) formed 0.60 ± 0.43 ng/ml paf-acether. Platelets and neutrophils, incubated together and both stimulated by their specific agonist, formed more than twice as much paf-acether as platelets and neutrophils separately (10.90 ± 4.25 ng/ml, n = 6, p < 0.001). The formation of lyso paf-acether and the release of lysozyme and LDH were unchanged under the cooperation conditions. The formation of paf-acether almost doubled(10.24 ± 8.79 ng/ml paf-acether versus 5.30 ± 5.23, p < 0.05, n = 4) when ZC-stimulated neutrophils were incubated with supernatants from thrombin-stimulated platelets as well as with synthetic lyso paf-acether. Extracted and purified lyso paf-acether from thrombin-stimulated platelets led to increase of biosynthesis of paf-acether by neutrophils (13.86 ± 3.92 ng/ml paf-acether versus 5.76 ± 0.66, p < 0.05, n = 3). These results indicate that cooperation between platelets and neutrophils is likely to occur via acetylation by neutrophils of excess lyso paf-acether originating from platelets. Thus neutrophils can increase their biosynthesis of paf-acether by acetylating lyso paf-acether either synthetic or released from other cells.
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Oura, Y., N. Sakiyama, R. Ueshima, M. Higuchi, E. Kakishitha, and K. Nagai. "Effect of Platelet Activating Factor(PAF) on the collagen induced platelet aggregation in whole blood." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643481.

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Studies of platelet aggregation are generally performed in p1ate1et-rich plasma(PRP) by the transmittance method. Recently, impedance aggregometry has been introduced which shows the platelet aggregability in whole blood. We compared the impedance aggregometry in whole blood with the transmittance method in PRP, with regard to collagen induced platelet aggregation. The aggregation rate in whole blood increased with increasing concentration of collagen, but remained unchanged in PRP. The factors which influence the platelet aggregation rate in whole blood were studied. CV-3988, that is the specific antagonist of PAF, acetylsalicylic acid (ASA) and phosphocreatine / creatine phosphokinase (CP/CPK) were used in order to evaluate the contribution of PAF, thromboxane and ADP in whole blood. CV-3988 dose-dependently inhibited platelet aggregation induced by collagen in whole blood, but did not inhibit the aggregation in PRP. ASA(10mM) inhibited the aggregation in whole blood incompletely too, but completely in PRP. And the inhibition of CP/CPK(CP/CPK : 1.5mM/50U/ml) was very weak in whole blood compared to that of other antagonists. The inhibitory effect of CV-3988 was investigated on the collagen induced platelet aggregation in whole blood which was pretreated with ASA ( 1 OmM ) and CP/CPK (1.5mM/50U/ml), resulting in a collagen induced aggregation in whole blood that was not completely inhibited. We conclude that there are some other different factors, which influence platelet aggregation in whole blood, in addition to thromboxane, ADP and PAF.
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Mushayakarara, E. C., and H. H. Mantsch. "An IR Spectroscopic Characterization Of The Blood Component Platelet Activating Factor." In 1985 International Conference on Fourier and Computerized Infrared Spectroscopy, edited by David G. Cameron and Jeannette G. Grasselli. SPIE, 1985. http://dx.doi.org/10.1117/12.970751.

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Reports on the topic "Platelet activating factor"

1

Snyder, F. Regional Neonatal Associates for cooperative study of platelet-activating factor (PAF). Summary report. Office of Scientific and Technical Information (OSTI), November 1992. http://dx.doi.org/10.2172/28403.

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