Relevant bibliographies by topics / Platelet activating factor structure analogs

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Platelet activating factor structure analogs'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Platelet activating factor structure analogs"

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Takatani, Muneo, Yoshio Yoshioka, Akihiro Tasaka, et al. "Platelet activating factor (PAF) antagonists: synthesis and structure-activity studies of novel PAF analogs modified in the phosphorylcholine moiety." Journal of Medicinal Chemistry 32, no. 1 (1989): 56–64. http://dx.doi.org/10.1021/jm00121a012.

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Zhang, Chunxiang, Daniel L. Baker, Satoshi Yasuda та ін. "Lysophosphatidic Acid Induces Neointima Formation Through PPARγ Activation". Journal of Experimental Medicine 199, № 6 (2004): 763–74. http://dx.doi.org/10.1084/jem.20031619.

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Neointimal lesions are characterized by accumulation of cells within the arterial wall and are a prelude to atherosclerotic disease. Here we report that a brief exposure to either alkyl ether analogs of the growth factor–like phospholipid lysophosphatidic acid (LPA), products generated during the oxidative modification of low density lipoprotein, or to unsaturated acyl forms of LPA induce progressive formation of neointima in vivo in a rat carotid artery model. This effect is completely inhibited by the peroxisome proliferator-activated receptor (PPAR)γ antagonist GW9662 and mimicked by PPARγ
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Hadváry, Paul, and Thomas Weller. "Conformationally Restricted Analogs of Platelet-Activating Factor (PAF)." Helvetica Chimica Acta 69, no. 8 (1986): 1862–71. http://dx.doi.org/10.1002/hlca.19860690814.

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Wissner, A., M. L. Carroll, K. E. Green, et al. "Analogs of platelet activating factor. 6. Mono- and bis-aryl phosphate antagonists of platelet activating factor." Journal of Medicinal Chemistry 35, no. 9 (1992): 1650–62. http://dx.doi.org/10.1021/jm00087a023.

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Nicotra, Francesco, Luigi Panza, Giovanni Russo, and Luca Zucchelli. "Chemoenzymic approach to carbohydrate-derived analogs of platelet-activating factor." Journal of Organic Chemistry 57, no. 7 (1992): 2154–58. http://dx.doi.org/10.1021/jo00033a043.

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Yanoshita, Ryohei, Ichiro Kudo, Koichi Ikizawa, et al. "Hydrolysis of Platelet Activating Factor and Its Methylated Analogs by Acetylhydrolases1." Journal of Biochemistry 103, no. 5 (1988): 815–19. http://dx.doi.org/10.1093/oxfordjournals.jbchem.a122352.

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Wissner, A., R. E. Schaub, P. E. Sum, C. A. Kohler, and B. M. Goldstein. "Analogs of platelet activating factor. 4. Some modifications of the phosphocholine moiety." Journal of Medicinal Chemistry 29, no. 3 (1986): 328–33. http://dx.doi.org/10.1021/jm00153a005.

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Snyder, Fred. "Platelet-activating factor and its analogs: metabolic pathways and related intracellular processes." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1254, no. 3 (1995): 231–49. http://dx.doi.org/10.1016/0005-2760(94)00192-2.

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Samanta, Uttamkumar, and Brian J. Bahnson. "Crystal Structure of Human Plasma Platelet-activating Factor Acetylhydrolase." Journal of Biological Chemistry 283, no. 46 (2008): 31617–24. http://dx.doi.org/10.1074/jbc.m804750200.

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Derewenda, Z. S., and U. Derewenda. "The structure and function of platelet-activating factor acetylhydrolases." Cellular and Molecular Life Sciences (CMLS) 54, no. 5 (1998): 446–55. http://dx.doi.org/10.1007/s000180050172.

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Dissertations / Theses on the topic "Platelet activating factor structure analogs"

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Riaz, Muhammad Suleman. "Investigating the effects of host factors (proteins and non-proteins) on mycobacteria." Thesis, Brunel University, 2018. http://bura.brunel.ac.uk/handle/2438/16060.

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Mycobacterium tuberculosis (M.tb), the causative agent of tuberculosis, is one of the leading causes of death due to a single infectious agent and results in more than 1 million human deaths every year. M.tb infection of the host initiates a local inflammatory response, resulting in the migration of a number of host plasma protein and non-protein factors to the site of infection. In addition, some of these factors are also produced locally at the site of infection. It is envisaged that these host factors are likely to come in direct contact with M.tb and immune cells and may modulate the outco
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Parent, Jean-Luc. "Étude de la relation structure/fonction du récepteur du platelet-activating factor humain par mutagénèse dirigée." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21859.pdf.

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Parent, Jean-Luc. "Étude de la relation structure/fonction du récepteur du "platelet-activating factor" humain par mutagenèse dirigée." Sherbrooke : Université de Sherbrooke, 1997.

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Parent, Jean-Luc. "Étude de la relation structure/fonction du récepteur du "platelet-activating factor" humain par mutagenèse dirigée." Thèse, Université de Sherbrooke, 1996. http://savoirs.usherbrooke.ca/handle/11143/4087.

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Le "platelet-activating factor" (PAF) est un puissant médiateur phospholipidique produisant un large éventail de réponses biologiques. Le récepteur du PAF (PAFR) fait partie de la superfamille des récepteurs couples aux protéines G (RCPGs). Ce récepteur lie le PAF avec haute affinité et est couplé à de multiples voies de signalisation menant à des réponses biologiques pouvant être inhibées par une variété d'antagonistes du PAF structurellement distincts.L'objectif principal de mes travaux de doctorat consistait à caractériser la relation structure/fonction du PAFR humain par voie de mutagenèse
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Ho, Yew Seng Jonathan. "Structure and function relationships of the catalytic subunits of brain platelet activating factor acetylhydrolase /." 1999. http://wwwlib.umi.com/dissertations/fullcit/9930079.

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Thesis (Ph. D.)--University of Virginia, 1999.<br>Spine title: X-ray structure of PAF acetylhydrolase. Includes bibliographical references (p. 161-175). Also available online through Digital Dissertations.
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"Model study and partial synthesis of prehispanolone and derivatives from hispanolone." Chinese University of Hong Kong, 1994. http://library.cuhk.edu.hk/record=b5895462.

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En Si Wang.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 1994.<br>Includes bibliographical references (leaves 126-140 (2nd gp.)).<br>Acknowledgements --- p.i<br>Contents --- p.ii<br>Abstract --- p.iv<br>List of Acronyms and Abbreviations --- p.vi<br>introduction --- p.1<br>Chapter I. --- "Platelet Activating Factor (PAF)´ؤPast, Present, and Future" --- p.1<br>Chapter I-1. --- What is PAF? --- p.1<br>Chapter I-2. --- Biochemistry of PAF --- p.2<br>Chapter I-2-1. --- Metabolic Cycle of PAF --- p.3<br>Chapter I-2-1-A. --- Biosynthesis of PAF --- p.4<br>Chapter I-2-1 -B. --- Inact
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Books on the topic "Platelet activating factor structure analogs"

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P, Braquet, ed. CRC handbook of PAF and PAF antagonists. CRC Press, 1991.

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Braquet, Pierre. Handbook of PAF and PAF Antagonist. CRC-Press, 1991.

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Book chapters on the topic "Platelet activating factor structure analogs"

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Lohmeyer, M., and P. Workman. "Antitumour Ether Lipids and Platelet-Activating Factor Analogues Have Different Cytotoxic Profiles and Calcium Mobilizing Effects — a Structure-Activity Study." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_135.

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Shimizu, Takao, and Hiroyuki Mutoh. "Structure and Regulation of Platelet Activating Factor Receptor Gene." In Advances in Experimental Medicine and Biology. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1813-0_30.

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Braquet, P., and J. J. Godfroid. "Conformational Properties of the PAF-Acether Receptor on Platelets Based on Structure—Activity Studies." In Platelet-Activating Factor and Related Lipid Mediators. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5284-6_9.

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Hanahan, Donald J. "Minor Phospholipids: Platelet activating factor (PAF) and PAF analogs, Lysophosphatidic acid and phosphatidic acid, Phosphatidylglycerol, Cardiolipin, Sphingosine-1-P." In A Guide to Phospholipid Chemistry. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195079814.003.0009.

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In the previous chapters, the emphasis was placed on establishing the chemical nature of phospholipids normally found in relatively high concentrations in mammalian cells. The methodology described for identification of these compounds can be applied, perhaps with some minor modifications to the structural characterization of phospholipids found in plants, fish, and bacteria. Interwoven into the fabric of these chapters was the subtle reference to their potential biological role in cellular behavior. As lipid biochemistry has developed over the past several years, there is no doubt that the field of signal transduction has had an enormous impact on phospholipid awareness. As might be expected, the potential for phospholipids or their metabolites to exhibit biological activity loomed large. As will be evident in this chapter, phospholipids can certainly have biological activity and this theme shall be explored in some depth. The title “Minor Phospholipids” is not meant to be belittling, but is only intended to reflect the fact that these phospholipids are present in very low concentrations. In fact, some are considered to be formed only after a cell has been stimulated by an extracellular agonist. As shall be seen, these compounds have considerable biological activity and hence are really of major importance in the cellular metabolic scene. The term platelet activating factor (PAF) was originally applied to a phosphoglyceride capable of activating platelets, leading to their aggregation. In addition, in certain species, there was also discharge of their dense granules (as indicated by serotonin release from the platelets). This nomenclature was unfortunate because it is now well established that many cells can produce this compound and that, likewise, PAF can stimulate many other cells. There are many other compounds, such as thrombin and arachidonic acid, which also can activate platelets. Notwithstanding this problem of nomenclature, there is a widespread (deeply entrenched) usage of this term to indicate a specific type of phospholipid with a particular biological activity. Given the status of this field at the current time, the use of the term PAF will be continued here.
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Gonzalez, Tara D., and Brian J. Bahnson. "Crystal Structure and Atomic Level Analysis of Plasma PAF-AH." In Platelet-Activating Factor Acetylhydrolases (PAF-AH). Elsevier, 2015. http://dx.doi.org/10.1016/bs.enz.2015.09.001.

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Bhatia, Suresh, and Joseph Hajdu. "Stereospecific Synthesis of Antitumor Active Thioether PAF Analogs." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch96.

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Godfroid, J., G. Dive, J. Lamotte-Brasseur, J. Batt, and F. Heymans. "PAF Receptor Structure." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch39.

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Shen, T. "Chemical and Biochemical Characterization of Lignan Analogs as Novel PAF Receptor Antagonists." In Platelet-Activating Factor and Structurally Related Alkyl Ehter Lipids. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439832042.ch37.

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Tilley, Jefferson W., and Margaret O’Donnell. "N-[ω-(Heteroaryl)Alkyl]Carboxamide Derivatives as Platelet Activating Factor Antagonists: Structure-Activity Relationships and Biological Data." In CRC Handbook of PAF and PAF Antagonists. CRC Press, 2019. http://dx.doi.org/10.1201/9780429265921-11.

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Conference papers on the topic "Platelet activating factor structure analogs"

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Wurzinger, L. J., R. Opitz, and H. Schmid-Schönbein. "ULTRASTRUCTURAL INVESTIGATIONS ON THE MECHANISM OF “SHEAR-INDUCED PLATELET ACTIVATION”." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642845.

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High shear forces are suspected to play a triggering role in the initiation of arterial thrombosis, by activating platelets and the coagulation system. In an earlier study a shear stress of 170 N/m2 acting for only 7 milliseconds (ms) on platelet rich plasma (PRP) was found to induce a significant increase in platelet factor 3 availability (Thromb. Haemost. 54: 381-386; 1985). To clarify the question whether platelets can be activated directly by mechanical forces in analogy to smooth muscle cells, electron micrographs of platelets subjected to laminar shear stress were analysed with morphomet
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Hawiger, J. "PLATELET RECEPTOR RECOGNITION DOMAINS AND THEIR SYNTHETIC PEPTIDE ANALOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643726.

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Adhesive molecules and their receptorsplay an essential role in hemostasis and thrombosis. Platelet thrombi are formed through the interaction of cell adhesion molecules (CAMs) with intercellular adhesion molecules (IAMs)and substrate adhesion molecules (SAMs). Platelet CAMs encompass membrane glycoproteins lb, lib, Ilia,and possibly la and IV, which constitutemembrane receptors for IAMs(e.g., fibrinogen) and for SAMs encompassingvon Willebrand Factor (vWF), fibronectin, vitronectin, collagen, and thrcmbospondin. Receptorfunction of platelet CAMs can be specific,i.e., only one adhesive protein
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Arnout, J., A. Van Hecken, I. Delepeleire, et al. "EFFECTIVENESS AND TOLERABILITY OF CV-3988, A SELECTIVE PAF ANTAGONIST, AFTER INTRAVENOUS ADMINISTRATION TO MAN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642878.

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Platelet activating factor (PAF) is a naturally occurring phospholipid with a wide spectrum of biological activities. Although PAF has been ascribed a potential role in various conditions including inflammation, asthma, glomerulonephritis and thrombosis, its precise function in physiologic/pathophysiologic processes remains unclear. The introduction of selective PAF receptor antagonists could represent a useful tool to extend our knowledge of the role of this mediator in health and disease.We have investigated the efficacy and tolerability of (RS)-2-methoxy-3-(octadecylcarbomoyloxy)propy1 2-(3
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Erickson, L. A., P. W. Bergum, E. V. Hubert, et al. "ENHANCEMENT AND INHIBITION OF THE ACTIVITY OF RECOMBINANT ANALOGS OF TISSUE PLASMINOGEN ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643844.

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Both the affinity of tissue plasminogen activator (tPA) for fibrin, which is associated with enhancement of its activity, and its susceptibility to inhibition contribute to the ability of this molecule to initiate vascular fibrinolysis. Full-length tPA is thought to consist of five structural regions designated the finger (F), growth factor-like (G), kringle 1 (K1), kringle 2 (K2), and protease (P) domains. Previous studies have suggested that the interaction of tPA with fibrin is primarily dependent upon the presence of the F and K2 domains, with its inhibition minimally requiring an intact a
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