Relevant bibliographies by topics / Adenosine diphosphate; ADP; Blood

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

Academic literature on the topic 'Adenosine diphosphate; ADP; Blood'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Adenosine diphosphate; ADP; Blood"

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Poelstra, K., JF Baller, MJ Hardonk, and WW Bakker. "Demonstration of antithrombotic activity of glomerular adenosine diphosphatase [published erratum appears in Blood 1991 Oct 15;78(8):2163]." Blood 78, no. 1 (1991): 141–48. http://dx.doi.org/10.1182/blood.v78.1.141.bloodjournal781141.

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We have demonstrated that reduced glomerular adenosine diphosphatase (ADPase) activity within the rat kidney is associated with an increased thrombotic tendency. To establish a possible causal relationship between these intraglomerular events, experiments were conducted to inhibit adenosine diphosphate (ADP) degradation without influencing other glomerular prothrombotic or antithrombotic mechanisms. Concurrently, we studied intraglomerular platelet aggregation. Two ways of selective inhibition of glomerular ADPase activity were applied: (1) by competitive substrates (ie, uridine diphosphate [U
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Poelstra, K., JF Baller, MJ Hardonk, and WW Bakker. "Demonstration of antithrombotic activity of glomerular adenosine diphosphatase [published erratum appears in Blood 1991 Oct 15;78(8):2163]." Blood 78, no. 1 (1991): 141–48. http://dx.doi.org/10.1182/blood.v78.1.141.141.

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Abstract We have demonstrated that reduced glomerular adenosine diphosphatase (ADPase) activity within the rat kidney is associated with an increased thrombotic tendency. To establish a possible causal relationship between these intraglomerular events, experiments were conducted to inhibit adenosine diphosphate (ADP) degradation without influencing other glomerular prothrombotic or antithrombotic mechanisms. Concurrently, we studied intraglomerular platelet aggregation. Two ways of selective inhibition of glomerular ADPase activity were applied: (1) by competitive substrates (ie, uridine dipho
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Cattaneo, Marco, Christian Gachet, Jeanne-Pierre Cazenave, and Marian A. Packham. "Adenosine diphosphate (ADP) does not induce thromboxane A2 generation in human platelets." Blood 99, no. 10 (2002): 3868–70. http://dx.doi.org/10.1182/blood-2002-01-0313.

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Darlington, Daniel N., Xiaowu Wu, Kevin L. Chang, James Bynum, and Andrew P. Cap. "Regulation of Platelet Function By Adenosine Receptors." Blood 134, Supplement_1 (2019): 2348. http://dx.doi.org/10.1182/blood-2019-131129.

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Introduction: We have recently shown that severe trauma and hemorrhage lead to inhibition of platelet aggregation and an elevation in cyclic adenosine monophosphate (cAMP). Adenosine is one of the few humoral agents known to stimulate cAMP in platelets. Because adenosine is released from damaged tissue, it may contribute to the platelet dysfunction seen after severe trauma. Platelets have four adenosine receptors (A1, A2a, A2b and A3). These receptors are G-Protein Coupled Receptors and have been proposed to stimulate adenylyl cyclase and increase intracellular cAMP. Although studies have show
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Cattaneo, Marco. "The platelet P2Y12 receptor for adenosine diphosphate: congenital and drug-induced defects." Blood 117, no. 7 (2011): 2102–12. http://dx.doi.org/10.1182/blood-2010-08-263111.

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Abstract P2Y12, the Gi-coupled platelet receptor for adenosine diphosphate (ADP), plays a central role in platelet function. Patients with congenital P2Y12 defects display a mild to moderate bleeding diathesis, characterized by mucocutaneous bleedings and excessive post-surgical and post-traumatic blood loss. Defects of P2Y12 should be suspected when ADP, even at high concentrations (≥ 10μM), is unable to induce full, irreversible platelet aggregation. Tests that evaluate the degree of inhibition of adenylyl cyclase by ADP should be used to confirm the diagnosis. Drugs that inhibit P2Y12 are p
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Goto, Shinya, Noriko Tamura, and Shunnosuke Handa. "Effects of adenosine 5′-diphosphate (ADP) receptor blockade on platelet aggregation under flow." Blood 99, no. 12 (2002): 4644–46. http://dx.doi.org/10.1182/blood-2001-12-0284.

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Muhsin, A., M. T. Eusni Raha, M. N. Sabariah, A. K. Faraizah, H. Roshida, and M. S. Salmiah. "Impaired Platelet Aggregation to Adenosine Diphosphate (ADP) Agonist in National Blood Centre, Malaysia." Asian Journal of Epidemiology 5, no. 4 (2012): 114–22. http://dx.doi.org/10.3923/aje.2012.114.122.

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Koessler, Juergen, Philipp Klingler, Marius Niklaus, et al. "The Impact of Cold Storage on Adenosine Diphosphate-Mediated Platelet Responsiveness." TH Open 04, no. 03 (2020): e163-e172. http://dx.doi.org/10.1055/s-0040-1714254.

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Abstract Introduction Cold storage of platelets is considered to contribute to lower risk of bacterial growth and to more efficient hemostatic capacity. For the optimization of storage strategies, it is required to further elucidate the influence of refrigeration on platelet integrity. This study focused on adenosine diphosphate (ADP)-related platelet responsiveness. Materials and Methods Platelets were prepared from apheresis-derived platelet concentrates or from peripheral whole blood, stored either at room temperature or at 4°C. ADP-induced aggregation was tested with light transmission. Ac
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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.505.

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Abstract The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-se
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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.bloodjournal822505.

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The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-selectin ex
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Dissertations / Theses on the topic "Adenosine diphosphate; ADP; Blood"

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Webb, Rachel J. "Characterisation of P2-receptors on human platelets." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342989.

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Pacheco-Rodriguez, Gustavo. "Synthesis, purification and characterization of small mono(ADP-ribosyl)ated molecules in the ADP-ribose elongation reaction catalyzed by poly(ADP-ribose)polymerase." Thesis, North Texas State University, 1993. https://digital.library.unt.edu/ark:/67531/metadc798168/.

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The ADP-ribose elongation catalyzed by poly(ADP-ribose) polymerase (PARP) [EC 2.2.2.30] has been partially characterized utilizing mono (ADP-ribosyl)ated polyamines. Arginine methyl ester (AME)-(ADP-ribose) and agmatine (AGMT)-(ADP-ribose) were synthesized enzymatically with a eukarytic mono(ADP-ribosyl) transferase and cholera toxin, respectively.
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Cervantes-Laurean, Daniel. "Preparation and Characterization of Model Conjugates for the Study of Proteins Modified by ADP-ribose." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc935701/.

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Modification of proteins by ADP-ribose has been shown to be a versatile modification with respect to the amino acid side chain. The results described here will allow the study of the biological importance of ADP-ribose glycation and also allow differentiation on crude extracts between enzymatic modifications from protein ADP-ribose glycation that can occur due to the presence of NAD glycohydrolases.
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Alvarez-Gonzalez, Rafael. "Complex polymers of ADP-ribose occur in vitro and in vivo." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc798086/.

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The work presented here included the development of a highly sensitive method to estimate the size and complexity of poly(ADP-ribose). This involved radiolabeling of the precursor pools, purification of polymers using a boronate resin, polymer fractionation according to size by molecular sieve chromatography and analysis of polymer complexity by enzymatic digestion to nucleotides which were quantified by strong anion exchange chromatography.
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Poole, Alastair W. "Responses of equine blood platelets induced by adenosine 5'-diphosphate." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260575.

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Scase, Timothy John. "Blood platelet responses induced by adenosine 5'-diphosphate : functional and molecular studies." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624899.

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Loflin, Paul T. (Paul Tracey). "Identification of Endogenous Substrates for ADP-Ribosylation in Rat Liver." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc277847/.

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Bacterial toxins have been shown to modify animal cell proteins in vivo with ADPR. Animal cells also contain endogenous enzymes that can modify proteins. Indirect evidence for the existence in vivo of rat liver proteins modified by ADPR on arginine residues has been reported previously. Presented here is direct evidence for the existence of ADP-ribosylarginine in rat liver proteins. Proteins were subjected to exhaustive protease digestion and ADP-ribosyl amino acids were isolated by boronate chromatography.
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Nylander, Sven. "Thrombin/ADP-induced platelet activation and drug intervention /." Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med885s.pdf.

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Chen, Hai-Ying. "Studies on Poly (ADP-ribose) Synthesis in Lymphocytes of Systemic Lupus Erythematosus Patients." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc501263/.

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A method for assaying poly (ADP-ribose) polymerase (PADPRP) activity in lymphocytes of systemic lupus erythematosus (SLE) patients has been developed. Using this method, PADPRP activity has been studied in lymphocytes from 15 patients and 13 controls. The mean activity in SLE lymphocytes was significantly lower than that in controls and 60% of the SLE patients demonstrated activities below the minimum of the control population. Possible mechanisms for this altered metabolism were investigated. The Km app of PADPRP for NAD; size distribution, branch frequency, and rates of turnover of polymers;
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Croset, Amélie. "Identification et caractérisation des mécanismes d'action des molécules appats, les SiDNA, dans l'inhibition des voies de réparation des cassures simple-brin." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T018.

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La plupart des traitements anticancéreux, comme la chimiothérapie ou la radiothérapie, sont cytotoxiques et causent des dommages à l'ADN dans le but d’induire la mort des cellules tumorales. Cependant, l’efficacité d’activité de réparation de l'ADN des tumeurs entraine des résistances intrinsèques et acquises aux traitements. L'une des étapes précoces de la réparation de l’ADN est le recrutement de protéines au niveau du site de dommage. Ce recrutement est coordonné par une cascade de modifications et est contrôlé par des protéines senseurs telles que la protéine kinase ADN dépendante (DNA-PK)
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Books on the topic "Adenosine diphosphate; ADP; Blood"

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1945-, Richter Ch, ed. ADP-ribosylation of proteins: Enzymology and biological significance. Springer-Verlag, 1987.

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1948-, Poirier Guy G., and Moreau Pierre 1952-, eds. ADP-ribosylation reactions. Springer-Verlag, 1992.

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Alvarez-Gonzalez, R. Adp-Ribosylation Reactions: From Bacterial Pathogenesis To Cancer. Springer, 2012.

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K, Jacobson Myron, and Jacobson Elaine L, eds. ADP-ribose transfer reactions: Mechanisms andbiological significance. Springer-Verlag, 1989.

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ADP-Ribose Transfer Reactions: Mechanisms and Biological Significance. Springer, 2012.

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Jacobson, Myron K., and Elaine L. Jacobson. ADP-Ribose Transfer Reactions: Mechanisms and Biological Significance. Springer, 2012.

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Alvarez-Gonzalez, R. ADP-Ribosylation Reactions: From Bacterial Pathogenesis to Cancer (Developments in Molecular and Cellular Biochemistry). Springer, 1999.

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Friedrich, Haag, Koch-Nolte Friedrich, and International Workshop on the Biological Significance of Mono ADP-Ribosylation in Animal Tissues (1996 : Hamburg, Germany), eds. ADP-ribosylation in animal tissues: Structure, function, and biology of mono (ADP-ribosyl) transferases and related enzymes. Plenum, 1997.

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(Editor), Friedrich Haag, and Friedrich Koch-Nolte (Editor), eds. ADP Ribosylation in Animal Tissues: Structure, Function, and Biology of Mono (ADP-Ribosyl) Transferases and Related Enzymes (Advances in Experimental Medicine and Biology). Springer, 1997.

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Koch-Nolte, Friedrich, and Friedrich Haag. ADP-Ribosylation in Animal Tissues: Structure, Function, and Biology of Mono Transferases and Related Enzymes. Springer, 2012.

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Book chapters on the topic "Adenosine diphosphate; ADP; Blood"

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Williams, Diane P., Patricia Bacha, Vicki Kelley, Terry B. Strom, and John R. Murphy. "Adenosine Diphosphate Ribosylation of Elongation Factor-2 as a Therapeutic Target: Genetic Construction and Selective Action of a Diphtheria Toxin-Related Interleukin-2 Fusion Protein." In ADP-Ribose Transfer Reactions. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-8507-7_89.

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Becker, Richard C., and Frederick A. Spencer. "Aspirin." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0012.

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Aspirin, considered the prototypic platelet antagonist, has been available for over a century and currently represents a mainstay both in the prevention and treatment of vascular events that include stroke, myocardial infarction, peripheral vascular occlusion, and sudden death. Aspirin irreversibly acetylates cyclooxygenase (COX), impairing prostaglandin metabolism and thromboxane A2 (TXA2) synthesis. As a result, platelet aggregation in response to collagen, adenosine diphosphate (ADP), and thrombin (in low concentrations) is attenuated (Roth and Majerus, 1975). Because aspirin more selectively inhibits COX-1 activity (found predominantly in platelets) than COX-2 activity (expressed in tissues following an inflammatory stimulus), its ability to prevent platelet aggregation is seen at relatively low doses, compared with the drug’s potential antiinflammatory effects, which require much higher doses (Patrono, 1994). Several alternative mechanisms of platelet inhibition by aspirin have been proposed, including: (1) inhibition of platelet activation by neutrophils and (2) enhanced nitric oxide production. In addition, aspirin may prevent the progression of atherosclerosis by protecting low-density lipoprotein (LDL) cholesterol from oxidation and scavenging hydroxyl radicals. Following oral ingestion, aspirin is promptly absorbed in the proximal gastrointestinal (GI) tract (stomach, duodenum), achieving peak serum levels within 15 to 20 minutes and platelet inhibition within 40 to 60 minutes. Enteric-coated preparations are less well absorbed, causing an observed delay in peak serum levels and platelet inhibition to 60 and 90 minutes, respectively. The antiplatelet effect occurs even before acetylsalicylic acid is detectable in peripheral blood, probably from platelet exposure in the portal circulation. The plasma concentration of aspirin decays rapidly with a circulating half-life of approximately 20 minutes. Despite the drug’s rapid clearance, platelet inhibition persists for the platelet’s life span (7 ± 2 days) due to aspirin’s irreversible inactivation of COX-1. Because 10% of circulating platelets are replaced every 24 hours, platelet activity (bleeding time, primary hemostasis) returns toward normal (≥50% activity) within 5 to 6 days of the last aspirin dose (O’Brien, 1968). A single dose of 100 mg of aspirin effectively reduces the production of TXA2 in many (but not all) individuals.
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Godeau, Francois, and S. S. Koide. "Xenopus Mono(Adenosine Diphosphate Ribosyl) Transferase: Purification, Assay, and Properties." In ADP-Ribosylation, DNA Repair and Cancer. CRC Press, 2020. http://dx.doi.org/10.1201/9781003079491-12.

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Webert, Kathryn E., and John G. Kelton. "Disorders of platelet number and function." In Oxford Textbook of Medicine. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.220603.

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Platelets are released from megakaryocytes in the bone marrow and circulate for 5 to 10 days before being cleared by the cells of the reticuloendothelial system. They play a critical role in haemostasis, with key features being (1) adhesion—when the wall of a blood vessel is damaged, platelets adhere to exposed collagen and other components of the subendothelium via the glycoprotein Ib receptor and other adhesive receptors; followed by (2) activation—release of thrombin, adenosine diphosphate, and arachidonic acid, which is converted by a cascade of enzymes into platelet activating agents including thromboxane A...
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Becker, Richard C., and Frederick A. Spencer. "Clopidogrel." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0013.

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Clopidogrel, a thienopyridine derivative, is a novel platelet antagonist that is several times more potent than ticlopidine but associated with fewer adverse effects. After repeated 75-mg oral doses of clopidogrel, plasma concentrations of the parent compound, which has no platelet-inhibiting effect, are very low. Clopidogrel is extensively metabolized in the liver. The main circulating metabolite is a carboxylic acid derivative with a plasma elimination half-life of 7.7 ± 2.3 hours. Approximately 50% of an oral dose is excreted in the urine and the remaining 50% in feces over the following 5 days. Dose-dependent inhibition of platelet aggregation is observed 2 hours after a single oral dose of clopidogrel, with a more significant inhibition achieved with loading doses (≥300 mg) by approximately 6 hours. Repeated doses of 75 mg of clopidogrel per day inhibit adenosine diphosphate (ADP)-mediated aggregation, with steady state being reached between day 3 and day 7. At steady state, the average inhibition to ADP is between 40% and 60%. Based on ex vivo studies, clopidogrel is approximately 100-fold more potent than ticlopidine. There are no cumulative antiplatelet effects with prolonged oral administration. The combined administration of clopidogrel (300 mg loading dose) and aspirin yields a readily discernible platelet-inhibiting effect within 90 to 120 minutes. Clopidogrel selectively inhibits the binding of ADP to its platelet receptor (P2Y12) and the subsequent G-protein–linked mobilization of intracellular calcium and activation of the glycoprotein (GP)IIb/IIIa complex (Gachet et al., 1992). The specific receptor has been cloned and is abundantly present on the platelet surface (Hollopter et al., 2001). Clopidogrel has no direct effect on cyclooxygenase, phosphodiesterase, or adenosine uptake. Clopidogrel is rapidly absorbed following oral administration with peak plasma levels of the predominant circulating metabolite occurring approximately 60 minutes later. Administration with meals does not significantly modify the bioavailability of clopidogrel. The available information suggests that clopidogrel offers safety advantages over ticlopidine, particularly with regard to bone marrow suppression and other hematologic abnormalities. Although thrombotic thrombocytopenic purpura (TTP) has been reported with clopidogrel (Bennett et al., 2000), its occurrence (11 cases per 3 million patients treated) is rare, and has not been reported in randomized clinical trials performed to date.
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Becker, Richard C., and Frederick A. Spencer. "Aggrenox and Cilostazol." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0015.

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The dipyridamole component of Aggrenox and cilostazol, both phosphodiesterase inhibitors, are used predominantly in patients with peripheral vascular and cerebrovascular disease. Aggrenox is a combination platelet antagonist that includes aspirin (25 mg) and dipyridamole (200 mg extended-release preparation). It is typically taken twice daily. Aspirin’s mechanism of action has been discussed previously. Dipyridamole inhibits cyclic adenosine monophosphate (cAMP)-phosphodiesterase (PDE) and cyclic-3´, 5´- guanylate monophospate (GMP)-PDE (Bunag et al., 1964). The pharmacokinetic profile of aspirin has been summarized previously. Peak dipyridamole levels in plasma are achieved within several hours of oral administration (400 mg dose of Aggrenox). Extensive metabolism via conjugation with glucuronic acid occurs in the liver. There are no significant pharmacokinetic interactions between aspirin and dipyridamole coadministered as Aggrenox. Dipyridamole inhibits platelet aggregation by two distinct mechanisms. First, it attenuates adenosine uptake into platelets (as well as endothelial cells and erythrocytes). The resulting increase elicits a rise in cellular adenylate cyclase concentrations, resulting in elevated cAMP levels, which inhibit platelet activation to several agonists, including adenosine diphosphate (ADP), collagen, and platelet-activating factor. Dipyridamole also inhibits PDE. The subsequent increase in cAMP elevates nitric oxide concentration, facilitating platelet inhibitory potential (Eisert, 2001). The European Stroke Prevention Study (ESPS)-2 reported that 79.9% of patients experienced at least one on-treatment adverse event. The most common side effects were gastrointestinal complaints and headache. Dipyridamole has vasodilatory effects and should be used with caution in patients with severe coronary artery disease in whom episodes of angina pectoris may increase. Patients receiving Aggrenox should not be given adenosine for myocardial perfusion studies. Plasma concentrations of dipyridamole are approximately 40% higher in patients greater than 65 years of age compared with younger individuals. Aggrenox has not been studied in patients with acute coronary syndrome (ACS). The ESPS-2 included 6,602 patients with ischemic stroke (76% of the total population) or transient ischemic attack who were randomized to receive Aggrenox, dipyridamole alone, aspirin alone, or placebo. Aggrenox reduced the risk of stroke by 22.1% compared with aspirin and by 24.4% compared with dipyridamole. Both differences were statistically significant (p = .008 and p = .002, respectively) (Diener et al., 1996).
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Dalton, David R. "Roots, Shoots, Leaves, and Grapes." In The Chemistry of Wine. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190687199.003.0015.

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As noted earlier and as anticipated by Charles and Francis Darwin it has been argued that plants sense the direction of gravity (gravitropism) by movement of starch granules found in cells called statocytes that contain compartments (organelles) called statoliths. The synthesis of statoliths appears to occur in the plastid (plant organelle) compartments called amyloplasts (Figure 7.1, 1). It has been suggested that this gravitropic signal then leads to movement of plant hormones such as indole-3-acetic acid (auxin) (Figure 7.2), through the phloem opposite to the pull of gravity to promote stem growth. Chloroplasts (Figure 7.1, 2) are cell compartments (plastids or organelles) in which photosynthesis is carried out. The process of photosynthesis, discussed more fully later, is accompanied by the production of adenosine triphosphate (ATP) from adenosine diphosphate (ADP) and inorganic phosphate (Pi) (Figure 7.3). ATP is consumed and converted to ADP and Pi in living systems. The cycle of production and consumption allows ATP to serve as an “energy currency” to pay for the reactions in living systems. Beyond this generally recognized critical function of chloroplasts, it has recently been pointed out that light/ dark conditions affect alternative splicing of genes which may be necessary for proper plant responses to varying light conditions. The organelles or plastids which contain the pigments for photosynthesis and the amyloplasts that store starch are only two of many kinds of plastids. Other plastids, leucoplasts for example, hold the enzymes for the synthesis of terpenes, and elaioplasts store fatty acids. Apparently, all plastids are derived from proplastids which are present in the pluripotent apical and root meristem cells. The cell wall (Figure 7.1, 3) is the tough, rigid layer that surrounds cells. It is located on the outside of the flexible cell membrane, thus adding fixed structure. A representation of a portion of the cell wall (as made up of cellulose and peptide cross-linking) is shown below in Figure 7.7. The cells will have different sizes as a function of where they are found (e.g., leaf, stalk, root), but in every case, the cell wall limits the size of the membrane that lies within.
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Becker, Richard C., and Frederick A. Spencer. "Platelet Glycoprotein IIb/IIIa Receptor Antagonists." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0014.

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The glycoprotein (GP) IIb/IIIa (αIIb/β3) receptor totalling 50,000 to 70,000 copies per platelet represents a common pathway for platelet aggregation in response to a wide variety of biochemical and mechanical stimuli. Accordingly, it represents an attractive target for pharmacologic inhibition that can be applied to patients with acute coronary syndromes. The evolution of GPIIb/IIIa receptor antagonists began with murine monoclonal antibodies and subsequently expanded to include small peptide or nonpeptide molecules with structural similarities to fibrinogen. There are three intravenous GPIIb/IIIa receptor antagonists that have been approved by the U.S. Food and Drug Administration: . . . • Abciximab (ReoPro) . . . . . . • Tirofiban (Aggrastat) . . . . . . • Eptifibatide (Integrilin) . . . Abciximab (ReoPro) is the Fab fragment of the chimeric human–murine monoclonal antibody c7E3. Following an intravenous bolus, free plasma concentrations of abciximab decrease rapidly with an initial half-life of less than 10 minutes and a second-phase half-life of 30 minutes, representing rapid binding to the platelet GPIIb/IIIa receptor. Abciximab remains in the circulation for 10 or more days in the platelet-bound state. Intravenous administration of abciximab in doses ranging from 0.15 mg/kg to 0.3 mg/kg produces a rapid dose-dependent inhibition of platelet aggregation in response to adenosine diphosphate (ADP). At the highest dose, 80% of platelet GPIIb/IIIa receptors are occupied within 2 hours and platelet aggregation, even with 20 μM ADP, is completely inhibited. Sustained inhibition is achieved with prolonged infusions (12 to 24 hours) and low-level receptor blockade is present for up to 10 days following cessation of the infusion; however, platelet inhibition during infusions beyond 24 hours has not been well characterized. Platelet aggregation in response to 5 μM ADP returns to greater than or equal to 50% of baseline within 24 hours of drug cessation. In nearly 2,100 patients undergoing either balloon coronary angioplasty or atherectomy at high risk for ischemic (thrombotic) complications, a bolus of abciximab (0.25 mg/kg) followed by a 12-hour continuous infusion (10 μg/min) reduced the occurrence of death, the occurrence myocardial infarction (MI), or the need for an urgent intervention (repeat angioplasty, stent placement, balloon pump insertion, or bypass grafting) by 35% (EPIC Investigators, 1994).
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"Commentary on and reprint of Born GVR, Aggregation of blood platelets by adenosine diphosphate and its reversal, in Nature (1962) 194:927–929." In Hematology. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012448510-5.50177-1.

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LICHTMAN, M., J. SPIVAK, L. BOXER, S. SHATTIL, and E. HENDERSON. "Commentary on and reprint of Born GVR, Aggregation of blood platelets by adenosine diphosphate and its reversal, in Nature (1962) 194:927–929." In Hematology. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012448510-5/50177-1.

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Conference papers on the topic "Adenosine diphosphate; ADP; Blood"

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Chamone, D. A. F., M. Ivany-Silva, C. Cassaro, G. Bellotti, C. Massumoto, and A. Y. Hoshikawa-Fujimura. "GUARANA (Paullinia cupana) INHIBITS AGGREGATION IN WHOLE BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644553.

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Guarana, a methylxanthine obtained from the seeds of Paullinia cupana has been largely used in the Amazon region by native indians during centuries as stimulant. We evaluated the effect of guarana on ex-vivo and in vitro platelet aggregation induced by adenosine-5-diphosphate (ADP) in human and rat whole blood with an impedance (Chrono-Log, model 500) and in their platelet rich plasma (PRP) with an optical aggregometer (Chrono-Log, model 440). Ex-vivo studies were carried out after single oral intake of guarana. Seven healthy volunteers (5 male and 2 female) aged 19-26 years who had taken no d
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Nelson, S. D., A. J. Moriarty, R. Hughes, and K. Balnave. "TRANSITORY INFLUENCE OF FIBRINOGEN/FIBRIN DEGRADATION PRODUCTS (FDPs) ON PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644548.

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This paper describes a pilot study to investigate the influence of FDPs on platelet aggregation in a small cohort of patients (N = 12) undergoing systemic thrombolytic therapy with streptokinase (600,000 I.U. or 1,500,000 I.U. delivered over 30 minutes) for acute myocardial infarction.Serial pre- and post-therapy blood samples were anticoagulated with sodium citrate, and whole blood aggregation studies carried out over 24 hours using a Crono-log 540 aggregometer and the standard adenosine diphosphate (ADP), adrenalin (A), collagen (C) and ristocetin (R) aggregating agents.Results, in the form
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Longmire, K., and M. M. Frojmovic. "PLATELET AGGREGATION DYNAMICS TO ADENOSINE DIPHOSPHATE IN NON-STIRRED SUSPENSIONS: LONG-RANGEINTERACTIONS FOR HUMAN, BUT NOT RABBIT, PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644464.

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The simplest experimental approach for a theoretical description of platelet aggregation is based on kinetics of early multiplet formation (‹4 platelets per aggregate)occurring with diffusion-dependent particle collisions (no flow). The Smoluchowski theory was used to calculate collision efficiencies, αβ, from a linear plot of platelet particle count (Nt)−1 vs time (t) following addition of adenosine diphosphate (ADP) to citrated platelet-rich-plasma (PRP) for 7 human (H) and 2 rabbit (R) donors. A 0.1 ml sample of PRP was stirred with ADP for 0.5s, then immediately transferred to a 37°C bath
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Herman, A. G., and H. Bult. "RED BLOOD CELL LYSIS MAY INFLUENCE PLATELET AGGREGATION IN WHOLE BLOOD AGGREGOMETER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644552.

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The electronic whole blood aggregometer (WBA) has the advantage that it enables the study of platelet aggregation in whole blood shortly after blood collection. Using the WBA varying results have been obtained with respect to the anti-aggregating activity of dipyridamole. As dipyridamole is an efficient inhibitor of adenosine uptake, we tested whether the degree of red blood cell lysis (and thus availability of adenine nucleotides) affected its efficacy. Citrate (10.7 mM) blood was stored in sealed tubes and used between 20 and 100 min after venipuncture. One ml was placed in a Chronolog Model
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Patel, R., and R. Bick. "PLATELET DYSFUNCTION INDUCED BY TETRAHYDROCANNABINOL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644877.

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Many drugs and other agents have been reported to induce platelet dysfunction and clinical bleedability; however, tetrahydrocannabinol (marijuana) has thus far not been reported. The patient herein described is a 28-year-old Caucasian female who wasreferred for evaluation of easy and spontaneous bruising. On history, the patient related that for a three-month period she had been developing spontaneous ecchymoses of the extremities and torso. She denied any medication other than heavy marijuana use. Hemostasis evaluation revealed her to have a normal prothrombin time, partial thromboplastin tim
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Gentry, P. A., and G. S. Bondy. "The aggregation of bovine platelets is not dependent on thromboxane B2 production." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644500.

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Bovine and human platelets appear to be equally sensitive to inhibition by several environmental toxins even though the bovine is not generally recognised as a species prone to thromboembolic and hemorrhagic disease. During the examination of the mechanism of action of the toxins it became necessary to establish parameters for normal bovine platelet function.Bovine platelets suspended in homologous plasma demonstrate various responses to different agonists. Bovine platelets aggregate effectively and irreversibly to fibrillar form collagen and adenosine-diphosphate (ADP), undergo reversible agg
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Ortega, M. P., C. Sunkel, and J. G. Priego. "INHIBITION OF HUMAN PLATELET FUNCTION BY PCA-4230." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643431.

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PCA-4230 (3-{2-(N-l,2-benzisothiazolyl-3(2H)one-1,1-dioxide) ethoxycarbonyl}-2,6-dimethyl-5-ethoxycarbonyl-4-methyl-l,4-dihy-dropyridine) is a new synthetic compound which has been selected after evaluation of .several series of molecules included in an ex tensive program of synthesis and biological screening.The purpose of this study was to investigate the In vUjiO effects of PCA-4230 on human platelet function.Platelet aggregation (PA) was measured, in platelet rich plasma (PRP) or washed platelets, according to Born’s technique. Release reaction (RR) was measured by the luminiscence method
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Saniabadi, A. R., G. D. O. Lowe, and C. D. Forbes. "EFFECT OF DIPYRIDAMOLE ON SPONTANEOUS PLATELET AGGREGATION IN WHOLE BLOOD DECREASES WITH THE TIME AFTER VENEPUNCTURE:EVIDENCE FOR THE ROLE OF ADP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644819.

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Spontaneous platelet aggregation (SPA) was studied in human whole blood at 3,5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter (Ultra Flo 100), SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of blood at 37°C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10-5M at each time interval; (b) 0.5-100 x 10-6M at 3 and 30 minutes, and (c) 15 x 10-6M in combination with 2 x 10-4M adenosine (Ad)
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Sakariassen, S. K., E. Fressinaud, D. Meyer, J. J. Sixma, and R. H. Baumgartner. "RHEOLOGY AND PLATELET-SURFACE ADHESION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643987.

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The process of platelet adhesion to sites of vascular injury is pivotal for the arrest of bleeding. The same process may, on the other hand, lead to formation of mural thrombi and may play a role in atherogenesis through the release of platelet-derived growth factor. The events of platelet-surface adhesion may be divided into initial attachment and the subsequent spreading on the surface. These interactions are mediated by a variety of factors, including glycoproteins (GP) in the platelet membrane, von Willebrand factor (vWF) in plasma, and the composition of the surface.However, in most insta
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Burroughs, A., L. Taylor, D. Sprengers, R. A. Hatton, N. McIntyre, and P. BA Kernoff. "HAEMOSTATIC CHANGES IN CIRRHOSIS AFTER REPEATED DOSES OF DESAMINO D-ARGININE VASOPRESSIN (DDAVP)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644128.

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Eight patients with stable cirrhosis received DDAVP (0.3ug/kg I. V. of Desmopressin acetate, Ferring Pharmaceuticals) and this dose was repeated after 4h and 24h. Blood for haemostatic studies was collected immediately before and lh after each dose. Results, shown below as medians (expressed in u/dl), with ranges in parentheses, were analysed using the Wilcoxon signed rank test for paired data. One hour after the first dose, von Willebrand factor antigen (VW:ag) and Ristocetin co-factor activity (Ricof) rose from 380 (182-1060) to 502 (230-1000), p<0.01 and from 400 (154-1200) to 494 (180-1
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