Relevant bibliographies by topics / Platelet factor 4

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

Academic literature on the topic 'Platelet factor 4'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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Journal articles on the topic "Platelet factor 4"

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Shimizu, T., Y. Ishikawa, Y. Morishima, T. Fukuda, and K. Kato. "Platelet factor 4 release from the platelets stored in platelet concentrates." Transfusion 25, no. 5 (September 1985): 420–23. http://dx.doi.org/10.1046/j.1537-2995.1985.25586020114.x.

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CAPITANIO, A., S. NIEWIAROWSKI, B. RUCINSKI, G. TUSZYNSKI, C. CIERNIEWSKI, D. HERSHOCK, and E. KORNECKI. "Interaction of platelet factor 4 with human platelets." Biochimica et Biophysica Acta (BBA) - General Subjects 839, no. 2 (April 17, 1985): 161–73. http://dx.doi.org/10.1016/0304-4165(85)90033-9.

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O'Brien, J. R. "PLATELET FACTOR 4 (PF 4) AND THE PLATELET MEMBRANE." Acta Medica Scandinavica 191, S525 (April 24, 2009): 65–66. http://dx.doi.org/10.1111/j.0954-6820.1972.tb05793.x.

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Sottile, Jane, Deane F. Mosher, Jan Fullenweider, and James N. George. "Human Platelets Contain mRNA Transcripts for Platelet Factor 4 and Actin." Thrombosis and Haemostasis 62, no. 04 (1989): 1100–1102. http://dx.doi.org/10.1055/s-0038-1647125.

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SummaryRNAs from a number of cells, including platelets, were analyzed by Northern blotting for the presence of transcripts to four platelet proteins - actin, thrombospondin, fibronectin, and platelet factor 4. RNA from platelets contains considerable amounts of mRNA for platelet factor 4, easily detectable mRNA for actin, and traces of mRNA for thrombospondin. mRNA for platelet factor 4 was not detected in human lymphocytes or in any of 5 human cell lines.
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Cowan, S. W., E. N. Bakshi, K. J. Machin, and N. W. Isaacs. "Binding of heparin to human platelet factor 4." Biochemical Journal 234, no. 2 (March 1, 1986): 485–88. http://dx.doi.org/10.1042/bj2340485.

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Platelet factor 4 is a small protein (Mr 7756) from the alpha-granules of blood platelets which binds strongly to and neutralizes the anticoagulant properties of heparin. From an analysis of X-ray crystallographic data a model for the binding of platelet factor 4 to heparin is proposed.
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Dickhout, Annemiek, Bibian M. E. Tullemans, Johan W. M. Heemskerk, Victor L. J. L. Thijssen, Marijke J. E. Kuijpers, and Rory R. Koenen. "Galectin-1 and platelet factor 4 (CXCL4) induce complementary platelet responses in vitro." PLOS ONE 16, no. 1 (January 7, 2021): e0244736. http://dx.doi.org/10.1371/journal.pone.0244736.

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Galectin-1 (gal-1) is a carbohydrate-binding lectin with important functions in angiogenesis, immune response, hemostasis and inflammation. Comparable functions are exerted by platelet factor 4 (CXCL4), a chemokine stored in the α-granules of platelets. Previously, gal-1 was found to activate platelets through integrin αIIbβ3. Both gal-1 and CXCL4 have high affinities for polysaccharides, and thus may mutually influence their functions. The aim of this study was to investigate a possible synergism of gal-1 and CXCL4 in platelet activation. Platelets were treated with increasing concentrations
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Day, H. James, H. Stormorken, and H. Holmsen. "Subcellular Localization of Platelet Factor 3 and Platelet Factor 4." Scandinavian Journal of Haematology 10, no. 4 (April 24, 2009): 254–60. http://dx.doi.org/10.1111/j.1600-0609.1973.tb00069.x.

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Leavitt, Andrew D. "What for platelet factor 4?" Blood 110, no. 4 (August 15, 2007): 1090. http://dx.doi.org/10.1182/blood-2007-05-091363.

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Robinson, C. "Recombinant Human Platelet Factor 4." Drugs of the Future 20, no. 2 (1995): 148. http://dx.doi.org/10.1358/dof.1995.020.02.284334.

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Lorenz, R., and M. Brauer. "Platelet factor 4 (PF 4) in septicaemia." Infection 16, no. 5 (September 1988): 273–76. http://dx.doi.org/10.1007/bf01645070.

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Dissertations / Theses on the topic "Platelet factor 4"

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Brousseau-Nault, Mathieu. "Chronic periodontitis is associated with platelet factor 4 (PF4) secretion." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59016.

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Aim: Platelets contribute to chronic inflammation but their role in periodontitis is not well understood. The aim of this study was to compare platelet recruitment and activation in healthy and inflamed periodontium. Materials and Methods: Gingival crevicular fluid (GCF) samples were obtained from sites of healthy periodontium, gingivitis and periodontitis. Platelets were quantified in the GCF by staining and microscopy. GCF concentrations of platelet factor 4 (PF4) [PF4]GCF and glycoprotein IIbIIIa ([GPIIbIIIa]GCF) were determined by ELISA. Blood samples were obtained from the 3 patient gro
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Javaid, Mohammad. "Platelet factor 4 upregulates matrix metalloproteinase-1 production in gingival fibroblasts." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/60244.

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Background and Objective: Periodontitis is a highly prevalent chronic inflammatory disease that causes tooth loss, morbidity and confers an increased risk for systemic disease. Tissue destruction during periodontitis is due in large part to collagen-degrading matrix metalloproteinases (MMPs) released by resident cells of the periodontium in response to pro-inflammatory cytokines. Platelets are immune-competent blood cells with a newly recognized role in chronic inflammation, however their role in the pathogenesis of periodontitis is undefined. Consequently, the objective of this study was to a
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Kreimann, Martin [Verfasser]. "Characterization of complexes between platelet factor 4 and heparin / Martin Kreimann." Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1065685513/34.

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Yasuba, Hirotaka. "INCREASED RELEASABILITY OF PLATELET PRODUCTS AND REDUCED HEPARIN-INDUCED PLATELET FACTOR 4 RELEASE FROM ENDOTHELIAL CELLS IN BRONCHIAL ASTHMA." Kyoto University, 1991. http://hdl.handle.net/2433/168713.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>医学博士<br>甲第4772号<br>医博第1273号<br>新制||医||500(附属図書館)<br>UT51-91-E143<br>京都大学大学院医学研究科内科系専攻<br>(主査)教授 三河 春樹, 教授 泉 孝英, 教授 大島 駿作<br>学位規則第5条第1項該当
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Rudmann, Sally V. "The effect of twenty minutes of aerobic exercise on in vivo platelet release in moderately trained females : radioimmunoassay of platelet factor 4 beta-thromboglobulin /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487266362337217.

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Charpin, Jean-Marie. "Physiopathologie de la bronchiolite obliterante chez les transplantes pulmonaires : implication de 4 mediateurs profibrosants : tgf-beta, igf-1,et-1 et pdgf." Paris 5, 2000. http://www.theses.fr/2000PA05N104.

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Etherington, Michael Denis. "An investigation into the measurement of plasma intraplatelet platelet factor 4 and beta-thromboglobulin in health and thrombotic disease." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278486.

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Kimmerle, Sabine. "Rapid determination of Anti-Heparin/Platelet factor 4 antibody titers in the diagnosis of Heparin-induced Thrombocytopenia$cSabine Kimmerle." Bern : [s.n.], 2003. http://www.stub.unibe.ch/html/haupt/datenbanken/diss/bestell.html.

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Newman, Peter Michael Pathology UNSW. "Antibody and Antigen in Heparin-Induced Thrombocytopenia." Awarded by:University of New South Wales. Pathology, 2000. http://handle.unsw.edu.au/1959.4/17485.

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Immune heparin-induced thrombocytopenia (HIT) is a potentially serious complication of heparin therapy and is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. Early diagnosis of HIT is important to reduce morbidity and mortality. I developed an enzyme immunoassay that detects the binding of HIT IgG to PF4-heparin in the fluid phase. This required techniques to purify and biotinylate PF4. The fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because
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Libraire, Julie. "Le facteur 4 plaquettaire (PF4/CXCL4) prévient la formation du complexe initial de l’inhibiteur de l’activateur du plasminogène (PAI-1) avec sa cible d’origine tissulaire (t-PA)." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P654.

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Le facteur 4 plaquettaire (PF4/CXCL4) est un tétramère constitué de quatre sous-unités identiques de 7,8 kDa qui est libéré en grande quantité par les plaquettes lors de l’hémostase primaire (ensemble des phénomènes permettant un colmatage initial d’une lésion vasculaire). L’étude de la formation d’un caillot de fibrine en présence de PF4 montre une augmentation de la turbidité finale du caillot : le PF4 modifie le réseau formé. Etant donné que la plupart des acteurs de la fibrinolyse se lie au caillot de fibrine et que le PF4 modifie sa structure, nous avons pensé qu’il serait intéressant de
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Books on the topic "Platelet factor 4"

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Hsiung, Marilyn S. Mechanisms of D(4) dopamine receptor-mediated platelet-derived growth factor receptor-beta transactivation. 2006.

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Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, wh
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Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.

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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inapprop
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Book chapters on the topic "Platelet factor 4"

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Pepper, D. S., and C. V. Prowse. "Beta-thromboglobulin and platelet factor 4." In ECAT Assay Procedures A Manual of Laboratory Techniques, 21–34. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2992-3_3.

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Ishii, Satoshi. "Platelet-Activating Factor (PAF) in Infectious Diseases." In Bioactive Lipid Mediators, 95–108. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55669-5_7.

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Terashita, Z., M. Kawamura, Y. Imura, and K. Nishikawa. "Possible Involvement of Platelet Activating Factor (PAF) in Tissue Factor Generation and the Pathogenesis of Disseminated Intravascular Coagulation (DIC)." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 58–63. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_10.

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Braquet, Pierre G. "Platelet-Activating Factor and Its Antagonists: Scientific Background and Clinical Applications of Ginkgolides." In Ginkgo Biloba A Global Treasure, 359–69. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-68416-9_27.

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Hirashima, Yutaka, Ryoko Kato, Tomoaki Ohmori, Takeshi Nagahori, Michiharu Nishijima, Shunro Endo, Akira Takaku, and Ken Karasawa. "The Role of Platelet-Activating Factor (PAF) in the Development of Chronic Subdural Hematoma." In Recent Advances in Neurotraumatology, 61–64. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68231-8_10.

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Abe, Mamoru, Masaharu Matsuzaki, Takashi Inoue, Hirotoshi Sano, and Tetsuo Kanno. "Significance of Platelet-Activating Factor (PAF) and PAF — Acethylhydrolase in the Pathogenesis of Chronic Subdural Hematoma." In Recent Advances in Neurotraumatology, 65–68. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68231-8_11.

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Miyazaki, Kohji, Kohji Fukunaga, Iqbal Munir, Hitoshi Okamura, and Eishichi Miyamoto. "Expression of Cyclooxygenase (COX)-2 in Human Endometrial Adenocarcinoma Cell Line HEC-1B: An In Vitro Model of the Expression of COX-2 by Platelet-Activating Factor, Human Chorionic Gonadotropin and Prostaglandin E2, and the Possible Signaling Pathways Involved." In Cell and Molecular Biology of Endometrial Carcinoma, 123–38. Tokyo: Springer Japan, 2003. http://dx.doi.org/10.1007/978-4-431-53981-0_8.

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Morita, Takashi, and Hideko Atoda. "The Structural Characterization of Coagulation Factor IX/Factor X-Binding Protein Isolated from the Venom of Trimeresurus Flavoviridis." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 35–40. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_6.

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Shen, Ming-Ching, Shu-Wha Lin, Pei-Chu Yang, and Chin-Chin Huang. "Studies of Factor VIII Inhibitors in Chinese Hemophilia a Patients." In Current Aspects of Blood Coagulation, Fibrinolysis, and Platelets, 49–54. Tokyo: Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68323-0_8.

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Vanhoutte, P. M. "Endothelium-Derived Vasoactive Factors, Platelets and Coronary Disease." In Coronary Circulation in Physiological and Pathophysiological States, 89–102. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68108-3_6.

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Conference papers on the topic "Platelet factor 4"

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Bryckaert, M. C., A. Wasteson, G. Tobelem, F. Rendu, and J. P. Caen. "PLATELET DERIVED GROWTH FACTOR (PDGF) BINDS TO HUMAN PLATELETS AND MODULATES PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643493.

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PDGF which is released during platelet activation like the other ∝ granule components (fibrinogen, F VIII/vWF, PF4) could bind to platelet membrane Following this hypothesis, we have studied the binding of 125I pure human PDGF to washed human platelets activated by collagen. This binding was specific and time dependent and reached a plateau with 20 μg/ml of collagen. With 200 fold excess of unlabeled PDGF, the binding of 125I-PDGF decreased progressively to 10 .whereas unlabeled Epidermal Growth Factor did not compete with 125I-PDGF. Saturation curve and scatchard analysis have shown one class
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Ordinas, A., E. Bastida, M. Garrido, J. Monteagudo, L. de Marco, and R. Castillo. "ASIALO VON WILLEBRAND FACTOR ENHANCES PLATELET ADHESION TO VASCULAR SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644098.

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Native Von Willebrand factor (NvWF) binds to platelets activated by thrombin, ADP or ristocetin, and also supports the adhesion of platelets to subendothelium at high shear rates. In contrast, asialo von Willebrand factor (AvWF) induces platelet aggregation in absence of platelet activators. We investigated the role of AvWF in supporting the adhesion of platelets to rabbit vessel subendothelium under flow conditions at a shear rate of 2000 sec-1 for 5 min using the Baumgartner perfusion system. We also studied the effects of blockage of platelet GPIb or GPIIb/IIIa on platelet adhesion using mo
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Boschetti, C., A. Vicari, E. Cofrancesco, A. Della Volpe, G. Moreo, E. Po-gliani, G. Pozza, and E. Polli. "HEPARIN-RELEASED PLATELET FACTOR 4 (HR-PF4) IN DIABETIC MICR0VAS-CULAR DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643498.

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When heparin is injected i.v. as a bolus, PF4 but not (β-throm boglobulin ((βTG) is released immediately. HR-PF4 is not liberated from platelets but from the endothelial cells of vessels which serve as storage sites. The role of platelet activation in diabetic microvascular disease is still controversial, however there is experimental evidence of vascular injury and hemostatic activation preceding the appearance of microvascular disease. The contradictory results so far obtained in man may be partly attributed to the heterogeneity of the diabetic patients studied. We studied 20 insulin-depende
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Bodzenta-Lukaszvk, A., K. Krupiński, and M. Bielawiec. "PLATELET FUNCTION AND KALLIKREIN SYSTEM IN PATIENTS WITH ESSENTIAL HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644258.

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Since the pathogenesis of hypertension is still discussed the aim of this study was to investigate behaviour of platelets and kallikrein system in patients suffering from this disease. In 30 patients with essential hypertension, aged 23-31 years and 20 normotensive healthy subjects, aged 21-35 years the following parameters of platelet function were studied: platelet aggregation induced with ADP,platelet activating factor (PAF) and arachidonic acid (AA) according Born's method, plasma beta-thromboglobulin (Beta-TG) and platelet factor 4 (PF4) , plasma thromboxane B2 (TXB2) and cyclic AMP using
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Vigh, Zs, and I. Scharrer. "INVESTIGATIONS ON MULTIMERIC STRUCTURE OF PLATELET VON WILLE-BRAND FACTOR IN PATIENTS WITH HEREDITARY DISORDERS OF PLATELET FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644087.

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Von Willebrand factor (vWF), a multimeric glycoprotein, plays an essential and multifunctional role in the hemostatic process. It is well known that platelet glycoproteins IB, IIB and IIIA contain receptors for vWF. Von Willebrand factor was also found in alpha granules of platelets. Therefore we investigated the multimeric structure of platelet vWF in 12 patients with different inherited disorders of platelet function. The patients had the following diagnosis: Hermansky Pudlak syndrome, Thrombasthenia and up to new undefined hereditary disorders of platelet function. The method is based upon:
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Gewirtz, A., W. Y. Xu, B. Rucinski, and S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.

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Platelet (plt) factor 4 (PF4) is an alpha granule protein which can modulate T lymphocyte function. T cells may help regulate megakaryocytopoiesis. Therefore, we hypothesized that T cell-PF4 interactions might play a role in autoregulating marrow megakaryocyte (MEG) production. To test this idea, we studied MEG colony formation in plasma clot cultures containing human serum derived solely from pit poor normal AB plasma, enriched hematopoietic progenitor cells (HPC), autologous T cells, and exogenous PF4. Highly purified PF4 (single band on SDS gel) was prepared from outdated human pits by a co
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Rucinski, B., G. J. Stewart, G. Boden, and S. Niewiarowski. "INTERACTION OF PLATELET FACTOR 4 WITH HEPATOCYTES AND ITS POSSIBLE SIGNIFICANCE IN HEMOSTASIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643500.

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Previous experiments have demonstrated the rapid clearance of himan platelet factor 4 (PF4) from rabbit and rat blood, its accumulation in the liver and its elimination of PF4 degradation products with urine. Injection of heparin resulted in a rapid loss of 125 i-pF4-radioactivity from the liver (Rucinski et al Amer. J. Physiol. 251, H800, 1986). Current experiments demonstrate the uptake of human 125i-pf4 by hepatocytes reaching maximum at 180 min. This uptake is 2-3 times greater at 37°C than at 4°C. At 37°C degradation of 125I-PF4 by hepatocytes was also observed as indicated by the increas
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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.
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Suzuki, Sozo, Kazuo Mori, Koji Sugai, Yasuyuki Akutsu, Masaaki Ishikawa, Hideaki Sakai, and Katsuhide Hiwatashi. "ELECTRONMICROSCOPIC STUDIES ON PLATELETS AND MEGAKARYOCYTES IN GIANT PLATELET SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644560.

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Giant platelet syndrome are characterized morphologically by many giant platelets associated with several functional abnormalities in the peripheral blood. However, the mechanism of large platelet production has not yet been clarified. In 1981, we reported acase with Bernard-Soulier syndrome(BSS) in whom giant platelets were considered to be formed by fusion of two or three platelets in the circulating blood. We examined the ultrastructure of platelets and megakaryocytes in another case with BSS (29 year-old female) and a case with May-Hegglin anomaly (31 year-old male). Whole blood and bone m
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Kim, Youngmi, Eunhee Kim, Olga Guryanova, Masahiro Hitomi, Andrew E. Sloan, Anita B. Hjelmeland, and Jeremy N. Rich. "Abstract 5192: Platelet derived growth factor receptors differentially inform intertumoral and intratumoral heterogeneity." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5192.

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