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Relevant bibliographies by topics / Platelet disorder

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Academic literature on the topic 'Platelet disorder'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Platelet disorder"

1

Gothwal, M., K. Sandrock-Lang, and B. Zieger. "Genetics of inherited platelet disorders." Hämostaseologie 34, no. 02 (2014): 133–41. http://dx.doi.org/10.5482/hamo-13-09-0049.

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SummaryThe current review describes inherited platelet disorders, illustrates their clinical phenotype and molecular genetic defects. Platelets are the key molecules mediating haemostasis via adhesion, activation and clot formation at the site of injury. The inherited platelet disorders can be classified according to their platelet defects: receptor/cytoskeleton defects, secretion disorder, and signal transduction defect.Patients with inherited thrombocytopathia present with mucous membrane bleedings (epistaxis, gingival bleeding) and may present with serious life threatening bleedings followi

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Zhaoyue Wang, Jumei Shi, Yue Han, Yingchun Wang, and Changgeng Ruan. "Spontaneous Platelet Aggregation With Congenital Giant Platelet Containing Large Granules and Thick Membrane." Clinical and Applied Thrombosis/Hemostasis 7, no. 4 (2001): 305–10. http://dx.doi.org/10.1177/107602960100700410.

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Inherited giant platelet disorders are a heterogeneous group of disorders. In the current study, a patient was reported with moderate bleeding tendency, giant platelets, and spontaneous platelet aggregation, which were not affected by the administration of aspirin or ticlopidine. The electron microscopy of platelets showed a black and thick plasma membrane with crystal-like fine hairs in the exterior coat and more large and variously shaped granules in the cytoplasm. The expression of glycoprotein (GP) Ib, GP IIb, and GP IIIa on platelet surface was normal, and no mutations in genes for GP Ibα

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Naina, Harris V. K., and Samar Harris. "Platelet and Red Blood Cell Indices in Harris Platelet Syndrome." Blood 108, no. 11 (2006): 3988. http://dx.doi.org/10.1182/blood.v108.11.3988.3988.

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Abstract Inherited giant platelet disorders are a group of rare disorders characterized by thrombocytopenia, giant platelets and variable bleeding symptoms. Naina et al., described a new giant platelet disorder called Harris Platelet Syndrome (HPS), the most common inherited giant platelet disorder occurring in up to one third of blood donors from north eastern part of Indian subcontinent. HPS is characterized by an autosomal dominant mode of inheritance with normal to severe thrombocytopenia (less than 50x109/L), giant platelets (mean platelet volume more than 10fL) and absent bleeding sympto

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Pham, Angie, and Jun Wang. "Bernard-Soulier Syndrome: An Inherited Platelet Disorder." Archives of Pathology & Laboratory Medicine 131, no. 12 (2007): 1834–36. http://dx.doi.org/10.5858/2007-131-1834-bsaipd.

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Abstract Bernard-Soulier syndrome is an inherited platelet disorder, which is transmitted in an autosomal recessive manner. This syndrome is characterized by variable thrombocytopenia and large defective platelets. Bernard-Soulier syndrome often presents early with bleeding symptoms, such as epistaxis, ecchymosis, menometrorrhagia, and gingival or gastrointestinal bleeding. Diagnosis can be confirmed by platelet aggregation studies and flow cytometry. The differential diagnosis includes the other inherited giant platelet disorders, as well as von Willebrand disease and immune thrombocytopenia

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Ranalli, Paola, Stefano Baldoni, Daniela Bruno, and Mauro Di Ianni. "MPN/MDS overlap syndrome anticipated by a severe bleeding diathesis: hypothesis of a pre-existing platelet disorder." Mediterranean Journal of Hematology and Infectious Diseases 16, no. 1 (2024): e2024067. http://dx.doi.org/10.4084/mjhid.2024.067.

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We report the case of a patient with a conclusive diagnosis of “MDS/MPN” Overlap Syndrome preceded by platelet disorder and hemorrhagic phenotype. We want to induce a reflection about diagnosis of oncohematological disorders in patient with a documented personal history of bleeding and/or platelet disorder, considering all the possible differential diagnosis: 1) Bleeding as the epiphenomenon of a still undiagnosed Myeloid Neoplasm or 2) Myeloid Neoplasm with germline predisposition and pre-existing platelet disorder; 3) Inherited platelet disorder successively developing MPN/MDS Overlap Syndro

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Antony-Debré, Iléana, Dominique Bluteau, Raphael Itzykson, et al. "MYH10 protein expression in platelets as a biomarker of RUNX1 and FLI1 alterations." Blood 120, no. 13 (2012): 2719–22. http://dx.doi.org/10.1182/blood-2012-04-422352.

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Abstract RUNX1 gene alterations are associated with acquired and inherited hematologic malignancies that include familial platelet disorder/acute myeloid leukemia, primary or secondary acute myeloid leukemia, and chronic myelomonocytic leukemia. Recently, we reported that RUNX1-mediated silencing of nonmuscle myosin heavy chain IIB (MYH10) was required for megakaryocyte ploidization and maturation. Here we demonstrate that runx1 deletion in mice induces the persistence of MYH10 in platelets, and a similar persistence was observed in platelets of patients with constitutional (familial platelet

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Handa, Makoto, Yohko Kawai, Tetuji Kamata та ін. "Platelet Unresponsiveness to Collagen: Involvement of Glycoprotein Ia-IIa (α2β1 Integrin) Deficiency Associated with a Myeloproliferative Disorder". Thrombosis and Haemostasis 73, № 03 (1995): 521–28. http://dx.doi.org/10.1055/s-0038-1653807.

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SummaryWe studied a 66-year-old man with a myeloproliferative disorder who presented with a prolonged bleeding time and marked thrombocytosis (platelet count, 3,890 × 109/1). There was no past history of a bleeding disorder. The patient had normal coagulation data. His platelets completely lacked collagen-induced platelet aggregation and adhesion, but showed normal responses to other agonists. All family members tested showed normal platelet aggregation with collagen.Analysis of 125I surface-labeled platelets by two-dimensional SDS gel electrophoresis disclosed absence of the spot correspondin

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Castilloux, Jean, Karen Moffat, Yang Liu, Jodi Seecharan, Menaka Pai, and Catherine Hayward. "A prospective cohort study of light transmission platelet aggregometry for bleeding disorders: Is testing native platelet-rich plasma non-inferior to testing platelet count adjusted samples?" Thrombosis and Haemostasis 106, no. 10 (2011): 675–82. http://dx.doi.org/10.1160/th11-06-0378.

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SummaryLight transmission platelet aggregometry (LTA) is important to diagnose bleeding disorders. Experts recommend testing LTA with native (N) rather than platelet count adjusted (A) platelet-rich plasma (PRP), although it is unclear if this provides non-inferior, or superior, detection of bleeding disorders. Our goal was to determine if LTA with NPRP is noninferior to LTA with APRP for bleeding disorder assessments. A prospective cohort of patients, referred for bleeding disorder testing, and healthy controls, were evaluated by LTA using common agonists, NPRP and APRP (adjusted to 250 x 109

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Massey, Gita, Laura Tyrrell, Yaser Diab, and William T. Gunning. "Medich Giant Platelet Syndrome: An Evolving Qualitative and Quantitative Platelet Disorder." Hematology Reports 14, no. 4 (2022): 349–57. http://dx.doi.org/10.3390/hematolrep14040049.

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Qualitative platelet disorders remain rare and varied. We describe here 2 additional patients with giant platelets, thrombocytopenia, deficiency in alpha granules and the presence of membranous inclusions within the cytoplasm. Collectively known as Medich syndrome, we further elucidated structural and clinical features of this rare syndrome. Platelets obtained from 2 patients with macro-thrombocytopenia were evaluated by electron microscopy. Structural findings were correlated with clinical characteristics. The defining morphologic feature found in the platelets of these patients is the presen

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Pujol-Moix, Nuria, Mariana Corrochano, Isabel Badell, Joan Carles Souto, and Josep F. Nomdedeu. "Platelet Ultrastructure in Familial Platelet Disorder with Associated Myeloid Malignancy (FPDMM)." Blood 136, Supplement 1 (2020): 37–38. http://dx.doi.org/10.1182/blood-2020-142248.

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The familial platelet disorder with associated myeloid malignancy (FPDMM) is an autosomal dominant platelet disorder, caused by germline RUNX1 mutations, with predisposition to develop hematologic malignancies, especially acute myeloid leukemia. In many of the FPDMM families reported, the platelet defect was a delta-storage-pool disease (d-SPD) which can also be found without leukemia propensity. However, it has not been studied whether the two types of d-SPD have a common nature. Platelet ultrastructure, previously very little studied, may be one of the aspects to be analyzed to solve this qu

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Dissertations / Theses on the topic "Platelet disorder"

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Neuger, Jolanta. "Platelet serotonin function and personality traits in affective disorder /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-181-0.

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Beutler, Lucinda. "Platelet and erythrocyte functional defects caused by mutations of GFI1B." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20481.

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GFI1B is a transcriptional repressor that is a major regulator of megakaryocytic and erythroid differentiation and development. The cause of a bleeding disorder in a four- generation Australian family, with cell changes consistent with aberrant platelet structure and function, and red blood cell morphology, showing autosomal dominant inheritance, was identified as being caused by a single nucleotide insertion into the GFI1B gene (c.880_881insC). The aims of this thesis were to study the effects of this mutant GFI1B on erythrocyte development in a cell culture model; to study how loss of Gfi1b

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Norazit, Anwar. "Vascular Endothelial Growth Factor (VEGF) and Platelet Derived Growth Factor (PDGF) in a Novel Model of Parkinson's Disease." Thesis, Griffith University, 2011. http://hdl.handle.net/10072/366312.

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Parkinson’s disease is a progressive neurodegenerative disorder, characterised histopathologically by the degenerating nigrostriatal pathway. Previous studies have shown a decrease in neurogenesis, dopaminergic neurons and neurotrophic factor levels in the Parkinson brain. This thesis investigates the capability of vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF) to stimulate endogenous neurogenesis and offer direct or indirect neuroprotection in a novel model of Parkinson’s disease. To assess the neurogenic capability of the postnatal substantia nigra, the e

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Sampaio, Thiago Pacheco de Almeida. "Relação entre a concentração de serotonina no plasma rico em plaquetas e a resposta à terapia comportamental baseada em exposição com prevenção de resposta no transtorno obsessivo-compulsivo." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-20022009-141000/.

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INTRODUÇÃO: Entre os tratamentos existentes para o transtorno obsessivocompulsivo (TOC) os mais eficazes são o farmacológico, com inibidores de recaptura de serotonina (IRS; inibidores seletivos de recaptura de serotonina [ISRS] e clomipramina), e o comportamental, baseado na técnica de exposição com prevenção de resposta (EPR). Ambas apresentam eficácia semelhante para os sintomas obsessivo-compulsivos e estudos demonstram que a EPR produz modificações neurobiológicas semelhantes às provocadas pelo tratamento com ISRS. Essas evidências sugerem que a resposta clínica à EPR está diretamente rel

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Cai, Huili. "Diagnostic des pathologies plaquettaires : optimisation de l'exploration des granules denses plaquettaires." Thesis, Université de Lorraine, 2015. http://www.theses.fr/2015LORR0067/document.

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Les plaquettes sont les cellules principales de l’hémostase. Leur anomalie qualitative et/ou quantitative est à l’origine d’une diathèse hémorragique. Le diagnostic des anomalies plaquettaires nécessite des tests biologiques. L’objectif de notre travail a été d’améliorer leur diagnostic, en particulier, de développer de nouveaux outils d’exploration des granules denses plaquettaires. Les pathologies plaquettaires héréditaires sont mal connues en Chine. Donc la cadre de notre collaboration Nancy /Wuhan nous avons publié un article en Chinois sur les thrombopénies héréditaires. Ensuite, nous avo

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Lynch, Susan Fraser. "Platelet and vascular studies in myeloproliferative disorders." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24860.

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We have studied a cohort of patients with polycythaemia vera (PV) primary thrombocythaemia (PT) and primary myelofibrosis (PMF) and described their clinical and laboratory features in comparison to other published observations. The demographic, haematological and molecular characteristics of our cohort were similar to other retrospective analyses, but the occurrence of thrombo-haemorrhagic complications was lower. The presence of vascular abnormalities in these patients was investigated using both established markers and an assay was devised to measure platelet, endothelial, leucocytes and red

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Longato-Stadler, Eva. "Psychopathology and Platelet MAO in a Criminal Male Population in Sweden." Doctoral thesis, Uppsala University, Department of Neuroscience, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2028.

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<p>The subjects were 130 male prisoners in Swedish jails were examined by SCID and the diagnoses given in terms of DSM-IV. The most common mental disorder was drug abuse. On Axis II several personality disorders were diagnosed. Personality assessments were made by KSP. High scores were mainly found for e.g. impulsiveness, sensation seeking, aggression and low scores in socialisation.</p><p>MAO assays were performed in 99 male criminal offenders and in 60 non-criminal volunteers. Offenders had lower MAO activity than controls also with the confounding factor smoking under control. It is propo

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Al, Ghaithi Rashid Hafidh Rashid. "Laboratory investigation of platelet function in patients with mild bleeding disorders." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8173/.

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Platelets play a crucial role in haemostasis by preventing bleeding at sites of vascular injury. Inherited or acquired platelet defects can impair haemostasis resulting in bleeding symptoms of varying severity ranging from mild to excessive which can be life threatening. Diagnosis of mild platelet-based bleeding disorders is challenging due to the absence of a gold standard technique and their variable bleeding symptoms and bleeding phenotypes observed in healthy individual as well as other haemostatic disorders. The work in this thesis built on the previous studies in the genotyping and plate

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Gurney, David Andrew. "Development and implementation of regional platelet diagnostic laboratory in order to enhance the diagnosis and treatment of inherited platelet function disorders." Thesis, University of Portsmouth, 2012. https://researchportal.port.ac.uk/portal/en/theses/development-and-implementation-of-regional-platelet-diagnostic-laboratory-in-order-to-enhance-the-diagnosis-and-treatment-of-inherited-platelet-function-disorders(d2bf09b6-16c1-4dcb-8eaa-61c3167d9fc9).html.

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This project sets out to create a reference laboratory service capable of detecting platelet function disorders using the latest techniques and based on the most current research. Platelet function disorders are difficult to diagnose due to differing phenotypic presentation and multiple causative agents. Platelet research has moved rapidly over the past decade and has included new reagents, analysers and techniques in the way platelet function disorders are diagnosed. A forward-looking diagnostic laboratory needs translate this ongoing research into routine laboratory practice, whilst ensuring

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Taylor, James Michael. "Validation of a new method for platelet HPA-1 phenotyping." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1133736.

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Polymorphisms of platelet glycoproteins (GPs) are frequently targets for anti-platelet antibodies. At least 19 antigenic polymorphisms have been identified on platelet GPs. Antibodies against the HPA-lb polymorphism (a Leu to Pro switch at amino acid residue 33 of the IIIa sub-unit of GP IIb/Illa) have been attributed to as much as 90% of all cases of neonatal alloimmune thrombocytopenic purpura and posttransfusion purpura in caucasians. The HPA-lb polymorphism has also been equivocally associated with coronary artery disease, particularly early onset (<60 years of age) myocardial infarction.

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Books on the topic "Platelet disorder"

1

D, Michelson Alan, ed. Platelets. 2nd ed. Academic Press/Elsevier, 2007.

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P, Caen J., ed. Platelet disorders. Baillière, 1989.

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D, Michelson Alan, ed. Platelets. Academic Press, 2002.

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European Symposium on Platelet Immunology (1st 1990 Paris, France). Platelet immunology: Fundamental and clinical aspects : proceedings of the First European Symposium on Platelet Immunology held in Paris, Palais du Luxembourg (France), March 1-2, 1990 = Immunologie plaquettaire : aspects fondamentaux et cliniques. John Libbey Eurotext, 1991.

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White, Melanie McCabe. Platelet protocols: Research and clinical laboratory procedures. Academic Press, 1999.

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1953-, Gresele Paolo, ed. Platelets in hematologic and cardiovascular disorders: A clinical handbook. Cambridge University Press, 2008.

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1953-, Gresele Paolo, ed. Platelets in hematologic and cardiovascular disorders: A clinical handbook. Cambridge University Press, 2008.

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R, Born Gustav V., and Neri Serneri G. G, eds. Antiplatelet therapy: Twenty years' experience : proceedings of a European conference, Florence, 26-28 March 1987. Excerpta Medica, 1987.

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European Thrombosis Research Organisation. Workshop. Monoclonal antibodies and human blood platelets: Proceedings of the European Thrombosis Research Organisation Workshop, under the patronage of the Institut national de la santé et de la recherche médicale, held in Lyon (France), 26-27 September 1985. Edited by McGregor John Louis and Institut national de la santé et de la recherche médicale (France). Elsevier Science Publishers, 1986.

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S, Authi Kalwant, Bruchhausen F. von 1929-, and Walter U. 1949-, eds. Platelets and their factors. Springer, 1997.

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Book chapters on the topic "Platelet disorder"

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Schott, K., M. Schnaidt, A. Batra, M. Bartels, and G. Buchkremer. "Platelet Antibodies In Mental Disorder." In Current Update in Psychoimmunology. Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6870-7_12.

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Pecknold, J. C., L. Luthe, and B. Suranyi-Cadotte. "Platelet Imipramine Binding Bmax Predicts Response to Anxiety in Alprazolam-Treated Panic Disorder Patients." In New Concepts in Anxiety. Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-11847-2_12.

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Regling, Katherine, and Meera Chitlur. "Platelet Disorders." In Benign Hematologic Disorders in Children. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49980-8_11.

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Eden, Robert D. "Platelet Disorders." In Principles of Medical Therapy in Pregnancy. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2415-7_184.

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Akkerman, Jan-Willem N., and Bernard De Bono. "Systems Biology to Study Platelet-Related Bleeding Disorders." In Platelet Proteomics. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470940297.ch12.

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Pecknold, J. C., L. Luthe, L. Iny, and M. H. Scott-Fleury. "Platelet [3H]-paroxetine and [3H]-imipramine binding in zacopride-treated patients with generalized anxiety disorder: preliminary results." In New Concepts in Anxiety. Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-11847-2_11.

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Singh, Avani M., and Kaaron Benson. "Platelet Transfusions." In Non-Neoplastic Hematologic Disorders. Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-62373-8_42.

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Robertson, Jeremy D., Victor S. Blanchette, and Walter H. A. Kahr. "Quantitative Platelet Disorders." In Practical Hemostasis and Thrombosis. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444306286.ch10.

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Cattaneo, Marco. "Qualitative Platelet Disorders." In Practical Hemostasis and Thrombosis. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444306286.ch11.

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Annamalai, Aniyizhai. "Platelet Function Disorders." In Medical Management of Psychotropic Side Effects. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51026-2_27.

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Conference papers on the topic "Platelet disorder"

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Batlle, J., M. F. López-Fernández, C. López-Berges, R. Sánchez, L. G. Villarón, and T. S. Zimmerman. "VON WILLEBRAND'S DISEASE TYPE IIB ASSOCIATED TO A COMPLEX THROMBOCYTOPENIC THROMBOCYTOPATHY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644642.

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A family bleeding disorder characterized by a new association between Type IIB von Willebrand's disease (vWD) and a complex platelet disfunction, with an intermittent thrombocytopenia is described in two patients from the same generation. The mother and a maternal aunt died having severe bleeding diathesis. The platelet abnormalities included: borderline or slightly low platelet count but moderate thrombocytopenia coincedent with the acute bleeding episodes, giant platelet site with a very heterogeneous distribution width, large number of vesicles in platelets by electron-microscopy recalling

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Okita, J. R., M. M. Frojmovic, S. Kristopeit, T. Wong, and T. J. Kunicki. "MONTREAL PLATELET SYNDROME: DECREASED ACTIVITY OF PLATELET CALPAINS ASSOCIATED WITH AGGREGATION ABNORMALITIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642822.

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The Montreal platelet syndrome (MPS) is an inherited disorder of platelet function characterized by a) severe thrombocytopenia, b) formation of "giant" platelets upon physical or biochemical stimulation, c) spontaneous aggregation (stir-induced microaggregate formation) and d) a lack of aggregation in response to thrombin. The Bernard-Soulier syndrome (BSS) is similar to MPS in that both syndromes are characterized by "giant" platelets and an abnormal aggregation response to thrombin. BSS patients have a deficiency of specific platelet glycoproteins (GPs). From our investigations we conclude M

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Kehrel, B., L. Ballesian, R. Kokott, W. Stenzinger, K. J. Clemetson, and J. Van De Loo. "REVERSIBLE DEFICIENCY OF INTACT THROMBOSPONDIN AND MEMBRANE GLYCOPROTEIN Ia IN PLATELETS OF A PATIENT WITH A BLEEDING DISORDER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644654.

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A 52 year old female patient with a severe bleeding tendency since the age of two was studied. Her history revealed recurrent petechial bleedings, two severe postoperative haemorrhagic episodes and intensivemenstrual bleedings which required blood transfusions. Coagulation studies ruled out any coagulation disorder including von Willebrand's disease. Platelet count and morphology(using light and electron microscopy) were normal. The patient had prolonged bleeding times (up to 15 min). Her platelets aggregated normally in response to ADP, arachidonic acid, thrombin, ionophore A 23187, epinephri

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Scharf, R. E., A. Wehmeier, and W. Schneider. "REDUCED PLATELET THROMBOXANE FORMATION IN ACUTE THROMBOTIC THROMBOCYTOPENIC PURPURA (TP): EVIDENCE FOR AN ABNORMAL PLATELET POPULATION WITH A TRANSIENT CYCLOOXYGENASE DEFECT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644588.

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We have recently shown that alpha-granule-depleted platelets circulate in acute TTP. These platelets are hemostatically defective due to partial loss of granular constituents and/or metabolic abnormalities. To further evaluate morphometric and metabolic changes of "exhausted" platelets, we studied their volume distribution and thromboxane A2 (TXA2) formation in a 35-year-old patient with primary TTP. Platelet volume distribution in whole blood was determined by the impedance method using citrate (0.38%)/glutaraldehyde (0.125%) as anticoagulant. TXB2 production was measured radioimmunologically

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Wachtfogel, Yanina T., Yizhar Floman, Meir Liebergall, Robert W. Colman, and Amiram Eldor. "PLATELET ALPHA2-ADRENERGIC RECEPTOR ABNORMALITIES IN PATIENTS WITH IDIOPATHK: SCOLIOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644567.

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Idiopathic scoliosis is a genetic multisystem disease involving skeletal, biochemical, central nervous svstem, muscle and blood platelet abnormalities. Platelets of patients with idiopathic scoliosis have been shown to have decreased adenosine diphosphate and epinephrine-induced aggregation. Similarities between the contractile protein system of platelets and muscle have made the platelet a popular model for certain aspects of muscle physiology. This study confirmed that 64% of the patient platelets tested exhibited a significantly decreased sensitivity to aggregation bv epinephrine. In seven

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Levy-Toledano, S., J. Enouf, M. Lebret, R. Bredoux, and J. P. Caen. "ABNORMAL CALCIUM TRANSPORT INTO MICROSOMES OF GRAY PLATELET SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644747.

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Gray platelets initially described as lacking α granules also show thrombin-induced aggregation and release lower than normal. One of the possible explanation is a modified intracellular Ca2+ concentration which is involved in platelet activation. We then decided to investigate the relationship between the morphological abnormality and a possible regulation of platelet Ca2+ concentration.We isolated a platelet membrane fraction (100,000 g) enriched in intracellular membranes which actively sequesters Ca2+. This Ca2+ uptake was mediated by a characterized (Ca2+ + Mg2+) ATPase.The isolated membr

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Weiss, H. J., V. T. Turitto, and H. R. Baumgartner. "FACTORS INFLUENCING FIBRIN DEPOSITION ON SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642950.

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During the past several years, we have initiated studies to determine the role of plasma factors and platelets, and the properties of the blood vessel, which influence the activation of the coagulation mechanism on the subendothelium. Studies were performed by exposing everted segments of de-endothelialized rabbit aorta, mounted in a perfusion chamber, to non-anticoagulated human blood for 5 to 10 minutes under a range of flow conditions, and measuring fibrin and platelet deposition on the subendothelium, and fibrinopepstide A (FPA) levels in post-chamber blood. In normal subjects, platelet de

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Cattaneo, M., A. Lecchi, L. J. McGregor, M. A. Randi, M. P. Mannucci, and A. Bianchi. "CHARACTERIZATION OF PLATELETS OF A PATIENT WITH A SELECTIVE DEFECT IN ADP-INDUCED AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643638.

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Abstract:

We studied a patient (V.R.) with a mild hemorrhagic disorder and prolonged bleeding time. Platelet aggregation induced by ADP (2-50 uM) in V.R.’s citrated PRP or washed platelets (WP) was greatly impaired; in contrast ADP (0.1-1 uM) induced normal platelet shape change of V.R. platelets. Collagen-induced aggregation was absent at low (1-2 ug/ml) but not at high concentration (10 ug/ml). Thrombin at high (1 U/ml) but not at low concentration (0.05 U/ml) induced normal aggregation of V.R.’s WP. Apyrase added to normal PRP or WP caused defective platelet aggregation similar to that observed for V

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Mehic, D., B. Eichinger, T. Dreier, et al. "Platelet function analyzer (PFA-100) in patients with bleeding disorder of unknown cause." In GTH Congress 2024 – 68th Annual Meeting of the Society of Thrombosis and Haemostasis Research – Building Bridges in Coagulation. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0044-1779167.

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Lillicrap, D., S. Windsor, Benford H. Hoogendorn, and A. R. Giles. "PLATELET VON WILLEBRAND FACTOR: STUDIES IN TYPE II VON WILLEBRAND′S DISEASE VARIANTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644108.

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Abstract:

Recent evidence suggests that platelet von Willebrand factor (vWf) plays an important role in maintenance of primary haemostasis. We have studied a normal population (N=24) and 15 patients with variant forms of von Willebrand's disease (vWd) to determine the utility of platelet vWf:Ag measurement in this disorder. Citrated blood was spun at 100 g for 10 mins at 20°C to prepare platelet rich plasma (PRP). The PRP was removed and platelet count and mean platelet volumes (MPV) were determined on a Coulter S+ counter. A platelet button was prepared by centrifugation of PRP at 3,500 g for 15 mins.

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