Relevant bibliographies by topics / Blood platelets

Academic literature on the topic 'Blood platelets'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Blood platelets"

Franco, Aime T., Adam Corken, and Jerry Ware. "Platelets at the interface of thrombosis, inflammation, and cancer." Blood 126, no. 5 (July 30, 2015): 582–88. http://dx.doi.org/10.1182/blood-2014-08-531582.

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Abstract Although once primarily recognized for its roles in hemostasis and thrombosis, the platelet has been increasingly recognized as a multipurpose cell. Indeed, circulating platelets have the ability to influence a wide range of seemingly unrelated pathophysiologic events. Here, we highlight some of the notable observations that link platelets to inflammation, reinforcing the platelet’s origin from a lower vertebrate cell type with both hemostatic and immunologic roles. In addition, we consider the relevance of platelets in cancer biology by focusing on the hallmarks of cancer and the ways platelets can influence multistep development of tumors. Beyond its traditional role in hemostasis and thrombosis, the platelet’s involvement in the interplay between hemostasis, thrombosis, inflammation, and cancer is likely complex, yet extremely important in each disease process. The existence of animal models of platelet dysfunction and currently used antiplatelet therapies provide a framework for understanding mechanistic insights into a wide range of pathophysiologic events. Thus, the basic scientist studying platelet function can think beyond the traditional hemostasis and thrombosis paradigms, while the practicing hematologist must appreciate platelet relevance in a wide range of disease processes.

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Heazlewood, Shen Y., Tanveer Ahmad, Monika Mohenska, Belinda B. Guo, Pradnya Gangatirkar, Emma C. Josefsson, Sarah L. Ellis, et al. "The RNA-binding protein SRSF3 has an essential role in megakaryocyte maturation and platelet production." Blood 139, no. 9 (March 3, 2022): 1359–73. http://dx.doi.org/10.1182/blood.2021013826.

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Abstract RNA processing is increasingly recognized as a critical control point in the regulation of different hematopoietic lineages including megakaryocytes responsible for the production of platelets. Platelets are anucleate cytoplasts that contain a rich repertoire of RNAs encoding proteins with essential platelet functions derived from the parent megakaryocyte. It is largely unknown how RNA binding proteins contribute to the development and functions of megakaryocytes and platelets. We show that serine-arginine–rich splicing factor 3 (SRSF3) is essential for megakaryocyte maturation and generation of functional platelets. Megakaryocyte-specific deletion of Srsf3 in mice led to macrothrombocytopenia characterized by megakaryocyte maturation arrest, dramatically reduced platelet counts, and abnormally large functionally compromised platelets. SRSF3 deficient megakaryocytes failed to reprogram their transcriptome during maturation and to load platelets with RNAs required for normal platelet function. SRSF3 depletion led to nuclear accumulation of megakaryocyte mRNAs, demonstrating that SRSF3 deploys similar RNA regulatory mechanisms in megakaryocytes as in other cell types. Our study further suggests that SRSF3 plays a role in sorting cytoplasmic megakaryocyte RNAs into platelets and demonstrates how SRSF3-mediated RNA processing forms a central part of megakaryocyte gene regulation. Understanding SRSF3 functions in megakaryocytes and platelets provides key insights into normal thrombopoiesis and platelet pathologies as SRSF3 RNA targets in megakaryocytes are associated with platelet diseases.

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D’Ambrosi, Silvia, R. Jonas Nilsson, and Thomas Wurdinger. "Platelets and tumor-associated RNA transfer." Blood 137, no. 23 (May 3, 2021): 3181–91. http://dx.doi.org/10.1182/blood.2019003978.

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Abstract Until recently, the nucleic acid content of platelets was considered to be fully determined by their progenitor megakaryocyte. However, it is now well understood that additional mediators (eg, cancer cells) can intervene, thereby influencing the RNA repertoire of platelets. Platelets are highly dynamic cells that are able to communicate and influence their environment. For instance, platelets have been involved in various steps of cancer development and progression by supporting tumor growth, survival, and dissemination. Cancer cells can directly and/or indirectly influence platelet RNA content, resulting in tumor-mediated “education” of platelets. Alterations in the tumor-educated platelet RNA profile have been described as a novel source of potential biomarkers. Individual platelet RNA biomarkers as well as complex RNA signatures may be used for early detection of cancer and treatment monitoring. Here, we review the RNA transfer occurring between cancer cells and platelets. We explore the potential use of platelet RNA biomarkers as a liquid biopsy biosource and discuss methods to evaluate the transcriptomic content of platelets.

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Delgado Lagos, Fredy, Amro Elgheznawy, Anastasia Kyselova, Dagmar Meyer zu Heringdorf, Corina Ratiu, Voahanginirina Randriamboavonjy, Alexander W. Mann, Beate Fisslthaler, Mauro Siragusa, and Ingrid Fleming. "Secreted modular calcium-binding protein 1 binds and activates thrombin to account for platelet hyperreactivity in diabetes." Blood 137, no. 12 (March 25, 2021): 1641–51. http://dx.doi.org/10.1182/blood.2020009405.

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Abstract Secreted modular calcium-binding protein 1 (SMOC1) is an osteonectin/SPARC-related matricellular protein, whose expression is regulated by microRNA-223 (miR-223). Given that platelets are rich in miR-223, this study investigated the expression of SMOC1 and its contribution to platelet function. Human and murine platelets expressed SMOC1, whereas platelets from SMOC1+/− mice did not present detectable mature SMOC1 protein. Platelets from SMOC1+/− mice demonstrated attenuated responsiveness to thrombin (platelet neutrophil aggregate formation, aggregation, clot formation, Ca2+ increase, and β3 integrin phosphorylation), whereas responses to other platelet agonists were unaffected. SMOC1 has been implicated in transforming growth factor-β signaling, but no link to this pathway was detected in platelets. Rather, the SMOC1 Kazal domain directly bound thrombin to potentiate its activity in vitro, as well as its actions on isolated platelets. The latter effects were prevented by monoclonal antibodies against SMOC1. Platelets from miR-223–deficient mice expressed high levels of SMOC1 and exhibited hyperreactivity to thrombin that was also reversed by preincubation with monoclonal antibodies against SMOC1. Similarly, SMOC1 levels were markedly upregulated in platelets from individuals with type 2 diabetes, and the SMOC1 antibody abrogated platelet hyperresponsiveness to thrombin. Taken together, we have identified SMOC1 as a novel thrombin-activating protein that makes a significant contribution to the pathophysiological changes in platelet function associated with type 2 diabetes. Thus, strategies that target SMOC1 or its interaction with thrombin may be attractive therapeutic approaches to normalize platelet function in diabetes.

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Sen Gupta, Anirban. "Synthetic Platelets for Treatment of Traumatic Hemorrhage and Thrombocytopenia." Blood 134, Supplement_1 (November 13, 2019): SCI—37—SCI—37. http://dx.doi.org/10.1182/blood-2019-121079.

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Platelets are primarily responsible for staunching bleeding by forming a 'platelet plug' and further amplifying thrombin generation on its surface to facilitate fibrin formation, leading to hemostatic clot formation at the site of vascular breach. Therefore, platelet transfusions are clinically used to mitigate bleeding risks in thrombocytopenia (prophylactic transfusion) and to mitigate hemorrhage in traumatic injuries (emergency transfusion). Currently these transfusions utilize donor-derived platelets, stored at 20-24oC with gentle agitation. In this condition, platelets have high risk of bacterial contamination and very short shelf-life (~ 5 days), which severely limit their logistical availability and use. Several parallel strategies are currently undergoing research to address these issues, including platelet storage at reduced temperatures (chilled or freeze-dried), pathogen reduction technologies and bioreactor-based in vitro platelet production from precursor cells. An alternative (and complimentary) approach that is the focus of our research is the engineering of I.V.-administrable synthetic hemostat nanoparticles that functionally mimic platelet's clotting mechanisms. These 'synthetic platelet' nanoparticle systems can be manufactured at large scale, sterilized without compromising functions and stored for long periods of time (6-9 months), thereby allowing significant logistical advantages in transfusion applications. Here we present in vitro and in vivo evaluation of such technology. For these studies, the 'synthetic platelet' nanoparticles were manufactured by decorating liposomes with a combination of VWF-binding, collagen-binding and fibrinogen-mimetic peptides, for integrative mimicry of platelet's hemostasis-relevant adhesive and aggregatory mechanisms. The nanoparticles were stored at room temperature in aqueous suspension as well as lyophilized powder, and particle stability was assessed over 6-9 months by dynamic light scattering (DLS). The nanoparticles were also exposed to E-beam sterilization, and particle stability as well platelet-mimetic bioactivity was assessed by DLS, aggregometry, microfluidics and rotational thromboelastometry (ROTEM). The systemic safety and targeted hemostatic efficacy of I.V.-administered nanoparticles were evaluated in mouse model of thrombocytopenia, and in mouse, rat and pig models of traumatic hemorrhage. DLS and electron microscopy confirmed that the synthetic platelet nanoparticles have a size of 150-200 nm diameter, and they remain stable over 6-9 months in storage. Microfluidic studies showed that these nanoparticles could rapidly adhere to 'vWF + collagen'-coated surfaces and enhance the recruitment and aggregation of active platelets on these surfaces. Aggregometry studies showed that the nanoparticles did not affect resting platelets but enhanced aggregation of ADP- or collagen-activated platelets (i.e. no thrombotic risk towards resting platelets). Flow cytometry studies confirmed this specificity of nanoparticle binding to active platelets. ROTEM studies showed that the 'synthetic platelet' nanoparticles significantly improved clot kinetics and firmness. In vivo, in all animal models, the nanoparticles showed no systemic pro-thrombotic effects, as assessed by hemodynamics as well as organ histology. In thrombocytopenic mice, prophylactically administered 'synthetic platelet' nanoparticles dose-dependently reduced tail bleeding time. In mouse, rat and pig trauma models, post-injury administration of 'synthetic platelet' nanoparticles reduced blood loss, stabilized blood pressure, delayed hypotension and thereby significantly improved survival. The nanoparticles could be further utilized as a platform for targeted presentation of phosphatidylserine (PS) to augment thrombin generation, or targeted delivery of tranexamic acid (TXA) for anti-fibrinolytic effect or delivery of inorganic polyphosphate (PolyP) to augment clot stability. These studies not only establish the potential of these nanoparticles as a platelet surrogate for transfusion applications, but also demonstrate their utilization as a platform for modular augmentation of various hemostatic outputs in prophylactic and emergency applications. Figure Disclosures Sen Gupta: Haima Therapeutics LLC: Equity Ownership.

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Maurya, Preeti, Sara Ture, Kathleen E. McGrath, James Palis, and Craig N. Morrell. "Adult, but Not Neonatal, Platelet Transfusions Drive a Monocyte Trafficking Phenotype in Vitro and In Vivo." Blood 138, Supplement 1 (November 5, 2021): 2144. http://dx.doi.org/10.1182/blood-2021-152913.

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Abstract Although, thrombocytopenia can affect all age groups, neonates, especially pre-term, have an increased incidence of thrombocytopenia. Platelet transfusions may reduce the bleeding risk in neonates, but are also associated with adverse short and long-term immune and inflammatory outcomes. A randomized trial of platelet transfusions in neonates found that transfusion was associated with an increased risk of necrotizing enterocolitis, unilateral/bilateral retinopathy, and bronchopulmonary dysplasia. Past work from our research team found that neonatal platelets expressed lower levels of mRNA for many immune related molecules compared to adult platelets. We therefore sought to determine whether the transfusion of adult platelets to neonates resulted in developmental immune dysregulation, with a focus on platelet and monocyte interactions. To explore the interactions between monocytes and platelets, we isolated monocytes from adult mouse bone marrow and co-incubated monocytes with adult (>8 weeks old) or neonatal mouse platelets (7 days old mice) and determined inflammatory and trafficking monocyte phenotypes by flow cytometry and qRT-PCR. Monocytes treated with adult platelets had an increased inflammatory (Ly6C hi) and trafficking phenotype (CCR2 hi), while monocytes treated with neonatal platelets adopted an inflammatory, but not trafficking phenotype. As expected, adult platelets increased the expression of monocyte inflammatory (Nos2, Cxcl1, Ccl2) and trafficking (Ccr2) mRNA, while neonatal platelets also increased inflammatory mRNA expression, but did not increase Ccr2 expression. Adult platelets express more Selp (P-selectin) than neonatal platelets and P-selectin is a major mediator of platelet and monocyte interactions. We confirmed that adult platelets expressed more P-selectin protein compared to neonatal platelets, and found that blocking P-selectin decreased adult platelet induced CCR2 expression to levels similar to monocytes treated with neonatal platelets. Using a transwell chamber we assessed adult and neonatal platelet effects on monocyte migration towards the CCR2 ligand CCL2. Monocytes were treated with adult platelets had significantly greater monocyte migration compared to monocytes co-incubated with neonatal platelets. To model platelet transfusions in the setting of thrombocytopenia, we used 14d old thrombopoietin receptor knockout mice (TPOR -/-) that have low platelet counts, and infused adult or neonatal platelets. We observed a significant increase in inflammatory and trafficking monocytes in mice transfused with adult platelets compared to those transfused with neonatal platelets. Using an in vivo model of monocyte chemotaxis, mice were treated with CCL2 intraperitoneal after platelet transfusion. Adult platelet transfusions, but not neonatal, increased monocyte peritoneal trafficking to CCL2. These data provide comparative insights as to how adult and neonatal platelet transfusions regulate monocyte functions. Adult platelet transfusions to neonates are associated with an inflammatory and trafficking monocyte phenotype that is platelet P-selectin dependent and may have a major impact on neonatal platelet transfusion complications. Disclosures Palis: Rubius Therapeutics: Consultancy.

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Denorme, Frederik, Bhanu Kanth Manne, Irina Portier, Alicia S. Eustes, Yasuhiro Kosaka, Benjamin T. Kile, Matthew T. Rondina, and Robert A. Campbell. "Platelet necrosis mediates ischemic stroke outcome in mice." Blood 135, no. 6 (February 6, 2020): 429–40. http://dx.doi.org/10.1182/blood.2019002124.

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Abstract Dysregulated platelet functions contribute to the development and progression of ischemic stroke. Utilizing mice with a platelet-specific deletion of cyclophilin D (CypD), a mediator of necrosis, we found that platelet necrosis regulates tissue damage and outcomes during ischemic stroke in vivo. Mice with loss of CypD in platelets (CypDplt−/−mice) exhibited significantly enhanced cerebral blood flow, improved neurological and motor functions, and reduced ischemic stroke infarct volume after cerebral ischemia-reperfusion injury. These effects were attributable, at least in part, to platelet-neutrophil interactions. Twenty-four hours after stroke, significantly more circulating platelet-neutrophil aggregates (PNAs) were found in CypDplt+/+ mice. Underscoring the role of platelet necrosis in PNA formation, we observed a significant number of phosphatidylserine (PS)+ platelets in PNAs in CypDplt+/+ mice. In contrast, significantly fewer platelets in PNAs were PS+ in CypDplt−/− counterparts. Accordingly, mice with CypD-deficient platelets had fewer neutrophils and PNAs recruited to their brain following stroke relative to wild-type counterparts. Neutrophil depletion in wild-type mice conferred protection from ischemic stroke to a similar degree as observed in mice with CypD-deficient platelets. Neutrophil depletion in CypDplt−/− mice did not further reduce infarct size. Transmission electron microscopy of ex vivo–formed PNAs revealed a propensity of necrotic platelets to interact with neutrophils. These results suggest that necrotic platelets interact with neutrophils to exacerbate brain injury during ischemic stroke. Because inhibiting platelet necrosis does not compromise hemostasis, targeting platelet CypD may be a potential therapeutic strategy to limit brain damage following ischemic stroke.

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Jacob, Shancy, Marina Tistao, Abigail Ajanel Gomez, Frederik Denorme, Yasuhiro Kosaka, Bhanu Kanth Manne, Li Guo, Robert A. Campbell, Matthew T. Rondina, and Jesse W. Rowley. "Mitochondrial Fission Protein Drp1 Regulates Platelet Function." Blood 142, Supplement 1 (November 28, 2023): 1201. http://dx.doi.org/10.1182/blood-2023-187556.

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Background: Mitochondria in platelets contribute to platelet function and are altered by diseases that involve dysregulated hemostasis or thrombosis. Mitochondrial integrity, governed by its size, number and distribution is modulated by fusion and fission proteins. Pharmacological inhibition of the mitochondrial fission protein Dynamin-related protein 1 (Drp1) has been shown to inhibit granule release in human platelets and impair thrombus formation in a murine model of thrombosis. However, the mitochondrial roles for Drp1 in platelet function are still largely unknown. Objective: To determine the mitochondrial roles of Drp1 in regulating platelet function. Methods: PF4-Cre mediated MK/platelet specific Drp1 null mice (Drp1 -/-) were used. Platelet morphology in Drp1 -/- and wild type (WT) platelets was analyzed by confocal microscopy. Procoagulant platelet formation (PS +ve platelets) after thrombin and the GPVI agonist convulxin (THR+CVX) stimulation was measured using Annexin V staining. Mitochondrial potential (ΔΨm) and mass at baseline and after stimulation was measured using TMRM and mitotracker green. Washed platelet activation in WT and Drp1 -/- platelets in response to convulxin was measured by flow cytometry. Platelet cytoplasmic calcium transients were measured using FURA-2AM after stimulation with THR+CVX. Phosphorylation of Drp1 (pDrp1 S616) in washed WT platelets in response to dual agonist THR+CVX was measured by western blotting. Results: Drp1 -/- platelets were bigger in size than WT platelets as measured by microscopy and had increased mitochondrial mass as determined by flow cytometry. Absence of Drp1 reduced activation of the αIIb/β3 fibrinogen binding receptor (P=0.035; n=5-6 per group) and reduced alpha granule release (P=0.025; n=5-6 per group) in response to CVX.Dual agonist stimulation resulted in reduced PS +ve platelets in Drp1 -/- compared to WT platelets (P=0.0035; n=7 per group). Since depolarization precedes PS exposure, we measured ΔΨm using TMRM in resting and dual agonist stimulated WT and Drp1 -/- platelets. No difference in ΔΨm was observed in resting Drp1 -/- vs WT platelets whereas, stimulated Drp1 -/- platelets exhibited significantly higher ΔΨm (P=0.038; n=4 per group) than stimulated WT platelets. Interestingly, in response to dual agonists, Drp1 -/- platelets also showed a significant increase (P<0.001) in cytoplasmic calcium transients than WT platelets. Western blot analyses of washed WT platelets stimulated with dual agonist showed phosphorylation of Drp1 at S616 (S616), indicating Drp1 activation. Conclusion: These findings highlight a role for Drp1 in murine platelet mitochondrial function, GPVI activation, and procoagulant platelet formation.

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Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Dynamics of leukocyte-platelet adhesion in whole blood." Blood 78, no. 7 (October 1, 1991): 1730–37. http://dx.doi.org/10.1182/blood.v78.7.1730.1730.

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Abstract The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a marked increase in the percentage of monocytes and neutrophils (PMN) binding platelets, as well as an increase in the number of platelets bound per monocyte and PMN. Lymphocytes were unaffected. Monocytes bound more platelets and at an initially faster rate than PMN. This increase in monocyte and PMN adhesion to platelets was completely inhibited by the blocking monoclonal antibody (MoAb), G1, to GMP-140. When the combination of epinephrine and adenosine diphosphate (epi/ADP) was used as a less potent agonist in the presence of RGDS, GMP-140 expression per platelet was less, and while monocyte-platelet conjugates formed, PMN-platelet conjugates did not. With epi/ADP in the absence of RGDS, there was an immediate, marked decrease in the percentage of all leukocytes with bound platelets, simultaneous with an increase in the percentage of unbound platelet aggregates. As these platelet aggregates dissociated, the percentage of monocytes and PMN with adherent platelets increased, with monocytes again binding at a faster initial rate than PMN. This recovery of monocyte and PMN adhesion to platelets was also inhibited by the G1 MoAb. We conclude that: (1) monocytes and PMN bind activated platelets in whole blood through GMP-140; (2) monocytes have a competitive advantage over PMN in binding activated platelets, particularly when less potent platelet agonists are used; and (3) platelet aggregate formation initially competes unactivated platelets off leukocytes; subsequent aggregate dissociation allows the now activated platelets to readhere to monocytes and PMN through GMP-140. These studies further elucidate the dynamic interaction of blood cells and possible links between coagulative and inflammatory processes.

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The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a marked increase in the percentage of monocytes and neutrophils (PMN) binding platelets, as well as an increase in the number of platelets bound per monocyte and PMN. Lymphocytes were unaffected. Monocytes bound more platelets and at an initially faster rate than PMN. This increase in monocyte and PMN adhesion to platelets was completely inhibited by the blocking monoclonal antibody (MoAb), G1, to GMP-140. When the combination of epinephrine and adenosine diphosphate (epi/ADP) was used as a less potent agonist in the presence of RGDS, GMP-140 expression per platelet was less, and while monocyte-platelet conjugates formed, PMN-platelet conjugates did not. With epi/ADP in the absence of RGDS, there was an immediate, marked decrease in the percentage of all leukocytes with bound platelets, simultaneous with an increase in the percentage of unbound platelet aggregates. As these platelet aggregates dissociated, the percentage of monocytes and PMN with adherent platelets increased, with monocytes again binding at a faster initial rate than PMN. This recovery of monocyte and PMN adhesion to platelets was also inhibited by the G1 MoAb. We conclude that: (1) monocytes and PMN bind activated platelets in whole blood through GMP-140; (2) monocytes have a competitive advantage over PMN in binding activated platelets, particularly when less potent platelet agonists are used; and (3) platelet aggregate formation initially competes unactivated platelets off leukocytes; subsequent aggregate dissociation allows the now activated platelets to readhere to monocytes and PMN through GMP-140. These studies further elucidate the dynamic interaction of blood cells and possible links between coagulative and inflammatory processes.

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Dissertations / Theses on the topic "Blood platelets"

Law, Robert. "PDE3A signalling in blood platelets." Thesis, University of Hull, 2016. http://hydra.hull.ac.uk/resources/hull:13761.

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Cyclic 3’, 5’ adenosine monophosphate (cAMP) signalling downstream of prostacyclin (PGI₂) is a key inhibitory pathway in blood platelets. This pathway is dynamically regulated by phosphodiesterase 3A (PDE3A), which hydrolyses cAMP into metabolically inactive AMP. Although PDE3A is an established drug target in anti-platelet therapies, the molecular mechanisms that underlie its function in platelets remain unclear. Therefore, the major aim of this study was to further explore PDE3A signalling in human platelets. Using a combination of cell fractionation and immunoblotting we identified two PDE3A splice variants in platelets, PDE3A1 and PDE3A2, that were differentially localised within the cell. PDE3A1 was located in the membrane fraction, whereas PDE3A2 was primarily located in the cytosolic fraction. Treatment of platelets with PGI2 induced a transient phosphorylation of PDE3A2 at Ser³¹² in a PKA dependent manner. In contrast, no phosphorylation of PDE3A1 was detected. The phosphorylation of PDE3A2 was associated with increased PDE3A enzymatic activity, which suggested that cAMP signalling activated only the cytosolic form of the enzyme. In many cells, A-kinase anchoring proteins (AKAPs) orchestrate a coordinated response between PKA and its effector proteins. The phosphorylation and activation of PDE3A2 in response to PGI2 was blunted by a cell permeable peptide inhibitor of PKA-AKAP interactions suggesting that PKA-mediated activation of PDE3A2 was dependent on an AKAP. Using a cAMP-pull down approach to enrich cAMP binding proteins combined with immunoblotting, we confirmed the presence of two AKAP7 isoforms (δ and γ) in platelets. Additionally, we found that AKAP7δ co-precipitated with PDE3A2 and possessed associated PDE3A activity. Furthermore, AKAP7 also possessed PKA activity, which was a result of its constitutive association with PKA-II. Critically, immunoprecipitated PDE3A was found to be co-associated with both PKA-II and AKAP7δ. The findings in this thesis suggest that blood platelets express multiple differentially-regulated PDE3A splice variants, of which PDE3A2 is regulated by PKA-II within a novel cytosolic AKAP7δ facilitated signalling complex. The selective inhibition of PDE3A splice variants and/or pharmacological disruption of PDE3A signalosomes may provide safer and more specific ways of controlling pathological platelet activation.

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Stott, Andrew James. "Studies on human blood platelets." Thesis, University of Warwick, 1990. http://wrap.warwick.ac.uk/57766/.

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This project was undertaken to increase the understanding of platelet function, with paticular emphasis on abnormal platelets in diabetes mellitus, and improving the quality of platelet concentrates for transfusion. {1} Potential platelet antagonists, including PGE1, verapamil, insulin and hirudin, were added to platelet concentrates in an attempt to improve the recovery and shelf-life of the concentrate. Each "preservative" caused some improvement in platelet concentrate quality, as measured by functional tests, and radio-immunoassay for the platelet activation marker, B- thromboglobulin. The best results were obtained with the addition of PGE1, which facilitated recovery of all samples to which it was added, suggesting a cheap way of ensuring consistently good platelet concentrates. {2} Various investigations were carried out regarding abnormal platelet function in diabetes mellitus. No significant differences were found in the responses of platelets from diabetics and age-matched controls to the calcium-channel blocking drug, Verapamil, in vitro. Similarly, the capacity of diabetic platelets to produce malondialdehyde, a by-product of thromboxane A2 synthesis, was not significantly different from control platelets. The use of insulin in aggregometry studies showed, surprisingly, that insulin could have a pro-aggregatory effect on platelets from diabetics, but not those from healthy controls. In addition, evidence for the existence of a platelet aggregation-enhancing factor in the plasma of diabetics and older controls was obtained. {3} Extensive tests to investigate the nature of spontaneous platelet aggregation (SPA) in whole blood have established the existence of two types of SPA, (i) ADP-dependent, and (ii) ADP-independent. The results obtained suggest a major role for erythrocytes in the development of inappropriate platelet aggregation.

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Kremer, Hovinga Johanna Anna. "Malondialdehyd fomation by blood platelets /." Bern, 1990. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Ramström, Sofia. "The role of platelets in whole blood coagulation /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med776s.pdf.

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Carter, A. J. "Thromboxane synthesis in human blood platelets and blood vessels." Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355288.

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Ledent-Semple, Elisabeth. "A study of factors influencing the quality of blood products during preparation, storage and filtration /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med667s.pdf.

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Taha, Mariam. "Bacterial Contamination of Platelet Concentrates: Role of Biofilm Formation and Manufacturing Process." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35192.

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Bacterial contamination of platelet concentrates (PCs) poses the highest transfusion-associated infectious risk with skin flora, such as Staphylococcus epidermidis and Staphylococcus capitis, being the predominant contaminants. These bacteria are able to form surface-attached aggregates or biofilms, which are present in the skin of healthy blood donors and can subsequently be isolated from contaminated PCs. Disinfection of the venipuncture area before donation with a combination of 2% chlorhexidine-gluconate and 70% isopropanol is used at Canadian Blood Services. However, not all bacteria are eliminated during skin disinfection since contaminated PCs are still captured during routine PC screening. In this thesis, the ability of biofilm-forming S. epidermidis and S. capitis to resist the currently used disinfectants was explored. It was demonstrated that although a combination of chlorhexidine and isopropanol has a bactericidal effect, it is unable to completely eradicate skin flora biofilms. Several countries have implemented Pathogen Inactivation Technologies (PITs) as a measure to help control transfusing bacterially-contaminated PCs by exposing PC units to ultra violet light. However, no investigations have been done to evaluate the ability of PITs against bacterial biofilms, which was one of the objectives of this thesis. Data revealed that the efficacy of a currently used PIT, the Mirasol® system, is similar for S. epidermidis present in PCs produced from whole blood inoculated with biofilm or non-biofilm cells. However, treatment effectiveness was strain dependent. In conclusion, further investigation to improve donor skin disinfection and PITs should be considered. Surveillance at Canadian Blood Services shows that contamination rates in single-donor apheresis PCs (Aph-PCs) is generally higher than in four-donor buffy coat platelet pools (BC-PCs). This study investigated whether the BC-PC production method contributes to this observation as BC-PCs are derived from WB that is left to rest overnight while Aph-PCs are collected directly from the donor. Data showed that WB hold during BC-PC production does not have a broad-spectrum bactericidal effect and therefore other factors contribute to low rates of contamination in BC-PCs. The work presented in this thesis provides an insight to bacterial residence and persistence during blood product manufacturing and makes suggestions for PC safety improvements.

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Lisiak, Karolina. "The role of platelets in the activation of TAFI in model thrombi." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24805.

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Bateson, E. A. J. "Cryopreservation of platelets : investigation of factors affecting recovery and function of frozen and thawed platelets." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233520.

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Sage, Stewart O. "Stimulus-response coupling in human blood platelets." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236016.

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Books on the topic "Blood platelets"

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

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D, Michelson Alan, ed. Platelets. San Diego: Academic Press, 2002.

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1942-, Phillips David R., and Shuman Marc A, eds. Biochemistry of platelets. Orlando: Academic Press, 1986.

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J, Westwick, ed. Mechanisms of stimulus-response coupling in platelets. New York: Plenum Press, 1985.

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

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

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Davie, E. W., and E. Kakishita. Blood coagulation, fibrinolysis, and platelets. Tokyo: Springer, 1996.

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1951-, Parnham Michael J., and Prop Gerrit, eds. Cologne Atherosclerosis Conference, Nr. 3, platelets. Basel: Birkhäuser, 1986.

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Ch, Kessler, Medizinische Universität zu Lübeck. Klinik für Neurologie., and Symposium on Platelet-Vessel Wall Interaction (1989 : Lübeck, Germany), eds. Platelets and atherosclerosis. Berlin: Springer-Verlag, 1990.

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M, Gibbins Jonathan, and Mahaut-Smith Martyn P, eds. Platelets and megakaryocytes. Totowa, N.J: Humana Press, 2004.

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Book chapters on the topic "Blood platelets"

Momi, Stefania, and Viroj Wiwanitkit. "Phylogeny of Blood Platelets." In Platelets in Thrombotic and Non-Thrombotic Disorders, 11–19. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_2.

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Ordinas, A., G. Escolar, and J. G. White. "Ultrastructure of platelets and platelet-surface interactions." In The Role of Platelets in Blood-Biomaterial Interactions, 3–13. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1745-6_1.

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White, James G. "The Cytoskeleton of Human Blood Platelets." In Blood Cell Biochemistry, 113–48. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9531-8_5.

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Moisan, A., T. Lamy, A. Devillers, J. Le Cloirec, P. Y. Le Prise, and J. Y. Herry. "Labeled Platelets in Idiopathic Thrombocytopenic Purpura." In Radiolabeled Blood Elements, 325–29. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2462-5_51.

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Davies, J. A. "Pharmacology of platelets." In The Role of Platelets in Blood-Biomaterial Interactions, 45–57. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1745-6_4.

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Louwes, H., and J. J. Schuurman. "Clinical Applications of 111In-Tropolonate Labelled Platelets." In Radiolabeled Blood Elements, 99–106. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2462-5_14.

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Moser, Kenneth M. "Indium-111 Platelets in Thromboembolism: Can Labeled Platelets be Used to Evaluate Antithrombotic Therapy?" In Radiolabeled Cellular Blood Elements, 155–76. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4922-8_9.

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Mustard, J. Fraser. "Pathophysiology, Biochemistry, and Pharmacology of Platelets." In Radiolabeled Cellular Blood Elements, 1–12. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4922-8_1.

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Kotzé, H. F., V. van Wyk, A. du P. Heyns, J. P. Roodt, M. G. Lötter, and P. N. Badenhorst. "Influence of Platelet Membrane Sialic Acid and Platelet Associated IgG on Ageing and Sequestration of Blood Platelets in Baboons." In Radiolabeled Blood Elements, 131–34. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2462-5_19.

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Aiuti, Alessandro, Serena Scala, and Christian Chabannon. "Biological Properties of Hematopoietic Stem Cells: Scientific Basis for Hematopoietic Cell Transplantation." In The EBMT Handbook, 57–66. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_7.

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AbstractHematopoiesis—from the Greek term for “blood making”—is the adaptive process by which mature and functional blood cells are continuously replaced over the entire lifetime of an individual. Erythrocytes, platelets, and the various subsets of leukocytes all have finite although different life spans. As a consequence, the daily production of red blood cells, platelets, and neutrophils under homeostatic conditions amounts to more than 300 billion cells.

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Conference papers on the topic "Blood platelets"

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

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Synthesis of platelet activating factor (PAF) by human blood platelets is a controversial issue. Whereas some groups have reported the synthesis, induced by thrombin, collagen or Ca2--ionophore Azsio?, others were unable to obtain for instance the thrombin-induced PAF synthesis. Also, synthesis of only up to 6 pMoles PAF/10 platelets has been reported, but leucocytes may synthesize up to 6000 pMoles PAF/10 cells. Only an 0.1% leucocyte contamination would thereby explain the “ platelet PAF synthesis” . We therefore optimized the PAF synthesis by human blood platelets and leucocytes, induced by thrombin and A23i07. As platelets have been reported to show an increased PAF synthesis upon treatment with phenylmethylsulfonylfluoride (PMSF), this was also investigated.Leucocytes were optimally stimulated with 10 uM Azale? (mean ± SD 4678 ± 2033, range 1698-7058 pMoles PAF/10 cells, n=6), but could not be stimulated by thrombin. PMSF treatment itself induced PAF synthesis by these cells, but this was not influenced by thrombin or A23ia7.Platelet suspensions, with <0.005% leucocyte contamination as determined by light microscopy after Jenner-Giemsa staining, could synthesize PAF when treated with PMSF and stimulated with 2.5 IU/ml thrombin (mean ± SD 0.6 ± 0.3, range 0.3-1.0 pMoles PAF/10 platelets, n=6), but in these suspensions A23io7-induced synthesis could not be demonstrated.The results indicate that synthesis of PAF by human blood platelets is not due to contaminating leucocytes, if thrombin is used as the stimulus. These results were confirmed by 3H-acetate uptake experiments.

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Asijee, G. M., T. Bruin, A. Sturk, J. E. ten Cate, and L. Muszbek. "VINCULIN ISOFORMS IN HUMAN BLOOD PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643902.

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In several cells vinculin has been implicated in the interaction between the cytoskeleton and the outer ceil membrane. We have recently demonstrated that vinculin becomes associated with the Triton X-100 insoluble cytoskeleton of blood platelets upon thrombin-induced activation (Asijee et al, Exp Cell Res, 1987, in press). In the present study we demonstrate by SDS-PAGE and immunoblotting that vinculin is also present in the membrane skeleton of both non-activated and activated human blood platelets. The membrane skeleton was prepared by the method of Fox (J Clin Invest, 1985: 76, 1673), and platelets were stimulated 5 min at 37 °c with 0.1 U/ml thrombin. The association was specifically inhibited by DNase I-induced depolymerization of the actin filaments.Protein analysis by the O’Farrell technique (first dimension IEF, second dimension SDS-PAGE) and subsequent immunoblotting demonstrated purified vinculin to consist of 4 major isoforms (pI 6.8 - 7.2). These isoforms differed in subcellular distribution. Upon thrombin-induced platelet activation, cytoskeletal vinculin consisted of the 2 most acidic isoforms, and cytoplasmic vinculin of 2 more basic isoforms. The membrane skeleton-associated vinculin contained all 4 isoforms.We conclude that: 1. vinculin is a component of the membrane skeleton of both non-activated and activated human blood platelets, 2. similar to chicken gizzard smooth muscle cells, human blood platelet vinculin consists of several isoforms with differing subcellular distribution.

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Shattil, S. J., J. A. Hoxie, M. Cunningham, C. S. Abrahms, J. O’Brien, and Z. Budzynski. "DETECTION OF ACTIVATED PLATELETS IN WHOLE BLOOD BY FLOW CYTOMETRY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643830.

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Platelets may become activated in a number of clinical disorders and participate in thrombus formation. We have developed a direct test for activated platelets in whole blood that utilizes dual-color flow cytometry and requires no washing steps. Platelets were distinguished from erythrocytes and white blood cells in the flow cytometer by labeling the platelets with biotin-AP1, an antibody specific for membrane glycoprotein lb, and analyzing the cells for phycoerythrin-streptavidin fluorescence. Membrane surface changes resulting from platelet activation were detected with three different FITC-labeled monoclonal antibodies: 1) PAC1, an antibody specific for the fibrinogen receptor on activated platelets; 2) 9F9, which binds to the D-domain of fibrinogen and detects platelet-bound fibrinogen; and 3) S12, which binds to an alpha-granule membrane protein that associates with the platelet surface during secretion. Unstimulated platelets demonstrated no PAC1, 9F9, or S12-specific fluorescence, indicating that they did not bind these antibodies. Upon stimulation with agonists, however, the platelets demonstrated a dose-dependent increase in FITC-fluorescence. The binding of 9F9 to activated platelets required fibrinogen. Low concentrations of ADP and epinephrine, which induce fibrinogen receptors but little secretion, stimulated near-maximal PAC1 or 9F9 binding but little S12 binding. On the other hand, a concentration of phorbol myristate acetate that evokes full platelet aggregation and secretion induced maximal binding of all three antibodies. When blood samples containing activated and non-activated platelets were mixed, as few as 0.8% activated platelets could be detected by this technique. There was a direct correlation between ADP-induced FITC-PAC1 binding and binding determined in a conventional 125I-PAC1 binding assay (r = 0.99; p < 0.001). These studies demonstrate that activated platelets can be reliably detected in whole blood using activation-dependent monoclonal antibodies and flow cytometry. This method may be useful to assess the degree of platelet activation and the efficacy platelet inhibitor therapy in thrombotic disorders.

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AlMomani, T., H. S. Udaykumar, J. Marshall, and K. B. Chandran. "Dynamic Simulation of Red Blood Cells/Platelet Interaction in Arteriolar Blood Flow." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175290.

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Hemodynamic forces have been proposed as a major factor in thrombosis (thrombus formation) in the human cardiovascular system [1]. It has been suggested that platelet activation, aggregation and adhesion to the surface of the implants result in the formation of the mural thrombi [2]. Red blood cells (RBCs) are thought to play a significant role in the dynamics and the activation of the platelets and hence thrombus formation in the human arterial system. Previous experimental works indicate that RBCs cause platelets to migrate and move toward the vessel walls [3]. Thrombus formation has also been shown to increase as the hematocrit (Hct) increases [4]. In order to simulate the platelet dynamics requires the computational analysis of the transport and collision of the formed elements under physiological flow. In the present study, a two-dimensional (2D) simulation of the RBC/platelet dynamics in the arterioles is described.

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Valkowiak, B., V. Kozubski, Z. Pawlowska, and C. S. Ciernlewski. "FIBRINOGEN RECEPTORS IN BLOOD PLATELETS OF MIGRAINE PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643525.

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The augmentation of platelet aggregability in migraine patients was found in many studies, by the use of both in vivo and in vitro techniques. In order to evaluate the platelet characteristics responsible for the increased aggregability of migraine platelets we determined their binding capacities and the apparent dissociation constant (KD app) of fibrinogen receptors. Twelve non-pregnant women in age ranged from 20 to 44 years with unequivocal history of common migraine and 10 control healthy age matched women were used in these studies. The patients were assessed in headache-free intervals. Blood was drawn into acid citrate dextrose containing apyrase (0.1 mg/ml) and platelets were isolated by differential centrifugation. The mean number of platelet fibrinogen receptors exposed by ADP in migraine patients ( 65197 ± 6276 ) was statistically ( p<0.05 ) higher than that obtained in healthy controls ( 40217 ± 7678 ). The apparent Kd for fibrinogen receptors in migraine platelets (6.01 ± 1.11 × 10−7 M ) was lower than that in control women about threefold < 2.17 ± 0.56 × 10−6 M). The difference was statistically significant ( p<0.02 ). With these results we conclude that the increased capacity and binding affinity of fibrinogen receptors may be responsible for the elevated number of circulating platelet aggregates in migraine patients and for the prevalance of various kinds of strokes during migraine attack.

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Mousel, J. A., H. S. Udaykumar, and K. B. Chandran. "Multiscale Modeling of Platelet Dynamics in Blood Flow With Application to Thrombus Formation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192780.

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From an averaged point of view, blood can often be treated computationally as a single-phase fluid of non-Newtonian character. Such a model may be appropriate if information regarding the bulk motion of the blood is all that is required. If, however, one seeks to describe the mechanisms leading to diseases such as thrombosis in the presence of foreign surfaces such as prosthesis, accurate predictions of platelet behavior in the dynamic environment of the blood are required. There are several effects that necessitate a careful treatment of platelet dynamics. For example, it is well known that the presence of red blood cells has a significant impact on radial distribution of platelets as well as the shear stress experienced by the platelets [1]. Therefore, the paths of and forces experienced by individual platelets are to be determined in order to predict the location and predilection for thrombus formation. However, since the length scales of the platelets are much smaller than the typical dimensions of the flow regions through which blood flows, it is not possible to capture platelet dynamics in a single-scale computation. Therefore, a multiscale technique for incorporating the dynamics of platelets and platelet-RBC interactions into large-scale flow simulations is required. We therefore examine a suspension of ellipsoidal and circular rigid particles that are representative of red blood cells and platelets carried in a Newtonian fluid to study the interaction or red blood cells and platelets.

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Klausen, Hanne, Per Flood, John O. Hjelle, and Holm Holmsen. "MORPHOLOGICAL CHANGES OF BLOOD PLATELETS IN MAN DURING DEEP SATURATION DIVING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643534.

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The small number of reports concerning blood platelets during deep saturation diving have shown that there may be a decrease in the number of circulating platelets. Gas bubbles are often present in theblood during decompression. In vitro, gas bubbles activate platelets, and alter the shape from discoidto spherical configuration with multiple, blunt spikes. This study was done to investigate if there are changes in the morphology of human blood platelets during deep diving. An 18 day long experimentalon-shore saturation dive to 360 msw was performed at NUTEC 1986. Bloodsamples were obtained from the 6 divers on 6 occations: pre-dive control, at 360 msw, 300 msw, 140 msw, 1 and 3 days after surfacing. Using 18 G Wasserman needles antecubital venous blood samples (3ml) were collected directly into the fixative agent (7 ml of 2% glutardialdehyde in cacodylate buffer) whilestill in the hyperbaric chamber. The samples were then decompressed,and the platelets separated from the blood by centrifugation at roomtemperature for 10 min at 190 g. Preparation to transmission electron microscopy included post-fixation in osmium tetroxide, staining uranyl-en-bloc and eventually lead, dehydration and embedding in Epon.Ultrathin sections were examined by a Philips 300 I electron microscope. The examination revealed alterations in both platelet size and shape in the course of the dive. The mean platelet area was increased during and immidiately after thedive, the greatest increase occuring at 360 msw. There was a high incidence of shape changed plateletswith spherical configuration and multiple, blunt spikes. This form was by far most abundant at 360 msw, and the morphology normalised towards surface. This rises the suspection of a pressure-related rather rhan bubble-related effect and the results indicate that plateletsin circulation can be activated bypressure itself

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Véricel, E., M. Croset, Ph Courpron, M. Dechavanne, and M. Lagarde. "BLOOD PLATELET FUNCTIONS: INFLUENCE OF AGING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644564.

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Aging has been associated with a high incidence of vascular diseases and it is suggested that platelet activation could contribute in the development of these diseases. The purpose of this study was to compare platelet functions from young adults (< 35 years) and elderly people (> 70 years). Aggregation of platelet rich plasma induced by arachidonic acid or epinephrine was significantly increased in the elderly. Similarly, an increase of platelet aggregation (platelets isolated from their plasma) induced by various agents (thrombin, U46619, arachidonic acid ...) was also noted. The same tendency was observed in whole blood aggregation. Platelet endogenous arachidonic acid metabolism under stimulation was evaluated. Production of thromboxane B2, measured by GLC, was significantly higher in the elderly people (510 ± 207 vs 242 ± 83 ng/10*platelets, p<0.02). On the other hand, platelet vitamin E, quantified by HPLC, was significantly decreased in elderly people (0.92 ± 0.21 vs 1.41 ± 0.55 nmoles/109 platelets, p<0.05). To further assess platelet and vascular function in vivo, we measured excretion of thromboxane B2 (TXB2), 2,3-dinor-TXB2 (M-TXB2), 6 keto-PGFlcr and 2,3-dinor-6 keto-PGFlα (M-6-k-PGFl±) in urine. These four metabolites were nearly all significantly increased in the older population (TXB2: 24.3 ± 2k.6 vs 3.1 ± 1.2 p<0.05; M-TXB2: 51.5 ± 43.2 vs 25.1 ± 14.5 NS; 6-k-PGFlα: 37.5 ± 29.3 vs 19.1 ± 4.2 p<0.05; and M-6- k-PGFlα: 193.6 ± 118.6 vs 116.4 ± 42.4 ng/mmole creatinine p<0.05). We conclude that changes in platelet functions reveal an enhanced platelet activity which may reflect a prethrombotic state in elderly people. The mechanisms of these modifications remain to be determined but the increased of specific peroxidation observed might be linked to the decrease of platelet vitamin E.

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Nichols, W. L., S. E. Kaese, D. A. Gastineau, L. A. Otteman, and E. J. W. Bowie. "BERNARD-SOULIER SYNDROME: WHOLE BLOOD DIAGNOSTIC ASSAYS OF PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644561.

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Diagnosis of Bernard-Soulier syndrome (BSS) is complicated by the difficulty of separating the giant platelets from other blood cells to pursue analyses of platelet function and structure. We report on the utility of three whole blood assay techniques for diagnosis of a patient with BSS. To our knowledge, these three techniques have not been simultaneously applied or compared for efficacy in laboratory diagnosis of BSS. (1) Whole blood platelet aggregation responses, studied with an electrical impedence aggregometer, were equivalent to those more laboriously obtained using platelet-rich plasma prepared by unit gravity sedimentation, studied with an optical light transmittance aggregometer. Platelet aggregation responses were normal with ADP or collagen stimulation, and absent with Ristocetin or bovine plasma stimulation. (2) Whole blood radioimmunoassay of platelet glycoprotein (GP) expression was performed using iodinated murine monoclonal antibodies HP1-1D (anti-GP IIb/IIIa) and 6D1 (anti-GPlb, kindly supplied by Dr. Barry Coller, Stony Brook, NY). After incubation with citrated whole blood, centrifugation was used to separate cell-bound antibody which was quantitated with a gamma counter. The patient’s whole blood had a normal level of cell-bound GP Ilb/IIIa, but a markedly reduced level of cell-bound GP lb (5% of normal mean; n = 20). (3) Whole blood smear immunocytochemical staining with the monoclonals (indirect immuno-alkaline phosphatase technique), and qualitative analysis by light microscopy, revealed a marked reduction of GP lb expression by the patient’s giant platelets, whereas GP Ilb/IIIa expression was normal. This latter technique might be especially valuable as a screening technique when the patient is not directly available for laboratory study. Together with the patient’s life-long history of thrombocytopenia and moderate bleeding diathesis, and other laboratory observations including markedly prolonged bleeding times and reduced whole blood prothrombin consumption, these data established diagnosis of BSS. We conclude that these three relatively simple assays of platelets in whole blood should be of particular value in the laboratory differential diagnosis of patients with congenital thrombocytopenias and giant platelet syndromes.

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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 marrow specimens were fixed with glutaraldehyde-osmium solution. Thin sections were prepared and stained with uranyl acetate and lead cytrate. Membrane systems of platelets and megakaryocytes in a case with BSS was investigated by staining of surface coating with ruthenium red.In a case with BSS, most platelets were very large and similar in morphology to those in formerly reported case. Giant platelets contained several-fold increased number of α-granules and mitochondria. Typical dense bodies were also observed. Contents of ATP/ADP, platelet factor-4(PF-4), B-thromboglobulin(B-TG) and platelet factor-3 availability(PF-3) were increased. Disorganization of microtubules was recognized. Some giant platelet contained membrane systems similar to demarcation membranes(DM) in megakaryocytes, characteristically. In mature megakaryocytes, areas divided by DM similar in size to those in normal megakaryocytes were observed. Several of these areas appeared to fuse together to form the giant platelets containing many granules and remnants of DM. In a case with May-Hegglin anomaly, typical Dohle’s bodies were shown in neutrophilic granulocytes. Giant platelets in this case also contained large number of α-granules and some of them contained membrane systems similar to DM. Areas similar in morphology to these giant platelets were clearly noted in the cytoplasm of mature megakaryocytes.In these cases, most giant platelets in the peripheral blood may be formed in the cytoplasm of megakaryocytes by fusion of several areas divided by DM, each of which may become normal sized platelets in normal megakaryocytes.

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Reports on the topic "Blood platelets"

Valeri, C. R., G. Ragno, H. MacGregor, and L. E. Pivacek. The Effect of Disinfection on Viability and Function of Baboon Red Blood Cells and Platelets. Fort Belvoir, VA: Defense Technical Information Center, July 1997. http://dx.doi.org/10.21236/ada360325.

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Viksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga, and Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, December 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.

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Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.

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Michelson, A. D., H. MacGregor, A. Kestin, M. R. Barnard, and M. J. Rohrer. Reversible Hypothermia-Induced Inhibition of Human Platelet Activation in Whole Blood in Vitro and in Vivo. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada360296.

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Khuri, Shukri F., Miguel Josa, Trevoc C. Axford, Samar Assousa, and Gina Ragno. Hematologic Changes During and Following Cardiopulmonary Bypass and Their Relationship to Non-Surgical Blood Loss. 1. Platelet Function and the Bleeding Time. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada360145.

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Peng, Ciyan, Jing Chen, Sini Li, and Jianhe Li. Comparative Efficacy of Chinese Herbal Injections Combined Western medicine for Non-small cell lung cancer: A Bayesian Network Meta-Analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0068.

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Review question / Objective: Advanced lung cancer has become the top malignant tumor in terms of morbidity and mortality, and Chinese herbal injections combined with western drugs have been widely used to treat advanced non-small cell lung cancer. For this purpose, we conducted a Bayesian network analysis to systematically evaluate the efficacy of different herbal injections combined with western drugs in the treatment of NSCLC. Subjects: Patients diagnosed with NSCLC by pathological or cytological examination, locally advanced or those who refused surgical treatment were included, regardless of gender, age, stage, race, nationality and sample size; Interventions: Chinese herbal injections combined with three types of commonly used western drugs (platinum, targeted and immune agents) were used in the experimental group, while the control group was treated with western drugs alone; Study type: to report the efficacy of Chinese herbal injections combined with western drugs in the treatment of non-small cell lung cancer efficacy in a randomized controlled trial (rct) Eligible. No restrictions were imposed on language, year of publication, or publication status. Ending indicators: Main ending indicators: (1) disease control rate (DCR), DCR = (complete remission + partial remission + stable)/total number of cases. Efficacy rate = (number of improvement cases + number of stable cases)/total number of cases. (2) Secondary outcome indicators: quality of life, determined according to the KPS behavioral status scale, improvement was defined as an increase of ≥10 points in KPS score after treatment; stability was defined as an increase or decrease of <10 points in KPS score; decline was defined as a decrease of ≥10 points in KPS score. (3) The incidence of adverse reactions, including gastrointestinal reactions, white blood cell (WBC) reduction, hemoglobin (HGB) reduction, platelet (PLT) reduction, etc.

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