Academic literature on the topic 'Platelet dynamics'
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Journal articles on the topic "Platelet dynamics"
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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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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.bloodjournal7871730.
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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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Bender, Markus, Anita Eckly, John H. Hartwig, Margitta Elvers, Irina Pleines, Shuchi Gupta, Georg Krohne, et al. "ADF/n-cofilin–dependent actin turnover determines platelet formation and sizing." Blood 116, no. 10 (September 9, 2010): 1767–75. http://dx.doi.org/10.1182/blood-2010-03-274340.
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Abstract The cellular and molecular mechanisms orchestrating the complex process by which bone marrow megakaryocytes form and release platelets remain poorly understood. Mature megakaryocytes generate long cytoplasmic extensions, proplatelets, which have the capacity to generate platelets. Although microtubules are the main structural component of proplatelets and microtubule sliding is known to drive proplatelet elongation, the role of actin dynamics in the process of platelet formation has remained elusive. Here, we tailored a mouse model lacking all ADF/n-cofilin–mediated actin dynamics in megakaryocytes to specifically elucidate the role of actin filament turnover in platelet formation. We demonstrate, for the first time, that in vivo actin filament turnover plays a critical role in the late stages of platelet formation from megakaryocytes and the proper sizing of platelets in the periphery. Our results provide the genetic proof that platelet production from megakaryocytes strictly requires dynamic changes in the actin cytoskeleton.
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Wilkins, Ngozi A., Brian Storrie, and Jeffrey A. Kamykowski. "Characterization of Platelet Alpha-Granule Dynamics." Blood 116, no. 21 (November 19, 2010): 327. http://dx.doi.org/10.1182/blood.v116.21.327.327.
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Abstract Abstract 327 Background: Platelets, anucleated cells that play a critical role in blood clotting, store proteins and small molecules in alpha-granules and dense granules, respectively, for secretion. Alpha-granules contain several proteins including von Willebrand factor and fibrinogen and dense granules contain serotonin. Rab4, a marker for the early endosomes has been implicated in regulating alpha granule secretions (Sirakawa et al, 2010). Previous fluorescence microscopy mapping of alpha-granule protein distributions suggested that there are either two different alpha-granule types or subdomains within a single granule population (Storrie and Seghal, 2007; Italiano et al, 2008). More recent work based on electron tomography (Kamykowski et al, manuscript in preparation) indicates that human platelets are comprised of one alpha granule population. We hypothesized that there was a single population of alpha-granules in which all fibrinogen is similarly compartmentalized. Hence, fibrinogen endocytocized by guinea pig megakaryocytes and platelets in vivo at 4 h (short label) and 24 h (long label) would map to the same location. Aims: We carried out several experiments to form a basis for future high-resolution (5 nm) electron tomography to establish packaging of HRP-conjugated fibrinogen or nanogold conjugated fibrinogen into platelet alpha-granules. (a) Using PD-10 columns, we prepared Cy3 conjugated fibrinogen. Using an in vivo guinea pig model to test the ability of guinea pig platelets to take up fluorescently labeled fibrinogen, we injected 10 mg/ml of Cy3 conjugated fibrinogen (short label, 4 h) and 10 mg/ml of commercially purchased AlexaFluor 488 conjugated fibrinogen (long label, 28 h) into guinea pigs. Platelets were then fixed, purified and confocal microscopy performed. (b) Using triple immunofluorescence, serotonin antibody was applied to fixed and purified resting state human and guinea pig platelets and immunofluorescence microscopy was performed to provide whole platelet information on the staining pattern of the dense granules in comparison to the alpha-granules and early endosomes. (c) Preliminary Electron Microscopy fixation conditions were also tested on guinea pig platelets. Results: For the uptake experiment, spinning-disk confocal microscopy was used to collect full platelet volume image stacks which were then deconvolved, pixel shift corrected for red and green channels and analyzed. Overlap of green and red fibrinogen conjugates was observed where the fluorescently tagged fibrinogens were taken up by structures presumed to be alpha-granules. For the triple labeling experiments, the distribution of serotonin, Rab4 and von Willebrand factor was observed in resting state platelets. Using spinning-disk confocal microscopy, full platelet volume image stacks were collected, deconvolved, pixel shift corrected for red, far red and green channels and analyzed. Serotonin antibody gave an abundant punctate staining pattern in both the triple-labeled human and guinea pig platelets. In both the human platelets and the guinea pig platelets, the serotonin positive punctate granules, presumed to be dense granules, had a more similar pattern to the von Willebrand factor positive punctate alpha granules, than to the Rab4 positive punctate granules, presumed to be the early endosomes. The triple label results were unexpected because previous electron microscopy studies have indicated that the dense granules in human platelets are fewer in number than the alpha-granules and fewer than the corresponding dense granules in guinea pig platelets. Results of the electron microscopy preparations are pending. Conclusions: Our results indicate that the guinea pig model, while its platelets are a much smaller size than human platelets, is a good system for loading alpha-granules with labeled proteins for electron tomography. The serotonin distribution results together with previous electron tomography also raise the question as to whether dense granules could be a specialized form of the alpha-granules. A summary of this research will be presented at the Promoting Minorities in Hematology event during the 2010 ASH meeting. Disclosures: No relevant conflicts of interest to declare.
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Dubois, Christophe, Laurence Panicot-Dubois, Barbara C. Furie, and Bruce Furie. "Dynamics of Calcium Mobilization in Platelets during Thrombus Formation in a Living Mouse." Blood 106, no. 11 (November 16, 2005): 649. http://dx.doi.org/10.1182/blood.v106.11.649.649.
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Abstract Platelet accumulation at sites of vascular injury arrests bleeding but also plays a critical role in the pathogenesis of thrombosis, leading to ischemia in myocardial infarction or stroke. Intracellular calcium mobilization in platelets is a critical step in the activation of platelets and formation of the platelet thrombus. Here we show the relationship of the dynamics of intracellular calcium mobilization with platelet accumulation into the developing thrombus in a living mouse. Following injection of 100 x 106 fura-2 loaded platelets into a living mouse we used high speed intravital multi-channel digital fluorescence microscopy to monitor calcium status in circulating and thrombus-bound platelets during thrombus development. One population of platelets binds transiently to the developing thrombus but does not mobilize calcium. The mean duration of platelet-thrombus interaction for these platelets is 11 sec. Another population of platelets undergoes calcium mobilization after binding to the developing thrombus. The time interval from attachment to calcium mobilization for individual platelets varied from 1.0 to 12 sec, with a median of 3.5 sec. More than 90% of platelets that undergo calcium mobilization do so with in 5 sec of attachment. The calcium mobilization in the thrombus bound platelets is reversible. About two thirds of the platelets return rapidly to the basal Ca2+ state while the remaining thrombus bound platelets maintain an elevated Ca2+ level for an extended period. The mean duration of platelet-thrombus interaction is 35 sec with a range of 1.5 sec to 284 sec (median duration 39.5 sec) as calculated from multiple independent observations of single platelets. In each platelet studied, only one calcium peak is detected per platelet. There is a close correlation between the duration of calcium mobilization in an individual platelet and the time that the platelet remains attached to the developing thrombus, suggesting a relationship of calcium-dependent events and platelet-thrombus affinity. A population of platelets binds to the thrombus, mobilizes calcium and remains associated with the thrombus. Using widefield deconvolution techniques to obtain planar images and increased numbers of dye-loaded platelets, individual platelets could be observed undergoing sustained calcium elevation within the thrombus. As the platelet thrombus reaches maximal size at about 120 sec, calcium mobilization continues in the stable core of the thrombus for several minutes, then decreases. These studies describe thrombus formation in a living animal under conditions in which the endothelium and vessel wall, blood cells and plasma components, and flowing blood are preserved in the absence of anticoagulants. Our results indicate that stable platelet thrombus formation is dependent upon durable calcium mobilization, and that intracellular calcium regulates thrombus development and maturation in vivo.
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Falet, Hervé, Gregory Chang, Brigitte Brohard-Bohn, Francine Rendu, and John H. Hartwig. "Integrin αIIbβ3signals lead cofilin to accelerate platelet actin dynamics." American Journal of Physiology-Cell Physiology 289, no. 4 (October 2005): C819—C825. http://dx.doi.org/10.1152/ajpcell.00587.2004.
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Cofilin, in its Ser3 dephosphorylated form, accelerates actin filament turnover in cells. We report here the role of cofilin in platelet actin assembly. Cofilin is primarily phosphorylated in the resting platelet as evidenced by a specific antibody directed against its Ser3 phosphorylated form. After stimulation with thrombin under nonstirring conditions, cofilin is reversibly dephosphorylated and transiently incorporates into the actin cytoskeleton. Its dephosphorylation is maximal 1–2 min after platelet stimulation, shortly after the peak of actin assembly occurs. Cofilin rephosphorylation begins 2 min after activation and exceeds resting levels by 5–10 min. Cofilin is dephosphorylated with identical kinetics but fails to become rephosphorylated when platelets are stimulated under stirring conditions. Cofilin is normally rephosphorylated when platelets are stimulated in the presence of Arg-Gly-Asp-Ser (RGDS) peptide or wortmannin to block αIIbβ3cross-linking and signaling or in platelets isolated from a patient with Glanzmann thrombasthenia, which express only 2–3% of normal αIIbβ3levels. Furthermore, actin assembly and Arp2/3 complex incorporation in the platelet actin cytoskeleton are decreased when αIIbβ3is engaged. Our results suggest that cofilin is essential for actin dynamics mediated by outside-in signals in activated platelets.
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Patel, Dipti, Heikki Väänänen, Markéta Jiroušková, Thomas Hoffmann, Carol Bodian, and Barry S. Coller. "Dynamics of GPIIb/IIIa-mediated platelet-platelet interactions in platelet adhesion/thrombus formation on collagen in vitro as revealed by videomicroscopy." Blood 101, no. 3 (February 1, 2003): 929–36. http://dx.doi.org/10.1182/blood.v101.3.929.
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Abstract The conventional description of platelet interactions with collagen-coated surfaces in vitro, based on serial static measurements, is that platelets first adhere and spread to form a monolayer and then recruit additional layers of platelets. To obtain dynamic information, we studied gravity-driven platelet deposition in vitro on purified type 1 collagen by video phase-contrast microscopy at 22°C. With untreated human and wild-type mouse platelets, soon after the initial adhesion of a small number of “vanguard” platelets, “follower” platelets attached to the spread-out vanguard platelets. Follower platelets then adhered to and spread onto nearby collagen or over the vanguard platelets. Thus, thrombi formed as a concerted process rather than as sequential processes. Treatment of human platelets with monoclonal antibody (mAb) 7E3 (anti–GPIIb/IIIa (αIIbβ3) + αVβ3) or tirofiban (anti–GPIIb/IIIa) did not prevent platelet adhesion but nearly eliminated the deposition of follower platelets onto vanguard platelets and platelet thrombi. Similar results were obtained with Glanzmann thrombasthenia platelets. Wild-type mouse platelets in the presence of mAb 1B5 (anti–GPIIb/IIIa) and platelets from β3-null mice behaved like human platelets in the presence of 7E3 or tirofiban. Deposition patterns of untreated human and wild-type mouse platelets were consistent with random distributions under a Poisson model, but those obtained with 7E3- and tirofiban-treated human platelets, 1B5-treated mouse platelets, or β3-null platelets demonstrated a more uniform deposition than predicted. Thus, in this model system, absence or blockade of GPIIb/IIIa receptors interferes with thrombus formation and alters the pattern of platelet deposition.
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Filipovic, N., M. Kojic, and A. Tsuda. "Modelling thrombosis using dissipative particle dynamics method." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1879 (July 2008): 3265–79. http://dx.doi.org/10.1098/rsta.2008.0097.
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Aim . Arterial occlusion is a leading cause of cardiovascular disease. The main mechanism causing vessel occlusion is thrombus formation, which may be initiated by the activation of platelets. The focus of this study is on the mechanical aspects of platelet-mediated thrombosis which includes the motion, collision, adhesion and aggregation of activated platelets in the blood. A review of the existing continuum-based models is given. A mechanical model of platelet accumulation onto the vessel wall is developed using the dissipative particle dynamics (DPD) method in which the blood (i.e. colloidal-composed medium) is treated as a group of mesoscale particles interacting through conservative, dissipative, attractive and random forces. Methods . Colloidal fluid components (plasma and platelets) are discretized by mesoscopic (micrometre-size) particles that move according to Newton's law. The size of each mesoscopic particle is small enough to allow tracking of each constituent of the colloidal fluid, but significantly larger than the size of atoms such that, in contrast to the molecular dynamics approach, detailed atomic level analysis is not required. Results . To test this model, we simulated the deposition of platelets onto the wall of an expanded tube and compared our computed results with the experimental data of Karino et al . ( Miscrovasc. Res. 17 , 238–269, 1977). By matching our simulations to the experimental results, the platelet aggregation/adhesion binding force (characterized by an effective spring constant) was determined and found to be within a physiologically reasonable range. Conclusion . Our results suggest that the DPD method offers a promising new approach to the modelling of platelet-mediated thrombosis. The DPD model includes interaction forces between platelets both when they are in the resting state (non-activated) and when they are activated, and therefore it can be extended to the analysis of kinetics of binding and other phenomena relevant to thrombosis.
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Suzuki, Aae, Lurong Lian, Liang Zhao, Sang H. Min, Yuhuan Wang, Mortimer Poncz, John K. Choi, Christopher L. Carpenter, and Charles S. Abrams. "Mice That Lack RhoA In Their Platelets Have Normal Actin Dynamics, but Have Macrothrombocytopenia." Blood 116, no. 21 (November 19, 2010): 549. http://dx.doi.org/10.1182/blood.v116.21.549.549.
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Abstract Abstract 549 In response to agonist stimulation, platelets undergo a rapid reorganization of their actin cytoskeleton. This process involves simultaneous disassembly and assembly of filamentous actin, and is one of the earliest phenomena seen in platelet activation. Ex vivo flow models suggest that the platelet cytoskeleton is required for platelet adhesion that can withstand the shear conditions found within the arterial vascular system. The signaling pathways that link external stimuli with actin assembly are believed to include polyphosphoinositides, small GTP-binding proteins, and actin binding proteins. Extrapolations of data, mostly derived from tissue culture cell lines, suggest that a central component of this signaling cascade is the small GTP binding protein, RhoA. A few studies using a RhoA-specific pharmacologic inhibitor, C3 exotoxin, suggest that RhoA is essential for platelet spreading and focal adhesion formation. These findings support the hypothesis that RhoA within platelets is critical for the cytoskeletal dependent processes that contribute to platelet plug formation. To determine the true in vivo role of RhoA within platelets, we utilized a murine genetic approach. Mice were genetically modified to contain conditional RhoA null mutation by inserting LoxP sites flanking exon 3. This exon encodes the P-loop and Switch 1 domains within this protein. RhoA fl/fl mice were crossed with Platelet factor 4 (PF4) expressing Cre mice. The PF4 promotor leads to Cre expression exclusively in platelets and megakaryocytes, thereby producing homologous recombination at the LoxP sites, and deletion the critical exon only within these cells. This end result of this breeding strategy produced RhoA fl/fl PF4 Cre+ mice that specifically lacked RhoA only in their platelets and megakaryocytes. RhoA fl/fl PF4 Cre+ mice were compared with their RhoA fl/fl PF4 Cre- littermates. RhoA fl/fl PF4 Cre+ mice appeared normal, but had platelet counts that were 30% +/− 3% lower than normal. The mean platelet volume was also increased by 25 % +/− 7 % in the RhoA-null platelets. Review of the peripheral blood smears confirmed that the mice had macrothrombocytopenia, but did not reveal any abnormalities in the erythrocytes or leukocytes of the mice. Examination of the bone marrows from RhoA fl/fl PF4 Cre+ mice demonstrated that they had at least as many megakaryocytes as RhoA fl/fl PF4 Cre- mice. But compared to the control cells, the RhoA-null megakaryocytes were larger, more lobulated, and had more cytoplasm. Furthermore, the thromobocytopenia is probably not due to splenic sequestration because the spleens of RhoA fl/fl PF4 Cre- mice were only minimally larger (less than 10%) than those of the control mice. These results suggest that the mechanism for thrombocytopenia is due to peripheral destruction. Platelets derived from RhoA fl/fl PF4 Cre+ mice were studied ex vivo, and were found to undergo shape change and aggregate normally in response to thrombin, collagen, and the thromboxane A2 analog, U46619. Surprisingly, platelet adhesion and cell spreading was also unaffected by the loss of RhoA. It is also remarkable that total F-actin (as assessed by phalloidin staining) was identical in the platelets derived from RhoA fl/fl PF4 Cre+ and RhoA fl/fl PF4 Cre- mice. Our results definitively refute the model that RhoA is an essential component of platelet actin dynamics and platelet adhesion. Instead our findings surprisingly indicate that loss of the platelet RhoA causes macrothrombocytopenia. Our data suggests that the development of macrothrombocytopenia is due to an intrinsic platelet abnormality that leads to a shortened platelet lifespan. Disclosures: No relevant conflicts of interest to declare.
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Patel-Hett, Sunita, Jennifer L. Richardson, Harald Schulze, Ksenija Drabek, Natasha A. Isaac, Karin Hoffmeister, Ramesh A. Shivdasani, et al. "Visualization of microtubule growth in living platelets reveals a dynamic marginal band with multiple microtubules." Blood 111, no. 9 (May 1, 2008): 4605–16. http://dx.doi.org/10.1182/blood-2007-10-118844.
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Abstract The marginal band of microtubules maintains the discoid shape of resting blood platelets. Although studies of platelet microtubule coil structure conclude that it is composed of a single microtubule, no investigations of its dynamics exist. In contrast to previous studies, permeabilized platelets incubated with GTP-rhodamine-tubulin revealed tubulin incorporation at 7.9 (± 1.9) points throughout the coil, and anti-EB1 antibodies stained 8.7 (± 2.0) sites, indicative of multiple free microtubules. To pursue this result, we expressed the microtubule plus-end marker EB3-GFP in megakaryocytes and examined its behavior in living platelets released from these cells. Time-lapse microscopy of EB3-GFP in resting platelets revealed multiple assembly sites within the coil and a bidirectional pattern of assembly. Consistent with these findings, tyrosinated tubulin, a marker of newly assembled microtubules, localized to resting platelet microtubule coils. These results suggest that the resting platelet marginal band contains multiple highly dynamic microtubules of mixed polarity. Analysis of microtubule coil diameters in newly formed resting platelets indicates that microtubule coil shrinkage occurs with aging. In addition, activated EB3-GFP–expressing platelets exhibited a dramatic increase in polymerizing microtubules, which travel outward and into filopodia. Thus, the dynamic microtubules associated with the marginal band likely function during both resting and activated platelet states.
Dissertations / Theses on the topic "Platelet dynamics"
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Wong, Truman. "Dynamics of platelet shape change and aggregation size-dependent platelet subpopulations." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61778.
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Lane, I. F. "The relationship between platelet-vessel wall interaction thrombosis and atherosclerosis." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233551.
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Kasirer-Friede, Ana. "Dynamics of von Willebrand factor-mediated platelet aggregation in laminar flow : physical and molecular determinants." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0020/NQ55344.pdf.
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Bark, David Lawrence Jr. "Mechanistic numerical study of trhombus growth." Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/22550.
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Sandmann, Rabea [Verfasser], Sarah [Akademischer Betreuer] Köster, and Florian [Akademischer Betreuer] Rehfeldt. "Blood Platelet Behavior on Structured Substrates : From Spreading Dynamics to Cell Morphology / Rabea Sandmann. Betreuer: Sarah Köster. Gutachter: Sarah Köster ; Florian Rehfeldt." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1078420084/34.
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Andersen, Brandon Thomas. "Multi-Processor Computation of Thrombus Growth and Embolization in a Model of Blood-Biomaterial Interaction Based on Fluid Dynamics." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3465.
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This work describes the development and testing of a real-time three-dimensional computational fluid dynamics simulation of thrombosis and embolization to be used in the design of blood-contacting devices. Features of the model include the adhesion and aggregation of blood platelets on device material surfaces, shear and chemical activation of blood platelets, and embolization of platelet aggregates due to shear forces. As thrombus develops, blood is diverted from its regular flow field. If shear forces on a thrombus are sufficient to overcome the strength of adhesion, the thrombus is dislodged from the wall. Development of the model included preparing thrombosis and embolization routines to run in a parallel processing configuration, and estimating necessary parameters for the model including the adhesion strength of platelet conglomerations to the device surfaces and the criterion threshold for the coalescence of neighboring thrombi. Validation of the model shows that the effect of variations in geometry may be accurately predicted through computational simulation. This work is based on previous work by Paul Goodman, Daniel Lattin, Jeff Ashton, and Denzel Frost.
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Fiusco, Francesco. "Hemodynamics of artificial devices used in extracorporeal life support." Licentiate thesis, KTH, Teknisk mekanik, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-301039.
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Extracorporeal Membrane Oxygenation (ECMO) is a life-saving therapy usedfor support in critical heart and/or lung failure. Patient’s blood is pumped viaan artificial lung for oxygenation outside of the body. The circuit is composedof a blood pump, cannulae for drainage and reinfusion, a membrane lung,tubing and connectors. Its use is associated with thromboembolic complicationsand hemolytic damage. Detailed numerical studies of two blood pumps anda lighthouse tip drainage cannula were undertaken to characterize the flowstructures in different scenarios and their link to platelet activation. The pumpsimulations were modelled according to manufacturer’s proclaimed use but alsoin off-design conditions with flow rates used in adult and neonatal patients.Lagrangian Particle Tracking (LPT) was used to simulate the injection ofparticles similar in size to platelets to compute platelet activation state (PAS).The results indicated that low flow rates impacted PAS similarly to high flowrates due to increased residence time leading to prolonged exposure to shearstress despite the fact that shear per se was lower at low flow rate. Regardingthe cannula, the results showed that a flow pattern similar to a jet in crossflowdeveloped at the side holes. A parameter study was conducted to quantifydrainage characteristics in terms of flow rate distribution across the holes wheninput variables of flow rate, modelled fluid, and hematocrit were altered. Thefindings showed, across all the cases, that the most proximal hole row drainedthe largest fraction of fluid. The effects due to the non-Newtonian nature ofblood were confined to regions far from the cannula holes and the flow structuresshowed very limited dependence on the hematocrit. A scaling law was found tobridge the global drainage performance of fluid between water and blood.QC 210906
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Hosseinzadegan, Hamid. "A Physio-chemical Predictive Model of Dynamic Thrombus Formation and Growth in Stenosed Vessels." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/89325.
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According to the World Health Organization (WHO), Cardiovascular Disease (CVD) is the leading cause of death in the world. Biomechanics and fluid dynamics of blood flow play an important role in CVD mediation. Shear stress plays a major role in platelet-substrate interactions and thrombus formation and growth in blood flow, where under both pathological and physiological conditions platelet adhesion and accumulation occur. In this study, a three-dimensional dynamic model of platelet-rich thrombus growth in stenosed vessels using computational fluid dynamics (CFD) methods is introduced. Platelet adhesion, aggregation and activation kinetics are modeled by solving mass transport equations for blood components involved in thrombosis. The model was first verified under three different shear conditions and at two heparin levels. Three-dimensional simulations were then carried out to evaluate the performance of the model for severely damaged (stripped) aortas with mild and severe stenosis degrees. For these cases, linear shear-dependent functions were developed for platelet-surface and platelet-platelet adhesion rates. It was confirmed that the platelet adhesion rate is not only a function of Reynolds number (or wall shear rate) but also the stenosis severity of the vessel. General correlations for adhesion rates of platelets as functions of stenosis and Reynolds number were obtained based on these cases. The model was applied to different experimental systems and shown to agree well with measured platelet deposition. Then, the Arbitrary Lagrangian Eulerian (ALE) formulation was used to model dynamic growth by including geometry change in the simulation procedure. The wall boundaries were discretely moved based on the amount of platelet deposition that occurs on the vessel wall. To emulate the dynamic behavior of platelet adhesion kinetics during thrombus growth, the validated model for platelet adhesion, which calculates platelet-surface adhesion rates as a function of stenosis severity and Reynolds number, was applied to the model. The model successfully predicts the nonlinear growth of thrombi in the stenosed area. These simulations provide a useful guide to understand the effect of growing thrombus on platelet deposition rate, platelet activation kinetics and occurrence of thromboembolism (TE) in highly stenosed arteries.Ph. D.
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Cosemans, Judith Maria Elisabeth Mathijs. "Dynamic regulation of thrombus stability focus on platelet receptors and downstream signaling /." Maastricht : Maastricht : Univeritaire Pers ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=14676.
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Naeem, Ali. "Optical properties and exciton dynamics of colloidal quantum dots, rods, and platelets." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/90269/.
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The linear optical properties and exciton dynamics of different semiconductor nanostructures have been studied. A model to describe the absoprtion spectra of cadmium selenide (CdSe) nanoplatelets (NPLs) has been developed, which allows the extraction of parameters relating to excitons confined within the thickness of the NPLs. Giant oscillator strength transitions (GOST) have been observed in NPLs with a lifetime limited dephasing of the ground state excitons at low temperature of about 1 ps, using transient resonant four wave mixing in heterodyne detection. The observation of the GOST effect has been affirmed by a decrease in the low temperature dephasing time with increasing NPL area. In addition, in cadmium selenide/cadmium sulphide (CdSe/CdS) quantum dot in rod (QDR) samples, dephasing dynamics at low temperature have been described by a Gaussian distribution of decay rates. Density dynamics have shown a fast initial decay followed by a signal rise attributed to an interplay between acoustic phonons and fast population dynamics related to the QDR fine structure. Density dynamics at longer delays have been attributed to an ensemble including both excitons and trions. The low temperature dephasing has been attributed to relaxation of excitons from a bright state to a lower lying dark state. Finally, a homebuilt scanning probe microscopy instrument has been modified to allow simultaneous optical and scanning probe imaging for the study of correlation between charge state and optical properties of nanostructures.
Books on the topic "Platelet dynamics"
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Kuiper, Gerhardus J. A. J. M., and Hugo ten Cate. Coagulation monitoring. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0266.
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Haemostasis is a dynamic process to stop bleeding after vessel wall damage. Platelets form a platelet plug via activation, adherence, and aggregation processes. The coagulation proteins are activated one-by-one, cascading towards fibrin polymerization, a process controlled by thrombin generation. Fibrinolysis is the process responsible for fibrin mesh degradation, which is also controlled by thrombin. Besides procoagulant proteins, anticoagulant proteins maintain a balance in the haemostatic system. Measuring platelet count and function can be done as part of the monitoring of haemostasis, while coagulation times are measured to assess the coagulation proteins. Degradation products of fibrin and lysis times give information about fibrinolysis. Point-of-care monitoring provides simple, rapid bedside testing for platelets and for whole blood using viscoelasticity properties. In trauma-induced coagulopathy (TIC) platelet counts and coagulation times are still common practice to evaluate haemostasis, but point-of-care measurements are being used more and more. Medication interfering with haemostasis is frequently used in intensive care unit patients. Each (group of) drug(s) has its own monitoring tests either based on classical or novel techniques.
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Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.
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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
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Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.
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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
Book chapters on the topic "Platelet dynamics"
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Sakata, Asuka, and Satoshi Nishimura. "Bone Imaging: Platelet Formation Dynamics." In Methods in Molecular Biology, 23–28. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7762-8_3.
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Sheriff, Jawaad, and Danny Bluestein. "Platelet dynamics in blood flow." In Dynamics of Blood Cell Suspensions in Microflows, 215–56. Boca Raton : CRC Press, [2020] j Includes bibliographical references and index.: CRC Press, 2019. http://dx.doi.org/10.1201/b21806-7.
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Fogelson, Aaron, Haoyu Yu, and Andrew Kuharsky. "Computational Modeling of Blood Clotting: Coagulation and Three-dimensional Platelet Aggregation." In Polymer and Cell Dynamics, 145–54. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8043-5_13.
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Qi, Qin M., and Eric S. G. Shaqfeh. "Microstructure and rheology of cellular blood flow, platelet margination and adhesion." In Dynamics of Blood Cell Suspensions in Microflows, 101–24. Boca Raton : CRC Press, [2020] j Includes bibliographical references and index.: CRC Press, 2019. http://dx.doi.org/10.1201/b21806-4.
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Nesbitt, Warwick S., Francisco J. Tovar-Lopez, Erik Westein, Ian S. Harper, and Shaun P. Jackson. "A Multimode-TIRFM and Microfluidic Technique to Examine Platelet Adhesion Dynamics." In Adhesion Protein Protocols, 39–58. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-538-5_3.
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Nesbitt, Warwick S., Ian S. Harper, Simone M. Schoenwaelder, Yuping Yuan, and Shaun P. Jackson. "A Live Cell Micro-imaging Technique to Examine Platelet Calcium Signaling Dynamics Under Blood Flow." In Methods in Molecular Biology, 73–89. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-307-3_6.
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Yablonka-Reuveni, Z., D. F. Bowen-Pope, and R. S. Hartley. "Proliferation and Differentiation of Myoblasts: The Role of Platelet-Derived Growth Factor and the Basement Membrane." In The Dynamic State of Muscle Fibers, edited by Dirk Pette, 693–706. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110884784-054.
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Felcher, G. P., and Y. Y. Huang. "Magnetism of thin film multilayers: an analogue of interacting platelets." In Structure and Dynamics of Strongly Interacting Colloids and Supramolecular Aggregates in Solution, 691–711. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2540-6_34.
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Boudot, Cécile, Stefanie Recht, Markus Eblenkamp, Miriam Haerst, and Erich Wintermantel. "Protein Adsorption and Adhesion of Blood Platelets on Silicone Rubber under Static and Dynamic Flow Conditions." In IFMBE Proceedings, 541–44. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11128-5_135.
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A. Matthay, Zachary, and Lucy Zumwinkle Kornblith. "Platelet Imaging." In Platelets. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91736.
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The knowledge gained through imaging platelets has formed the backbone of our understanding of their biology in health and disease. Early investigators relied on conventional light microscopy with limited resolution and were primarily able to identify the presence and basic morphology of platelets. The advent of high resolution technologies, in particular, electron microscopy, accelerated our understanding of the dynamics of platelet ultrastructure dramatically. Further refinements and improvements in our ability to localize and reliably identify platelet structures have included the use of immune-labeling techniques, correlative-fluorescence light and electron microscopy, and super-resolution microscopies. More recently, the expanded development and application of intravital microscopy in animal models has enhanced our knowledge of platelet functions and thrombus formation in vivo, as these experimental systems most closely replicate native biological environments. Emerging improvements in our ability to characterize platelets at the ultrastructural and organelle levels include the use of platelet cryogenic electron tomography with quantitative, unbiased imaging analysis, and the ability to genetically label platelet features with electron dense markers for analysis by electron microscopy.
Conference papers on the topic "Platelet dynamics"
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Bluestein, Danny, João S. Soares, Peng Zhang, Chao Gao, Seetha Pothapragada, Na Zhang, Marvin J. Slepian, and Yuefan Deng. "Multiscale Modeling of Flow Induced Thrombogenicity Using Dissipative Particle Dynamics and Molecular Dynamics." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93094.
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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Molecular dynamics (MD) and dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.
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Bluestein, Danny, João S. Soares, Peng Zhang, Chao Gao, Seetha Pothapragada, Na Zhang, Marvin J. Slepian, and Yuefan Deng. "Multiscale Modeling of Flow Induced Thrombogenicity With Dissipative Particle Dynamics (DPD) and Molecular Dynamics (MD)." In ASME 2013 Conference on Frontiers in Medical Devices: Applications of Computer Modeling and Simulation. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fmd2013-16176.
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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Molecular dynamics (MD) and dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.
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Zhang, Peng, Jawaad Sheriff, João S. Soares, Chao Gao, Seetha Pothapragada, Na Zhang, Yuefan Deng, and Danny Bluestein. "Multiscale Modeling of Flow Induced Thrombogenicity Using Dissipative Particle Dynamics and Coarse Grained Molecular Dynamics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14187.
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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Coarse Grained Molecular dynamics (CGMD) and discrete/dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.
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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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Badimon, J. J., L. Badimon, A. Galvez, J. Camunas, and V. Fuster. "DYNAMICS AND LOCALIZATION OF PLATELET DEPOSITION ON A SYNTHETIC VASCULAR GRAFT: CONTINUOUS IMAGING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643954.
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The in vivo dynamics of thrombus formation have not been extensively studied, mainly due to technical limitations. We assessed the dynamics and localization of platelet deposition on a prosthetic vascular graft for the first 24 hours after implantation in swine, with continuous monitoring during the initial 6 hours, and the effect of heparin. Polytetrafluoro-ethylene (PTFE) grafts (5cm. L × 0.5 cm. ID) were inplanted in one of the common carotids of 13 normal pigs; 8 received iv heparin (150uAg) perioperatively. 111 In-labelled autologous platelets were injected 5 min before reperfusion of the graft. From 10 min to 24 hrs after unclamping the vessel sequential gamma camera images of the neck were taken and stored in an on-line computer. Pinpoint analysis of the platelet deposition was performed by creating seven regions of interest of 5 × 5 pixels over both graft and contralateral carotid territories. We obtained the ratio of the 111 In-activity in each region of the graft, including both anastomoses, with respect to its contralateral homologous region. The ratios differed along the graft in both groups of animals, with maximal values at the anastomosis. Peak ratios were reached within 1 to 3 hrs, and were significatively lower in heparinized pigs (anastomosis: 1.95±0.36; graft: 1.3±0.66) than in rion-heparinized-pigs (anastomosis: 3.23±0.66; graft: 2.16±0.41; p<0.05). Heparinized pigs showed a progressive decrease of the ratios up to 24 hrs. In contrast, platelet deposition in non-heparinized-pigs continued up to 6 hrs. Patency at 24 hrs was 88% in heparinized-pigs versus 20% in non-heparinized-pigs. We conclude that computer assisted pinpoint analysis of platelet deposition may help to a better understanding of the thrombotic process differentiating platelet-graft interaction from platelet anastomosis interaction. The deposition of platelets and graft patency is strongly influenced by the stabilizing effect of procoagulant moieties, and the presence of the anastomosis (release of vessel wall procoagulant and platelet activating products and induction of blood flow disturbances) induces localized activation and deposition of platelets.
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Hoore, Masoud, Dmitry A. Fedosov, and Gerhard Gompper. "Video: Mechanical Dissociation of Platelet Aggregates in Blood Stream." In 70th Annual Meeting of the APS Division of Fluid Dynamics. American Physical Society, 2017. http://dx.doi.org/10.1103/aps.dfd.2017.gfm.v0008.
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Longmire, K., and M. M. Frojmovic. "PLATELET AGGREGATION DYNAMICS TO ADENOSINE DIPHOSPHATE IN NON-STIRRED SUSPENSIONS: LONG-RANGEINTERACTIONS FOR HUMAN, BUT NOT RABBIT, PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644464.
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The simplest experimental approach for a theoretical description of platelet aggregation is based on kinetics of early multiplet formation (‹4 platelets per aggregate)occurring with diffusion-dependent particle collisions (no flow). The Smoluchowski theory was used to calculate collision efficiencies, αβ, from a linear plot of platelet particle count (Nt)−1 vs time (t) following addition of adenosine diphosphate (ADP) to citrated platelet-rich-plasma (PRP) for 7 human (H) and 2 rabbit (R) donors. A 0.1 ml sample of PRP was stirred with ADP for 0.5s, then immediately transferred to a 37°C bath for no-stir (diffusion) studies or further stirred with ADP for stir-induced aggregation studies. Samples were fixed with 0.5 ml 0.8% glutaraldehyde with particle count (Nt) determined with a resistive counter and % aggregation (PA) computed (reproducibility/sensitivity ‹ 5%). For stir conditions, R platelets were as sensitive and as rapidly aggregated by ADP (2-10 μM) as H platelets, with ∼ 1 s time lag for onset of PA. However, for no-stir conditions, linear regression analysis of data for ADP (5-10 μM) induced PA for H platelets for 0-30 s gave αβ = 7.5±4.6 (r = 0.9±0.05). Analysis at longer “diffusion” times showed a second phase (60-300 s) in some H donors with aB = 0.5±0.4 (4/9 donors), while R platelets showed only 1 phase with αβ = 0.65±0.15 (0-60 to 0-900 s) (r = 0.8±0.1). The ADP sensitivity ([ADP]½ corresponding to 50% of maximal changes) for the abnormally rapid PA in no stir H PRP for early times, measured over 0.4-100 μM range, was found to be ∼9 μM (5-17 μM range) and 3.5 μM (3-10 μM) for measurements respectively at 5-10 and 20-30s; these values were ∼ 3-8 × greater than lADPji measured for stirred suspensions for rate/extent of PA or rate of turbidometrically-measured macroaggregation (TA), while › [ADP] threshold for secondary aggregation in TA (10 H donors). These abnormally large aB values and their ADP sensitivity observed for human platelets are consistent with long-range interactions mediated by“chemotactic” agents released from the cells but distinct from normal dense granule release requiring macroaggregation, or by as yet uncharacterized membrane or polymetric bridges.
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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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Palankar, R., M. Medvidov, J. Wesche, and A. Greinacher. "Single-molecule Labeling and Tracking of FcγRIIA on Human Platelets Reveals Differential Mobility Dynamics, which Depends on Platelet Cytoskeletal Integrity." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680095.
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Palankar, R., M. Medvidov, J. Wesche, and A. Greinacher. "Single-molecule Labeling and Tracking of FcγRIIA on Human Platelets Reveals Differential Mobility Dynamics, which Depends on Platelet Cytoskeletal Integrity." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680196.
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