Circulating platelets consist of subpopulations with different age, maturation state and size. In this review, we address the association between platelet size and platelet function and summarize the current knowledge on platelet subpopulations including reticulated platelets, procoagulant platelets and platelets exposing signals to mediate their clearance. Thereby, we emphasize the impact of platelet turnover as an important condition for platelet production in vivo. Understanding of the features that characterize platelet subpopulations is very relevant for the methods of platelet concentrate production, which may enrich or deplete particular platelet subpopulations. Moreover, the concept of platelet size being associated with platelet function may be attractive for transfusion medicine as it holds the perspective to separate platelet subpopulations with specific functional capabilities.

OBJECTIVE-The goal of this study was to specifically estimate the effectiveness of platelet releasate, a widely available treatment administered by a proprietary group of wound care centers (WCCs) for the treatment of diabetic neuropathic foot ulceration.. RESEARCH DESIGN AND METHODS-Treatment effectiveness was estimated in a retrospective cohort study controlling for treatment selection bias using logistic regression-derived propensity scores.. RESULTS-Platelet releasate was more effective than standard care. The relative risk for a wound to heal after treatment with platelet releasate compared with standard care at a WCC varied from 1.14 (95% CI 1.03-1.27) to 1.59 (1.49-1.70). The effect was greatest in those with the most severe wounds, i.e., large wounds that affect deeper anatomical structures.. CONCLUSIONS-Within the limitations of the ability of propensity score analysis to control for selection bias, platelet releasate is more effective than standard therapy. This effect is more ...

In this study, we show that the platelet surface expression of glycoprotein (GP) V is regulated by two independent mechanisms. While confirming that both thrombin and neutrophil elastase proteolyse GPV, we show that neutrophil cathepsin G, thrombin receptor activating peptide (TRAP), and a combination of ADP and epinephrine can each result in a decrease in the platelet surface expression of GPV by a nonproteolytic mechanism: a cytoskeletal-mediated redistribution of platelet surface GPV to the surface-connected canalicular system (SCCS). Four independent lines of evidence documented the nonproteolytic nature of this decrease in the platelet surface expression of GPV. First, flow cytometric studies showed that cathepsin G, TRAP, and ADP/epinephrine decreased the platelet surface expression of GPV without changing the total platelet content of GPV. Second, immunoelectron microscopy directly demonstrated translocation of GPV from the platelet surface to the SCCS. Third, the cathepsin G-, TRAP-, and ADP

TY - JOUR. T1 - Relationship between high platelet turnover and platelet function in high-risk patients with coronary artery disease on dual antiplatelet therapy. AU - Cesari, Francesca. AU - Marcucci, Rossella. AU - Caporale, Roberto. AU - Paniccia, Rita. AU - Romano, Eloisa. AU - Gensini, Gian Franco. AU - Abbate, Rosanna. AU - Gori, Anna Maria. PY - 2008/5. Y1 - 2008/5. N2 - A high platelet turnover rate produce a population of immature reticulated platelets (RP) that could confer, despite of antiplatelet drugs, a residual platelet reactivity (RPR) in coronary artery disease (CAD) patients. To assess the influence of RP on platelet reactivity in CAD patients on dual antiplatelet therapy we measured RP in 372 patients by using the Sysmex XE-2100 haematology analyzer and platelet function by optical platelet aggregometry (PA) on platelet-rich-plasma induced by 1 mmol arachidonic acid (AA-PA) and 10 μM ADP (ADP-PA). RPR was defined as either AA-PA ,20% or ADP-PA ,70%. RP were expressed as a ...

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TY - JOUR. T1 - Influence of rheologic changes and platelet-neutrophil interactions on cell filtration in sepsis. AU - Kirschenbaum, Linda A.. AU - Aziz, Mohammed. AU - Astiz, Mark E.. AU - Saha, Dhanonjoy C.. AU - Rackow, Eric C.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - We examined the role of erythrocyte (red blood cell; RBC) aggregation and deformability, neutrophil (polymorphonuclear neutrophil; PMN) deformability, whole-blood viscosity, and platelet-neutrophil interactions on cell filtration in subjects who were critically ill with sepsis (CIS), critically ill noninfected subjects (CINS), and healthy controls (C). We assessed cell deformability by filtration through filters of 5-μm pore size. Whole blood, RBC, PMN, and combinations of PMN and RBC were studied. Viscometry was done on isolated RBC. Platelet-PMN interactions were assessed with monoclonal antibodies to CD41 and activated CD53 platelet receptors, and to CD66b PMN receptors. Filtration pressure (Pi) for CIS was significantly greater ...

Platelet membrane receptor P2Y12 H1/H2 polymorphisms is highly associated with cerebral infarction: a case-control study Shu-Jun Lu, Xiao-Sheng Zhou, Qi Zheng, Hong-Liang Chen, Yan-Lei Geng Department of Neurology, Binzhou Medical University Hospital, Binzhou, Peoples Republic of China Objectives: This study aimed to determine the relationship between the polymorphisms of the H1/H2 gene of platelet membrane receptor P2Y12 and cerebral infarction (CI) in a Han population in North Shandong Province, Peoples Republic of China. Patients and methods: A case-control study, which involved 168 nonstoke subjects (contrast group) and 152 CI patients (CI group), was conducted. The state of subjects in the CI group was validated by computed tomography or MRI. The clinical data were categorized into two groups. The data included age, gender, smoking, drinking, shrinkage pressure, diastolic blood pressure, blood glucose, cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, serum uric

Partial purification and characterization of serine protease activity in platelets and platelet releasates from patients with Quebec platelet disorder Conference Paper ...

Approach and Results-To model standard antiplatelet therapy, platelets were treated in vitro with aspirin, the P2Y12 receptor blocker prasugrel active metabolite, and aspirin plus prasugrel active metabolite. Different proportions of uninhibited platelets were then introduced. Light transmission aggregometry analysis demonstrated clear positive associations between proportions of drug-free platelets and percentage platelet aggregation in response to a range of platelet agonists. Using differential platelet labeling coupled with advanced flow cytometry and confocal imaging, we found aggregates formed in mixtures of aspirin-inhibited platelets and drug-free platelets were characterized by intermingled platelet populations. This distribution is in accordance with the ability of drug-free platelets to generate thromboxane A2 and so drive secondary platelet activation. Conversely, aggregates formed in mixtures of prasugrel active metabolite-inhibited or aspirin plus prasugrel active ...

Introduction: S100A1 is a member of the S100 family of calcium-binding proteins. S100A1 controls Ca2+ dynamics in cardiomyocytes and plays an important role in heart failure. S100A1 is also strongly expressed in mouse platelets, but its role in platelet biology has not been investigated.. Goal: To determine the role of S100A1 in platelet activation and thrombosis.. Methods and Results: Platelet activation in response to threshold levels of convulxin, a specific agonist for the collagen receptor GPVI, showed significantly increased activation of αIIbβ3 integrin and α-granule release in S100A1-deficient (SKO) platelets compared with wild-type (WT) platelets. Consistently, SKO platelets also showed a more robust aggregation response to convulxin and collagen. In contrast, SKO platelets responded normally to stimulation with PAR4 receptor-activating peptide or ADP. Adhesion of SKO platelets to collagen under flow conditions was not significantly different to that of WT platelets. However, we ...

Oxidized LDL and platelets play a central role in the pathogenesis of atherosclerosis and ischemic cardiovascular diseases. Lysophosphatidic acid (LPA) is a thrombogenic substance that accumulates in mildly-oxidized LDL and in human atherosclerotic lesions, and is responsible for the initial platelet activation, shape change, induced by mildly-oxidized LDL and extracts of lipid-rich atherosclerotic plaques (Siess et al., 1999 Proc Natl Acad Sci USA 1999). LPA directly induced platelet shape change in blood and platelet-rich plasma (PRP) obtained from all blood donors. Albumin was one of the main inhibiting factors of platelet shape change in plasma. Interestingly LPA, at concentrations slightly above plasma levels, induced platelet shape change and aggregation in blood. 1-alkyl-LPA (16:0) was almost 20-fold more potent than 1-acyl-LPA (16:0). LPA-stimulated platelet aggregation in blood and PRP was donor-dependent. LPA-induced aggregation in blood could be completely blocked by the ADP- ...

A method for determining platelet activation by utilizing numeric counts of platelets before a sample of platelets has been activated and after the activatable platelets are activated with a platelet activation agonist and using the difference between such counts as an, indication of the platelet activity of the sample. There is also disclosed a method for using the electronic impedance cell counting technique for determining platelet activation wherein EDTA is used as a preservative by counting the platelets in an EDTA preserved sample using an electronic impedance cell counting technique and subtracting from that number the number of platelets remaining after the activatable platelets in a second sample have been activated with a platelet agonist in the absence of EDTA and using that difference as a measure of platelet activity.

Most heart attacks and strokes are caused by blood clots (thrombi) that block the vasculature. Because disease-causing arterial thrombosis depends on blood platelets, platelet inhibitors such as aspirin and clopidogrel effectively decrease the risk of thrombosis; however, they also impair platelet-dependent hemostasis that staunches bleeding from wounds and can therefore produce excessive bleeding. Experimental studies show that a reduction in the number of platelets also inhibits thrombosis, but these treatments also interfere with platelet function. Because normal hemostasis requires that the platelet concentration remain within a physiological range in the circulation, we evaluated whether lowering the number of circulating platelets-but only to a value still within the normal range-by inhibiting platelet formation in the bone marrow inhibits acute thrombogenesis in baboons. We reduced the platelet count with an inhibitor against the megakaryocyte-promoting hormone thrombopoietin and then ...

Platelets play a key and beneficial role for primary hemostasis on the disruption of the integrity of vessel wall. Platelet adhesion and activation at sites of vascular wall injury is initiated by adhesion to adhesive macromolecules, such as collagen and von Willebrand factor (vWF), or by soluble platelet agonists, such as ADP, thrombin, and thromboxane A2. Different receptors are stimulated by various agonists, almost converging in increasing intracellular Ca2+ concentration that stimulate platelet shape change and granule secretion and ultimately induce the inside-out signaling process leading to activation of the ligand-binding function of integrin alpha IIb beta 3. Binding of alpha IIb beta 3 to its ligands, mainly fibrinogen, mediates platelet adhesion and aggregation and triggers outside-in signaling, resulting in platelet spreading, additional granule secretion, stabilization of platelet adhesion and aggregation, and clot retraction ...

human platelet receptor for type III collagen: MW 68-72 kDa; platelet receptor involved in platelet interaction with type III collagen, localized within platelet lipid rafts where it could interact with other platelet receptors for collagen (GP VI and alpha2beta1 integrin) for efficient platelet activation

Reuters) - Scientists have for the first time created blood platelet cells by reprogramming stem cells derived from adult cells, offering the potential for a renewable supply of the fragile blood component.. Researchers at the Center for iPS Cell Research and Application at Kyoto University in Japan presented data here at a meeting of the American Society of Hematology showing they were able to create the cells in the laboratory and confirm they had the same life span as normal human platelets when infused in mice.. The next step will be to conduct a trial to determine whether our platelets can function in the human body and potentially provide a stable supply of platelets at a predefined quality and quantity that can then be used for transfusion therapy, D. Koji Eto, professor at the Kyoto center and senior author of the study, said in a statement.. Induced pluripotent stem cells, or iPS cells, are produced by manipulating ordinary human skin or blood cells back to a state in which they are ...

inbook{d2d8fceb-9b60-4916-ad95-3b1f6f9113f7, abstract = {,p,Many pathogenic bacteria have been reported to interact with human platelets to mediate platelet activation and aggregation. The importance of these interactions to the immune response or pathogenesis of bacterial infection has not been clarified. It may therefore be valuable to assess platelet responses mediated by diverse strains of bacteria. Here, I describe a method to study platelet integrin activation and granule release using flow cytometry, and a complementary method to study platelet aggregation using a dedicated platelet aggregometer. The combination of these methods represents a rapid and cost-effective strategy to provide mechanistic insight on the type of platelet response mediated by the bacteria.,/p,}, author = {Shannon, Oonagh}, issn = {10643745}, keyword = {Bacteria,Coagulation,Flow cytometry,Platelets,Streptococci}, language = {eng}, pages = {267--273}, publisher = {Humana Press}, series = {Methods in Molecular ...

The present study demonstrates that in type 2 DM patients with CAD receiving maintenance aspirin and clopidogrel therapy, the presence of moderate/severe CKD is associated with higher degrees of platelet reactivity compared with patients with normal renal function/mild CKD. In particular, after adjustment for potential confounders, patients with creatinine clearance ,60 ml/min had an almost 4-fold increase in the likelihood of showing high platelet reactivity after ADP stimuli and over a 2-fold increase in high platelet reactivity after collagen stimuli. Importantly, these patients with high platelet aggregability also have increased markers of platelet activation. Overall, these findings are indicative not only of dysfunctional purinergic signaling mediated ADP receptors but also of the presence of a hyper-reactive platelet phenotype with upregulation of multiple signaling pathways. Therefore, these pharmacodynamic observations might explain the elevated prevalence of ischemic complications, ...

OBJECTIVE-: Protease-activated receptor 4 (PAR4) is a key regulator of platelet reactivity and is encoded by F2RL3, which has abundant rare missense variants. We aimed to provide proof of principle that rare F2LR3 variants potentially affect on platelet reactivity and responsiveness to PAR1 antagonist drugs and to explore underlying molecular mechanisms. APPROACH AND RESULTS-: We identified 6 rare F2RL3 missense variants in 236 cardiac patients, of which the variant causing a tyrosine 157 to cysteine substitution (Y157C) was predicted computationally to affect most on PAR4 structure. Y157C platelets from 3 cases showed reduced responses to PAR4-activating peptide and to α-thrombin compared with controls, but no reduction in responses to PAR1-activating peptide. Pretreatment with the PAR1 antagonist vorapaxar caused lower residual α-thrombin responses in Y157C platelets than in controls, indicating greater platelet inhibition. HEK293 cells transfected with a PAR4 Y157C expression construct had ...

TY - JOUR. T1 - Four types of human platelet lysate, including one virally inactivated by solvent-detergent, can be used to propagate Wharton jelly mesenchymal stromal cells. AU - Chen, Ming Sheng. AU - Wang, Tsung Jen. AU - Lin, Hsiu Chen. AU - Thierry, Burnouf. PY - 2019/3/25. Y1 - 2019/3/25. N2 - There is accumulating experimental evidence that human platelet lysate (HPL) made from platelet concentrates can replace fetal bovine serum (FBS) as a xeno-free clinical-grade supplement of growth media to expand mesenchymal stromal cells (MSCs). However, uncertainties exist in regard to impacts that various manufacturing methods of HPL can exert on the expansion and differentiation capacity of MSCs. In particular, there is a need to evaluate the possibility of implementing virus-inactivation treatment during HPL production to ensure optimal safety of industrial HPL pools. Expired human platelet concentrates from four different donors were pooled and subjected to freeze-thaw cycles (-80/+37 °C), ...

The typical reconstruction model of an unstimulated human platelet is presented. It shows a strict spatial order of organelles and enodmembrane systems. The surface-connected vesicle system is predominantly found in the periphery. The dense tubules constitute a continuous, interconnected system found just under the surface of the platelet. They are particularly pronounced in the vicinity of the marginal microtubules. All organelles are in contact with the dense tubular system (DTS). Granules, vesicles and plasmalemma fuse into the tubules. The platelet organelles are centrally located. Lysosomal granules are primarily shperical and all of them contain a nucleoid. This speaks in favor of a single type of storage organelle in the platelet. The dense bodies and their remnants (large, solitary vesicles) are not joined by the other endomembrane systems, as in the case of the granules. A particular pathways for the release of substances from these organelles is now morphologically plausible. Mitochondria are

TY - JOUR. T1 - Platelet function after cardiac surgery and its association with severe postoperative bleeding. T2 - the PLATFORM study. AU - for The Surgical and Clinical Outcome Research (SCORE) Group. AU - Ranucci, Marco. AU - Pistuddi, Valeria. AU - Di Dedda, Umberto. AU - Menicanti, Lorenzo. AU - De Vincentiis, Carlo. AU - Baryshnikova, Ekaterina. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Platelet dysfunction after cardiac surgery is a determinant of postoperative bleeding. The existing guidelines suggest the use of desmopressin and/or platelet concentrate transfusions in case of platelet dysfunction in bleeding patients, but no cut-off values for platelet activity exist in the literature. The Platelet Function in the Operating Room (PLATFORM) study aims to identify the relationship between platelet function after cardiopulmonary bypass and severe bleeding, finding adequate predictive values of platelet function for severe bleeding. The PLATFORM is a prospective cohort study on 490 adult patients ...

The frequency and severity of bacteremic infections has increased over the last decade and bacterial endovascular infections (i.e., sepsis or endocarditis) are associated with high morbidity and mortality. Bacteria or secreted bacterial products modulate platelet function and, as a result, affect platelet accumulation at sites of vascular infection and inflammation. However, whether bacterial products regulate synthetic events in platelets is not known. In the present study, we determined if prolonged contact with staphylococcal α-toxin signals platelets to synthesize B-cell lymphoma (Bcl-3), a protein that regulates clot retraction in murine and human platelets. We show that α-toxin induced αIIbβ3-dependent aggregation (EC50 2.98 µg/mL ± 0.64 µg/mL) and, over time, significantly altered platelet morphology and stimulated de novo accumulation of Bcl-3 protein in platelets. Adherence to collagen or fibrinogen also increased the expression of Bcl-3 protein by platelets. α-toxin altered Bcl-3

Methods were developed for measuring changes in platelet sensitivity to a release-inducing stimulus and in platelet cyclic AMP in fresh whole blood samples from rabbits. These techniques permitted detection of the effects of exogenous and endogenous prostacyclin on circulating platelets. In these methods, rabbit platelets were labeled in vitro by incubation with [14C]serotonin and [3H]adenine and then transfused into other rabbits. Release of platelet [14C]serotonin by a standard dose of synthetic platelet-activating factor (40 pmol/ml) and the platelet cyclic [3H]AMP levels were then measured in citrated blood from the conscious animals within 2 min of arterial puncture. Bolus intravenous injections of prostacyclin (1-10 nmol/kg) caused concentration-dependent increases in platelet cyclic AMP after 2 min, which decreased approximately 75% by 5 min, and disappeared after 30 min. Significant inhibition of the platelet release reaction was detected 2 min but not 5 min after injection of 10 nmol of ...

TY - JOUR. T1 - Transfection of human platelets with short interfering RNA. AU - Hong, Wei. AU - Kondkar, Altaf A.. AU - Nagalla, Srikanth. AU - Bergmeier, Wolfgang. AU - Jin, Ying. AU - Herman, Jay H.. AU - Bray, Paul F.. PY - 2011/6. Y1 - 2011/6. N2 - Platelets contain mRNAs and are capable of translating mRNA into protein, and it has been previously demonstrated that platelets increase their levels of integrin β3 overtime while in blood bank storage conditions. We are unaware of prior attempts to introduce nucleic acids into platelets. Considering the potential clinical and research utility of manipulating platelet gene expression, we tested whether small interfering RNAs (siRNAs) could be transfected into normal human platelets. Multiple conditions were tested, including lipofectamine versus electroporation, different amounts of siRNA, the effect of different buffers and the presence of plasma during transfection, and the time for optimal siRNA incorporation after transfection. Using flow ...

Release: Dec. 3, 1999. UI participates in multi-center study testing new platelet sterilizing strategy. IOWA CITY, Iowa The University of Iowa Hospitals and Clinics is participating in a multi-center trial testing the efficacy and safety of a new way to cleanse infectious organisms from donated platelets before the blood product is administered to patients.. The UI department of pathology has received a one-and-half-year grant from health care companies Baxter and Cerus for the study titled Determination of the therapeutic efficacy and safety of photochemically treated platelets in thrombocytopenic patients.. Thrombocytopenia is a condition characterized by low blood platelet counts. Platelets are the clotting particles in blood.. The new photochemical strategy attempts to sterilize donated platelets against bacteria and viruses, which may be present in blood products. The goal of the study is to establish that the platelets are not damaged from the sterilization process. Preliminary data ...

The TEMPLATE study design will enable unbiased comparison of the effects of TIC versus TIC + ASP on platelet activity in patients with coronary artery disease. It will also enable a longitudinal comparison of the effects TIC and TIC + ASP with the effects of ASP alone in the same patients. The laboratory tests selected for this study will enable measurement of functional platelet responses to a panel of activating agonists using LTA, flow cytometry and flow chamber tests, selected to measure the extent of inhibition of the multiple platelet activation pathways. We will also measure the extent of baseline platelet activity by testing unstimulated platelets by flow cytometry and with the soluble platelet activation biomarker tests. Together, these data will provide a comprehensive description of the overall pharmacodynamic effects of the different antiplatelet treatments. This information has not been reported previously in cohorts of patients with coronary artery disease receiving TIC or TIC + ...

Blood platelets commonly called megakaryocytes are one of the three tiny cellular components of the blood which helps in the stoppage of bleeding.. Other cellular components of blood are the red blood cells and white blood cells. All the cellular components bathe in the plasma.. Nearly half a billion blood platelets are being formed in the bone marrow every day. These play a primary role in the formation of blood clot. Here I would like to define the two common terms related to the platelet plug formation when the blood vessel in injured.. * Adhesion means sticking of blood platelets with the wall of the bleeding vessel.. * Aggregation means sticking of the platelets with each other.. Normally, in the circulating blood, platelets keep on flowing without any adhesion or aggregation. However, injury to the wall of blood vessel is the point when blood platelets start clinging to the injured part of the vessel wall. At the same time the platelets aggregate with one another and completely seal the ...

The normal circulating platelet count is maintained within relatively narrow limits (150,000-450,000 platelets/μL in Northern Europeans and 90,000-300,000 platelets/μL in people of Mediterranean descent). This difference is related to an inherited slight variation in individual platelet volume (size). The platelet volume is inversely related to the platelet count, so the mass of circulating platelets is the same for these 2 populations. Approximately one-third of platelets are sequestered in the spleen at any one time. Splenic sequestration of platelets can increase dramatically with splenomegaly. Since a platelet has a lifespan of approximately 9-10 days, some 15,000-45,000 platelets/μL must be produced each day to maintain a steady state. New platelet production is the responsibility of the megakaryocyte, a very large multinucleated cell (10,750 fL) found in relatively small numbers in the marrow (0.1% of marrow cells) (Figure 31-1). As with other hematopoietic cells, megakaryocytes are ...

Research in the Laboratory for Hemostasis and Platelet Biology, led by Dr. Andrew Johnson, focuses on understanding genetic and genomic underpinnings of this individual variability in therapeutically targeted CVD pathways ...

Although tumor dormancy is highly prevalent, the underling mechanisms are still mostly unknown. It is unclear which lesions will progress and become a disseminated cancer, and which will remain dormant and asymptomatic. Yet, an improved ability to predict progression would open the possibility of timely treatment and improvement in outcomes. We have recently described the ability of platelets to selectively uptake angiogenesis regulators very early in tumor growth, and proposed their use as an early marker of malignancy. In this review we will summarize current knowledge about these processes and will discuss the possibility of using platelet content to predict presence of occult tumors.

OBJECTIVES: We sought to examine whether patients with stable coronary artery disease (CAD) have increased platelet reactivity and an enhanced propensity to form monocyte-platelet aggregates. BACKGROUND: Platelet-dependent thrombosis and leukocyte infiltration into the vessel wall are characteristic cellular events seen in atherosclerosis. METHODS: Anticoagulated peripheral venous blood from 19 patients with stable CAD and 19 normal control subjects was incubated with or without various platelet agonists and analyzed by whole blood flow cytometry. RESULTS: Circulating degranulated platelets were increased in patients with CAD compared with control subjects (mean [+/- SEM] percent P-selectin-positive platelets: 2.1 +/- 0.2 vs. 1.5 +/- 0.2, p andlt; 0.01) and were more reactive to stimulation with 1 micromol/liter of adenosine diphosphate (ADP) (28.7 +/- 3.9 vs. 16.1 +/- 2.2, p andlt; 0.01), 1 micromol/liter of ADP/epinephrine (51.4 +/- 4.6 vs. 37.5 +/- 3.8, p andlt; 0.05) or 5 micromol/liter of thrombin

Our data clearly show that human platelets can both bind and degrade full-length rhTPO. The affinity constants derived from the binding data indicate that rhTPOs affinity for platelet receptors was similar to that for the cloned c-Mpl receptor construct, gD-Mpl. The binding constants were also similar for rhTPO binding to PRP at 37°C and WP at 22°C. These data show that platelets bind rhTPO, likely via c-Mpl with high affinity (∼350 pmol/L), and that this binding is saturable. Scatchard analysis predicted a low number of (∼23 to 224) binding sites per platelet. However, this estimate may be low, because c-Mpl binding sites on circulating platelets are likely partially occupied by endogenous circulating TPO.9,10 If we assume the number of available c-Mpl receptors is ∼25 to 200 per platelet and that the approximate number of platelets per liter of blood in humans is 200 × 109, then the predicted binding capacity would be ∼8 to 64 pmol per liter of blood. This approximation suggests ...

Subjects for all study groups will be male and between the ages of 25 and 65. Hypertension & Depression Group: Hypertension controlled with an ACE-inhibitor anti-hypertensive; no co-morbid medical conditions known to influence psychological functioning or platelet calcium responses including uncontrolled diabetes, MI or CVA within 6 months of enrollment, secondary hypertension; depression as diagnosed by structured interview and HDRS score of 18; no active participation in another clinical trial; no current suicidal/ homicidal ideation. Hypertension Group: Hypertension controlled with an ACE-inhibitor anti-hypertensive; no co-morbid medical conditions known to influence psychological functioning or platelet calcium responses including uncontrolled diabetes, MI or CVA within 6 months of enrollment, secondary hypertension; no active participation in another clinical trial; no current suicidal/ homicidal ideation. Depression Group: No co-morbid medical conditions known to influence psychological ...

Platelets may interact directly with their targets and perform its killing function. For example, platelets may bind and wrap bacteria (Youssefian et al., 2002) or induce their aggregation (OBrien et al., 2002), leading to degranulation. During malaria infection, platelets have also been described to perform the direct killing of plasmodium parasites in their blood stage forms in a PF4-dependent manner (McMorran et al., 2009, 2012), leading to the general perception that platelets play protective roles during an infection. However, a recent in vivo study in mice paradoxically found that platelet depletion did not lead to higher parasitemia levels (Gramaglia et al., 2017). Instead, links were found between the presence of platelets and malarial pathogenesis via CD40 interactions. Because about two thirds (Jadhav et al., 2004) of malarial infections are accompanied by thrombocytopenia, it thus remains a quandary for clinicians to decide if they should be boosting or inhibiting platelet function ...

1. A new fixing solution is described, which preserves the platelets and prevents contact hemolysis of the erythrocytes, so that counts of both corpuscles may be made in the same preparation.. 2. Comparative counts of platelets in arteries and veins show that arterial blood contains a larger number of platelets than venous blood. This difference is accentuated under experimental conditions that cause a reduction in the number of platelets. It is concluded that new platelets are added to the blood in the capillary areas of the lungs, and that there is a corresponding destruction of platelets as the blood passes through the capillary areas of the systemic circulation.. 3. Perfusion of the lungs with a platelet-preserving solution, compared with that of other organs, gives evidence of the existence of a source of platelet material in the lungs.. 4. Histological examination of the lungs with a technique adequate to give a differential staining of platelet material demonstrates the presence of giant ...

New studies in mice suggest that blood platelets can destroy deadly malaria parasites, but a single dose of aspirin may be enough to thwart their killing power., , , , The findings could have important im...

ANTICOAGULANTS AND THROMBOLYTIC DRUGSHaemostasisVascular injury results firstly in vasoconstriction and formation of platelet plug at the site of injury (primary haemostasis). The platelet plug is then stabilized by the formation of a fibrin meshwork, resulting from activation of the coagulation cascade.Fibrin is eventually cleared through digestion by fibrinolytic enzymes.Primary HaemostasisWhen endothelial integrity is breached, platelets adhere to exposed subendothelial collagen. The adherent platelets become activated result in;1) Exposure of fibrinogen receptors, allowing fibrinogen to bind and cross-link adjacent platelets. The process is known as platelet aggregation. The platelet fibrinogen receptor consists of a complex of glycoproteins IIb and IIIa on the platelet membrane.2) Release of contents of secretory granules including substances such as adenosine diphosphate (ADP) which promote further platelet activation.3) Synthesis of thromboxane A2 which also acts to promote further ...

AimsTo assess whether platelet reactivity is increased in offspring of patients with early acute myocardial infarction (AMI) and its possible relation with endothelial dysfunction.Methods and resultsWe studied 23 healthy children (15 ± 3 years, 13 males) of patients with early AMI (≤50 years old; Group 1) and 21 healthy children of healthy subjects without any history of cardiovascular disease (14 ± 3 years, 10 males; Group 2). Platelet reactivity was assessed by flow cytometry as the increase in monocyte-platelet aggregates (MPA) and CD41 and PAC-1 platelet expression in response to exercise stress test (EST), adenosine diphosphate (ADP) stimulation (10 -7 M), or both. Endothelial function was assessed by measuring brachial artery dilation during post-ischaemic forearm hyperaemia [flow-mediated dilation (FMD)]. Both EST and ADP induced a higher percentage increase in platelet receptor expression in Group 1, compared with Group 2, with the most significant difference being shown for the ...

As conventional tissue biopsies have several drawbacks, much effort has been directed toward the development of minimal-invasive liquid biopsy platforms for detecting and profiling cancer.. Platelets are the second most abundant cells in blood and have very versatile functions both in physiological and pathophysiological conditions. When exposed to tumors and their environment, platelets exchange biomolecules with tumor cells changing the platelets RNA profile, resulting in tumor-mediated education of the platelets. Our research group and collaborators have previously shown that platelets sequester material while in circulation and with that ability accumulate cancer specific information. Platelet RNA profiles or detection of tumor-derived biomarkers within them may provide insight into ongoing cancer-related processes in a patient, allowing for implementation of personalized therapy strategies.. This thesis evaluates whether circulating platelets could have a potential role (as a liquid biopsy ...

Platelets, also called thrombocytes (thromb- + -cyte, blood clot cell), are a component of blood whose function (along with the coagulation factors) is to stop bleeding by clumping and clotting blood vessel injuries. Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, and then enter the circulation. These unactivated platelets are biconvex discoid (lens-shaped) structures, 2-3 µm in greatest diameter. Platelets are found only in mammals, whereas in other animals (e.g. birds, amphibians) thrombocytes circulate as intact mononuclear cells. On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells. The smear is used to examine platelets for size, shape, qualitative number, and clumping. The ratio of platelets to red blood cells in a healthy adult is 1:10 to 1:20. The main function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of ...

After deposition of a platelet monolayer over the exposed VWF and collagen, the next step required for thrombus formation is the recruitment of additional platelets from the flowing blood, which upon activation acquire the ability to stick to each other in a process commonly referred to as platelet aggregation. This is made possible by the local accumulation of soluble agonists that are secreted/produced by adherent-activated platelets, including ADP, TxA2, epinephrine and thrombin. The final step is activation of αIIbβ3, causing a conformational change that enables it to bind fibrinogen and VWF, allowing stable bridges between platelets. The great number of αIIbβ3 copies on the platelet surface, (40,000-80,000), allows the assembly of large aggregates at the site of vascular injury. Activation of αIIbβ3 integrin requires agonist-driven activation events in recruited platelets, referred to as inside-out signaling, including the sequential activation of one or more PLC isoforms yielding a ...

Fig.10 Design of CREKA-Lipo-T nanoparticles and their proposed antimetastatic mechanism within tumor tissues. (A) Proposed mechanism of action of CREKA-Lipo-T nanoparticles. Normally, tumor growth factor (TGF)-b secreted by platelets induces transition of tumor cells to a mesenchymal-like phenotype (I). Platelets can also protect tumor cells against attack from natural killer (NK) cells (II). At distant sites, platelets assist metastatic cells to cross the local endothelium by secreting numerous cytokines. Following treatment, CREKA-Lipo-T actively targets microthrombi in tumor vessel walls and releases ticagrelor slowly and locally. Ticagrelor binds to tumor-associated platelets and inhibits their functions. The release of TGF-b from platelets and the interaction between platelets and tumor cells are abolished, leading to decreased epithelial-mesenchymal-like transition of tumor cells and thus inhibiting their invasion capacity. When tumor cells are present in circulation, compromised platelets ...

TY - JOUR. T1 - Preferential binding of platelets to monocytes over neutrophils under flow. AU - Ahn, Kyung C.. AU - Jun, Andy J.. AU - Pawar, Parag. AU - Jadhav, Sameer. AU - Napier, Susan. AU - McCarty, Owen J.T.. AU - Konstantopoulos, Konstantinos. PY - 2005/4/1. Y1 - 2005/4/1. N2 - This study was undertaken to systematically investigate the binding kinetics of platelet recruitment by monocytes relative to neutrophils in bulk suspensions subjected to shear as well as the molecular requirements of leukocyte-platelet binding. Hydrodynamic shear-induced collisions augment the proportion of monocytes with adherent platelets more drastically than that of neutrophils with bound platelets. These heterotypic interactions are further potentiated by platelet activation with thrombin or to a lesser extent by monocyte stimulation with N-formyl-methionyl-leucyl-phenylalanine (fMLP). Monocyte-platelet heteroaggregation increases with increasing shear rate and shear exposure time. Platelet P-selectin ...

Cooper, N., Heddle, N. M., de Haas, M., Reid, M. E., Lesser, M. L., Fleit, H. B., Woloski, B. M. R. and Bussel, J. B. (2004), Intravenous (IV) anti-D and IV immunoglobulin achieve acute platelet increases by different mechanisms: modulation of cytokine and platelet responses to IV anti-D by FcγRIIa and FcγRIIIa polymorphisms. British Journal of Haematology, 124: 511-518. doi: 10.1111/j.1365-2141.2004.04804.x ...

Tortuous blood vessels are often seen in humans in association with thrombosis, atherosclerosis, hypertension, and aging. Vessel tortuosity can cause high fluid shear stress, likely promoting thrombosis. However, the underlying physical mechanisms and microscale processes are poorly understood. Accordingly, the objectives of this study were to develop and use a new computational approach to determine the effects of venule tortuosity and fluid velocity on thrombus initiation. The transport, collision, shear-induced activation, and receptor-ligand adhesion of individual platelets in thrombus formation were simulated using discrete element method. The shear-induced activation model assumed that a platelet became activated if it experienced a shear stress above a relative critical shear stress or if it contacted an activated platelet. Venules of various levels of tortuosity were simulated for a mean flow velocity of 0.10 cm s−1 , and a tortuous arteriole was simulated for a mean velocity of 0.47 ...

Article see p 476. As megakaryocytes form platelets, they transfer STAT3 to proplatelet tips. Consequently, STAT3 is found in platelets that circulate in the bloodstream (Figure). The presence of STAT3 in platelets raises the question of whether it regulates functional responses in platelets or is simply a vestigial remnant of megakaryocytes. An argument for the leftover without function hypothesis is the anucleate status of platelets: simply stated, with no nucleus and no nuclear DNA there is no place for STAT3 to stick in platelets. The problem with this argument is that simple is no longer a common word used to describe platelets. Moreover, why would platelets expend energy to carry a protein that they do not need, especially since previous studies have shown that STAT3 undergoes signal-dependent phosphorylation in these anucleate cytoplasts?4 Well, any doubt regarding why STAT3 is present in platelets has been cleared up. Using a combination of pharmacological and genetic based tools, ...

Background: Coated-platelets, a subset of activated platelets observed with dual-agonist stimulation with collagen and thrombin, represent 30% of the platelet population in normal controls. In recently published work, we have shown that elevated coated-platelet levels (,45%) are predictive of stroke in asymptomatic carotid stenosis. We now investigate if platelet count and mean platelet volume (MPV) are related to coated-platelet levels.. Methods: Coated-platelet levels were measured in a cohort of asymptomatic outpatients referred for carotid ultrasound studies. Platelet count and mean platelet volume for each subject were recorded from the VA electronic medical record at the closest possible time period (within ≤6 months) to the date of coated-platelet sample. Correlations between each parameter and coated-platelet levels were determined and those reaching significance at p≤0.1 were included in a multiple regression model with LDL and systolic blood pressure (SBP), variables previously ...

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TY - JOUR. T1 - A study of whole blood platelet and white cell aggregation using a laser flow aggregometer. AU - Sun, J.. AU - Abel, E. W.. AU - Bancroft, A.. AU - McLaren, M.. AU - Belch, J. J. F.. PY - 2003. Y1 - 2003. N2 - Both platelet aggregation and white blood cell aggregation are involved in pathological processes such as thrombosis, atherosclerosis and chronic inflammation. People in older age groups are likely to suffer from cardiovascular diseases and may have increased white cell and platelet aggregation which could contribute to this increased risk. This study aimed to compare white cell and platelet aggregation between different age and gender groups. Whole blood white cell aggregation and platelet aggregation were carried out on healthy volunteers using cytometric techniques. It was found that both white cell and platelet aggregation in the elderly group (white cell aggregation median value, 0.08; range, 0.02-0.14; platelet aggregation median value, 0.32; range, 0.1-0.39) were ...

Systematic review (Open Access) on the comparison of different platelet transfusion thresholds prior to insertion of central lines in patients with thrombocytopenia from Cochrane Database of Systematic Reviews Comparison of different platelet transfusion thresholds prior to insertion of central lines in patients with thrombocytopenia #vascularaccess #FOAMva #FOAMed #FOAMcc #POCUS #patientsafety

Megakaryocytes generate platelets by remodeling their cytoplasm into long proplatelet extensions, which serve as assembly lines for platelet production. Although the mechanics of proplatelet elongation have been studied, the terminal steps of proplatelet maturation and platelet release remain poorly understood. To elucidate this process, released proplatelets were isolated, and their conversion into individual platelets was assessed. This enabled us to (a) define and quantify the different stages in platelet maturation, (b) identify a new intermediate stage in platelet production, the preplatelet, (c) delineate the cytoskeletal mechanics involved in preplatelet/proplatelet interconversion, and (d) model proplatelet fission and platelet release. Preplatelets are anucleate discoid particles 2-10 \(\mu\)m across that have the capacity to convert reversibly into elongated proplatelets by twisting microtubule-based forces that can be visualized in proplatelets expressing GFP-\(\beta\)1-tubulin. The ...

In patients with thrombocytopenia, it can be difficult to predict a patients bleeding risk based on platelet count alone. Platelet reactivity may provide additional information; however, current clinical assays cannot reliably assess platelet function in the setting of thrombocytopenia. New methods to study platelet reactivity in thrombocytopenic samples are needed. In this study, we sought to develop a laboratory model of thrombocytopenia using blood from healthy subjects that preserves the whole blood environment and reproducibly produces samples with a specific platelet count and hematocrit. We compared the activation state of unstimulated and agonist-stimulated platelets in thrombocytopenic samples derived from this method with normocytic controls. Whole blood was diluted with autologous red blood cell concentrate and platelet-poor plasma, which were obtained via centrifugation, in specific ratios to attain a final sample with a predetermined platelet count and hematocrit. P-selectin exposure and

TY - JOUR. T1 - Functional alterations of human platelets following 111In labeling with different ligands and incubation media. AU - Mieno, M.. AU - Isaka, Y.. AU - Kimura, K.. AU - Matsumoto, M.. AU - Etani, H.. AU - Uehara, A.. AU - Hashikawa, K.. AU - Hata, R.. AU - Moriwaki, H.. AU - Ashida, K.. AU - Imaizumi, M.. AU - Kamada, T.. AU - Kozuka, T.. PY - 1990/1/1. Y1 - 1990/1/1. N2 - We studied the effects of various 111In-water soluble chelates and incubation media on labeling efficiency of platelets and in vitro platelet aggregability. High labeling efficiency of platelets in ACD-saline was achieved with 111In-oxine sulfate, 111In-tropolone and 111In-MPO (2-mercaptopyridine-N-oxide). In the condition with 4.8 x 106/mm3 platelets in ACD-plasma, 111In-oxine-sulfate had low labeling efficiency and inconsistent labeling, while 111In-tropolone and 111In-MPO had high labeling efficiency. In vitro platelet aggregability (ADP 2 μM) was reduced when platelets were labeled in the absence of plasma. ...

With platelet activation, there is modulation of platelet surface molecule expression. In flow cytometric analyses of in vivo platelet activation, results are often confounded by activation induced in vitro by the preparative procedures. It is particularly important therefore to prevent or retard platelet activation as soon as possible after withdrawal of the blood sample. Taking blood into paraformaldehyde, or fixing the cells with paraformaldehyde as soon as possible after withdrawal, has been employed to prevent platelet activation in vitro, but paraformaldehyde-fixed platelets cannot be further used in functional studies. We investigated the efficacy of Diatube-H, a commercially available combination of platelet antagonists (theophylline, adenosine, and dipyridamole), in preventing or retarding platelet activation in vitro, along with its effects on modulation of platelet membrane glycoproteins (GP) and adhesion molecules. In contrast to blood taken into EDTA, blood taken into Diatube-H ...

The present study clarifies several aspects of the effects on platelet aggregation of arising and assuming the upright posture in the morning: 1) On arising, increased platelet aggregation can readily be observed in whole blood; 2) this increased aggregation is not accompanied by platelet activation, as evidenced by changes in activation-dependent markers on the platelet surface; 3) the observed increase in aggregation in whole blood may be partly explained by increases in platelet count and hematocrit that accompany arising. In addition, the study confirmed previous reports of increased fibrinolysis on standing and provided new evidence of an opposing increase in thrombin generation on standing.. Comparison with previous studies. Studies reporting the effects of arising in the morning on platelet aggregation (7-11,13) have exclusively studied aggregation in PRP, and to our knowledge, the present study is the first to report the effects of arising on platelet aggregation in whole blood. Of the ...

FIG. 2. Cleavage of α2-8-linked sialic acid from platelet surfaces results in a reduction of S. mitis binding. Binding of SF100 (□) to untreated human platelets (lane 1) or platelets pretreated with sialidase A (lane 2), sialidase V (lane 3), or sialidase C (lane 4). Binding of PS344 (▪) to platelets (lane 5) or platelets pretreated with sialidase A (lane 6), sialidase V (lane 7), or sialidase C (lane 8). Values presented are expressed as a percentage of wild-type binding to untreated platelets (mean ± SD). Data represent three experiments performed in triplicate on different occasions from a different donor each time. Note that these donors are different from those shown in Fig. 1. ...

Normal primary platelet aggregation requires agonist-mediated activation of membrane GPIIb-IIIa, binding of fibrinogen to GPIIb-IIIa, and cellular events after ligand binding. PAC1 monoclonal antibody distinguishes between resting and activated states of GPIIb-IIIa, and other antibodies preferentially recognize GPIIb (PMI-1) or IIIa (anti-LIBS1) after the binding of fibrinogen or fibrinogen-mimetic peptides, such as GRGDSP. Using these antibodies and platelet flow cytometry, we studied two distinct persistent platelet aggregation abnormalities. Platelets from a thrombasthenic variant, which contained near-normal amounts of GPIIb-IIIa, failed to aggregate or bind PAC1 in response to agonists. In addition, GRGDSP, which binds to normal GPIIb-IIIa without prior cell activation, failed to increase the binding of PMI-1 or anti-LIBS1 to the thrombasthenic platelets, suggesting a primary defect in ligand binding. Chromatography of detergent-solubilized platelets on a KYGRGDS affinity column confirmed ...

Platelets are cell fragments which are mainly an essential component when it comes to blood clotting and coagulation. The platelets along with the red blood cells and white blood cells, function together for the regulation and normal functioning of blood in our body. The blood cells have each of their own different life span as well as different functions. Among these three, the platelets are the smallest but one of the most important factors in blood clotting. If the platelets dont get regulated properly, such as when they dont get renewed at normal intervals, then the blood dysfunction or disorder might occur.. The general lifespan of a platelet is about 10 days. The normal platelet count in the human blood ranges from 150,000 to 450,000 per micro liter of blood. The platelet count varies in different locations and organs. But in cases of medical conditions, the platelets count may either increase or decrease in the blood. One of the most common condition of platelet count changes is the ...

SUMMARY Acquired qualitative platelet disorders are frequent causes of abnormal platelet function measured in vitro, although by themselves are usually associated with little or no clinical bleeding. However, there are important exceptions. Nevertheless, their major clinical impact becomes apparent in the additional presence of thrombocytopenia, or additional acquired or congenital disorders of hemostasis. Acquired disorders of platelet function can be conveniently classified into those that result from drugs, hematologic diseases, and systemic disorders. Drugs are the most frequent cause of acquired qualitative platelet dysfunction. Aspirin is the most notable drug in this regard because of its frequent use, its irreversible effect on platelet prostaglandin synthesis, and its documented effect on hemostatic competency, although this effect is minimal in normal individuals. Other nonsteroidal antiinflammatory drugs reversibly inhibit platelet prostaglandin synthesis and usually have little ...

Platelets are an important blood component that helps in controlling bleeding. The most abundant particle in our blood is the platelet that causes the blood to clot whenever theres a cut or injury, thereby stopping the bleeding in minutes. Now, there are tens and thousands of platelets in normal which help in this process. But in cases of certain diseases and illness like dengue etc the platelets gets destroyed by the infective germ, making the body prone to bleeding. Such a low count of platelet can cause serious brain damage and other organ damage. Apart from a blood transfusion, the most trusted way to increase your platelet count is by eating low platelets treatment food. Foods to increase platelet count are often used as basic preventive care and home remedy for diseases like dengue. But how do these home remedies to increase platelets work is a very basic understanding of…. ...

A low blood platelet count, known as thrombocytopenia, prevents blood from clotting normally. This can be an indication of serious medical conditions.SignificanceThe three main reasons for a low blood platelet count include reduced platelet production at bone marrow, blockage of platelets at enlarged spleen and an overuse or elimination of platelets by the body.Conditions Affecting Bone MarrowHIV and cancers such as leukemia and lymphoma reduce the capacity of bone marrow to produce platelets.Conditions Affecting the SpleenMyelofibrosis and certain forms of cirrhosis can enlarge the spleen. This hinders the passage of platelets into the bl...

While the heterozygous Q43P β1-tubulin carriers have a reduced function, the β1-tubulin-deficient mice present with only minor abnormalities in platelet hemostatic functions. Besides the fact that human platelets are more easy to handle and study in detail than mouse platelets, this can probably be explained by the fact that the loss of β1-tubulin expression in mouse platelets was overcome by overexpression of the other platelet β-tubulin variants,7 while the Q43P carrier platelets not only show reduced β1-tubulin but also total β-tubulin protein levels. In addition, incorporation of GFP-tagged Q43P β1-tubulin into wild-type tubulin structures seems to be inefficient and delocalized.. Due to the platelet dysfunction phenotype, the Q43P β1-tubulin variant could not only be conceived as a genetic risk factor for the development of thrombocytopenia but also as a protective genetic factor against cardiovascular disease. Indeed, a case-control study showed that the prevalence of Q43P ...

Activated blood platelets mediate the primary response to vascular injury. Although molecular abnormalities of platelet proteins occur infrequently, taken collectively, an inherited platelet defect accounts for a bleeding diathesis in ≈1:20,000 individuals. One rare example of a platelet disorder, Glanzmann thrombasthenia (GT), is characterized by life-long morbidity and mortality due to molecular abnormalities in a major platelet adhesion receptor, integrin αIIbβ3. Transfusion therapy is frequently inadequate because patients often generate antibodies to αIIbβ3, leading to immunemediated destruction of healthy platelets. In the most severe cases allogeneic bone marrow transplantation has been used, yet because of the risk of the procedure it has been limited to few patients. Thus, hematopoietic stem cell gene transfer was explored as a strategy to improve platelet function within a canine model for GT. Bleeding complications necessitated the use of a mild pretransplant conditioning ...

Significance: Levels of platelet noncoding RNAs (ncRNAs) are altered by disease, and ncRNAs may exert functions inside and outside of platelets. Their role in physiologic hemostasis and pathologic thrombosis remains to be explored. Recent Advances: The number of RNA classes identified in platelets has been growing since the past decade. Apart from coding messenger RNAs, the RNA landscape in platelets comprises ncRNAs such as microRNAs, circular RNAs, long ncRNAs, YRNAs, and potentially environmentally derived exogenous ncRNAs. Recent research has focused on the function of platelet RNAs beyond platelets, mediated through protective RNA shuttles or even cellular uptake of entire platelets. Multiple studies have also explored the potential of platelet RNAs as novel biomarkers. Critical Issues: Platelet preparations can contain contaminating leukocytes. Even few leukocytes may contribute a substantial amount of RNA. As biomarkers, platelet RNAs have shown associations with platelet activation, but ...

Activation of platelets with thrombin and other agonists causes a rapid increase in the phosphorylation of multiple proteins on tyrosine. To identify candidate protein-tyrosine kinases (PTKs; EC 2.7.1.112) that may be responsible for these phosphorylation events, we analyzed the expression of seven Src-family PTKs and examined the association of these kinases with known platelet membrane glycoproteins. Five Src-related PTKs were detected in platelets: pp60SRC, pp60FYN, pp62YES, pp61HCK, and two LYN products of Mr 54,000 and 58,000. The Fgr and Lck PTKs were not detected. Although strict comparative quantification of protein levels was not possible, pp60SRC was detected at higher levels than any of the other kinases. In addition, glycoprotein IV (GPIV, CD36), one of the major platelet membrane glycoproteins, was associated in a complex with the Fyn, Yes, and Lyn proteins in platelet lysates. Similar complexes were also found in two GPIV-expressing cell lines, C32 melanoma cells and HEL cells. ...

Phosphatidylinositol 3-kinaseβ (PI3Kβ) plays a predominant role in integrin outside-in signaling and in platelet activation by GPVI engagement. We have shown that the tyrosine kinase Pyk2 mediates PI3Kβ activation downstream of integrin αIIbβ3, and promotes the phosphorylation of the PI3K-associated adaptor protein c-Cbl. In this study, we compared the functional correlation between Pyk2 and PI3Kβ upon recruitment of the two main platelet collagen receptors, integrin α2β1 and GPVI. PI3Kβ-mediated phosphorylation of Akt was inhibited in Pyk2-deficient platelets adherent to monomeric collagen through integrin α2β1, but occurred normally upon GPVI ligation. Integrin α2β1 engagement led to Pyk2-independent association of c-Cbl with PI3K. However, c-Cbl was not phosphorylated in adherent platelets, and phosphorylation of Akt occurred normally in c-Cbl-deficient platelets, indicating that the c-Cbl is dispensable for Pyk2-mediated PI3Kβ activation. Stimulation of platelets with CRP, a ...

TY - JOUR. T1 - Potentiation of TRAP-6-induced platelet dense granule release by blockade of P2Y12 signaling with MRS2395. AU - Mitrugno, Annachiara. AU - Rigg, Rachel A.. AU - Laschober, Nicole B.. AU - Ngo, Anh T.P.. AU - Pang, Jiaqing. AU - Williams, Craig D.. AU - Aslan, Joseph E.. AU - McCarty, Owen J.T.. N1 - Funding Information: This work was supported by grants from the National Institutes of Health (R01HL101972 and R01GM116184 to O.J.T.M.), the American Heart Association (13EIA12630000 to O.J.T.M. and 17SDG33350075 to J.E. A.) and the Altarum Institute (C.D.W. and O.J.T.M.). N.B.L. is a Johnson scholar. R.A.R is a Whitaker International Scholar. Funding Information: Super resolution microscopy studies were supported in part by the M.J. Murdock Charitable Trust. Publisher Copyright: © 2018 Taylor & Francis. Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 2018/5/19. Y1 - 2018/5/19. N2 - The release of ADP from platelet dense granules and its binding to platelet P2Y12 ...

Angiotensin II (Ang II) is a critical component of the reninangiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were _disibledevent=font-size:10pt;line-height:1.5;font-family:Verdana;>5-HT in platelets, an event

Results: 22 hypoxemic patients were selected for the study based on their diagnosis of COPD (from history and spirometry) along with age and sex matched controls. Presence of comorbidities and other factors that cause platelet activation were excluded. Level of platelet aggregation was determined by several experiments. By an aggregometer using platelet agonists (thrombin and ADP) it was found that platelet aggregation was significantly higher in hypoxemic COPD patients than normal healthy controls. Fluorescence spectrophotometer was used to measure intracellular calcium as a marker of platelet activation and it was found that hypoxemic COPD patients had significantly higher platelet aggregation than normal healthy controls. However no significant difference was found in other markers of platelet activation studied namely P-selectin exposure and PAC-1 binding between the two groups ...

ABSTRACT. Angiotensin II (Ang II) is a critical component of the renin-angiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were not changed. However, the aggregation response to collagen was reduced in isolated ...

Glycoprotein Ib-IX-V (GPIb-IX-V) is a platelet adhesion receptor complex that initiates platelet aggregation. Glycoprotein Iba (GPIba) is the central component of the GPIb-IX-V complex, anchoring the complex to the cytoskeleton and harboring the binding site for von Willebrand factor (vWF). Previous studies suggest that the coagulation function in pigs differs from that in humans, especially with respect to the interaction between vWF and platelets. However, we have little knowledge about the function of porcine platelets, which is important with regard to studies of cardiovascular disease, clotting, and surgery that use pigs as animal models. To extend this information, we cloned and analyzed the porcine GPIba sequence. Porcine GPIba contains 1891 nucleotides and includes an open reading frame that encodes 627 amino acids. The nucleotide sequence showed 67% identity with human GPIba, whereas the deduced amino acid sequences were 59% identical. The vWF binding domain shares the highest identity ...

BioAssay record AID 336312 submitted by ChEMBL: Antiplatelet activity against bovine citreated platelet assessed as inhibition of ADP-induced platelet aggregation up to 278 ug/ml after 6 mins.

TY - JOUR. T1 - Extensive characterization of the composition and functional activities of five preparations of human platelet lysates for dedicated clinical uses. AU - Delila, Liling. AU - Wu, Yu Wen. AU - Nebie, Ouada. AU - Widyaningrum, Rifa. AU - Chou, Ming Li. AU - Devos, David. AU - Burnouf, Thierry. N1 - Funding Information: LD and ON were supported by MS and PhD fellowships from Taipei Medical University, and RW by PhD fellowship from Ministry of Education of Taiwan. Publisher Copyright: © 2020 Taylor & Francis Group, LLC. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.. PY - 2021. Y1 - 2021. N2 - Human platelet lysates (HPLs), rich in various growth factors and cell growth-promoting molecules, encompass a new range of blood products that are being used for regenerative medicine, cell therapies, and tissue engineering. Well-characterized dedicated preparations, tailor-made to best fit specific therapeutic applications, are needed for optimal clinical efficacy and safety. ...

To delineate the critical top features of platelets necessary for balance and formation of thrombi, thromboelastography and platelet aggregation measurements were employed in whole blood of normal individuals and of those with Bernard-Soulier Syndrome (BSS) and Glanzmanns Thrombasthenia (GT). generation of stable thrombi, a potentially significant feature in individual medical results. Introduction An initial step in thrombus formation in the hurt vascular endothelium is the adhesion of platelets to shown subendothelial elements, e.g., von Willebrand Aspect (vWF), under high prices of shear, via the connections from the platelet glycoprotein (GP) 1b/V/IX receptor complicated with subendothelial vWF [1]. This tethering of platelets after that promotes their firmer binding to subendothelial collagen (COL) fibres via platelet receptors, e.g., GPVI [2], [3] and integrin II1 [4]. In this procedure, platelets are turned on, resulting in platelet shape adjustments, aggregation, discharge of aggregation ...

Octadecadienoic acids (linoleic acid and linolelaidic acid) and the diacylglycerol, 1-oleoyl-2-acetyl-rac-glycerol (OAG) concentration-dependently induced activation of gel-filtered human platelets, i.e. aggregation and phosphorylation of 20 kDa and 47 kDa peptides. In contrast, octadecenoic acids (oleic and elaidic acid) and octadecanoic (stearic) acid were inactive. Octadecadienoic acid-induced platelet activation was suppressed by the protein kinase C inhibitor, polymyxin B, but not by the cyclooxygenase inhibitor, indomethacin. OAG-induced activation was potentiated by octadecadienoic acids present at non-stimulatory concentrations. Our data suggest that octadecadienoic acids and diacylglycerol synergistically induce platelet activation via protein kinase C. Furthermore, linolelaidic acid may provide a useful experimental tool to study fatty acid regulation of protein kinase C in intact cells. ...

Staphylococcus aureus is an opportunistic pathogenic bacterium known for its ability to interact with platelets and modulate their function. S. aureus lipoproteins are one of the major groups of bacterial surface molecules and are released into the extracellular milieu where they are recognized by host immune cells. The aim of this study was to determine the role of S. aureus lipoproteins in S. aureus-platelet interactions. Platelet aggregation and binding assays using S. aureus wild type and lgt strains showed that, S. aureus lipoproteins contribute towards binding of the pathogen to platelets. Lipoproteins present in extracellular milieu also bind platelets. Platelet spreading, thrombus formation, agonist induced platelet aggregation and αIIbβ3 activation were inhibited by cell-free lipoproteins. CD36 was identified as the major platelet surface molecule interacting with S. aureus lipoproteins. Antibody neutralization demonstrated that functional inhibition of platelet activation caused by ...

Seventy-five consecutive patients with normal platelet counts were investigated for easy bruising. All had a normal coagulation profile, and all except four were women. None were on aspirin or other antiplatelet agents. Two specific groups could be delineated. In type I (44 patients, mean age, 35), platelet function was normal to supranormal. Megathrombocyte number was elevated in 60% of patients and correlated with the presence of antiplatelet antibody in 30% of patients. In type II (31 patients, mean age, 34), platelet function was abnormal: impaired epinephrine aggregation (primary and secondary wave) in 97%, impaired connective tissue aggregation in 77%, and impaired ADP aggregation in 42%. Megathrombocyte number was elevated in 71%, and antiplatelet antibody was present in 38% of patients. The easy bruising syndrome can be differentiated into two categories: type I, in which a platelet abnormality is unlikely, and type II, in which a platelet abnormality exists. Elevated incidence of ...

The work herein examines in vitro platelet aggregation in response to fluid shearing motion. Our specific aim is to characterize shear-induced aggregation by means of kinetic measurements. In doing so we consider plausible physicochemical mechanisms for platelet activation in the shear field. Besides resolving some questions concerning the activation of platelets by shear forces, this study further implicates fluid mechanical factors in thrombosis and arterial disease. Specific results may also apply to the design and evaluation of blood-contacting artificial devices. The experimental procedure centers on the use of a rotational viscometer to apply a controlled shearing motion to platelet suspensions for prescribed times. We quantify aggregation through changes in particle size histograms and associated measures (e.g. total number of particles). Additional insight into the aggregation response comes from interpreting kinetic data using the coalescence equation, a population balance specific for ...

It has been proposed that adsorbed glycoproteins such as fibrinogen and gamma-globulin induce platelet adhesion at blood-polymer interfaces. The importance of oligosaccharide groups in the glycoproteins proved to be responsible for platelet adhesion and aggregation via possible complex formation. Several studies have provided evidence that the proposed mechanism was involved in platelet adhesion on polymer surfaces. To minimize or prevent platelet adhesion on polymers, prostaglandins (PGs), potent inhibitors of platelet aggregation and PG-heparin (HEP) conjugate, were combined with polymers via physical dispersion or chemical immobilization on the surfaces. Albumin-HEP conjugate-adsorbed surfaces also showed significant reduction of platelet adhesion.

Human platelet-rich plasma (PRP) was irradiated in vitro with a fiberoptic Nd:YAG laser-heated metal cap to study its effects on platelets. The energy of the laser was 5 and 10 watts with an irradiation time of 0, 3, 6, and 9 seconds and 14 watts with an irradiation time of 0, 3, 4, and 5 seconds, respectively. The irradiated PRPs were analyzed for platelet count, aggregation reaction, thromboxane (TX)B2 measurement and electron microscopy. Various degrees of decrease in platelet count were observed in all groups. Except the 5Wx3S group, the other groups showed an increase in the maximum aggregation rate of platelets, which corresponded to the enhancement of TXB2 formation. It was also demonstrated by a transmission electron microscopy in 10Wx3S, 10Wx6S, 10Wx9S, 14Wx3S, 14Wx4S, and 14Wx5S energy groups that alpha- and dense-particles in irradiated platelets became sparse in number or even disappeared, less electron density, irregularity in size and shape, and a tendency for these particles to ...

This study was conducted to examine the mechanism(s) of synergistic interaction of adrenaline and platelet-activating factor (PAF) mediated human platelet aggregation. We found that platelet aggregation mediated by subthreshold concentrations of PAF (5-8 nM) plus adrenaline (0.5-2 μM) was inhibited by both α2-adrenoceptor blocker (yohimbine) and PAF receptor antagonist (WEB2086). While examining the role of the downstream signalling pathways, we found that this synergism was inhibited by calcium channel blockers, verapamil, and diltiazem. In addition, platelet aggregation by co-addition of adrenaline and PAF was also inhibited by very low concentrations of phospholipase C (PLC) inhibitor (U73122; IC50 = 0.2 μM), the MAP kinase inhibitor, PD98059 (IC50 = 3 μM) and cyclooxygenase (COX-1) inhibitors including indomethacin (IC50 = 0.25 μM), flurbiprofen (IC50 = 0.7 μM) and piroxicam (IC50 = 7 μM). However, the COX-2 inhibitor, nimesulide, was also effective in inhibiting the aggregation. The

The latter work was performed with murine species and, of note, many differences have been emphasized in megakaryocyte localization and ultrastructure of proplatelet formation, between mice and humans.32 The present study performed on human MKs sheds additional light on how these large protrusions can be induced to fragment into small platelets by shear forces in flowing blood. This is also in keeping with evidence that the pulmonary circulation could be an important site of platelet production, as the lung capillaries would be the first to be encountered by cells leaving the bone marrow.28 Indeed, the large cytoplasmic fragments and the isolated platelet-sized fragments that we observed in real time to form on the coverslip during the flow assay resembled those seen downstream of the pulmonary circulation in vivo.33 In our conditions, high shear rates were essential to proplatelet and platelet formation during an exposure time of 20 minutes. In contrast, no proplatelet or platelet was generated ...

REPORT DESCRIPTIONPlatelet rich plasma (PRP) is a blood plasma product in which concentration of platelets is elevated four to eight times higher than the normal blood platelet concentration. PRP is also called platelet rich gel, platelet enriched plasma and platelet enriched gels; and is used in effective treatment...

What Discussion about plateletsThrombocytopenia, platelet count, normal platelet count, high platelet count, low platelets, and other aspect

T cell depletion with antithymocyte globulins (ATG) can be complicated by thrombopenia and. hypercoagulability. The underlying mechanism is still unclear. We found that binding of ATG to. platelets caused platelet aggregation, alpha-granule release, membrane phosphatidylserine exposure. and the rapid release of platelet microvesicles (MV). Platelet activation and MV release. were complement-dependent and required membrane insertion of C5b-8 but not stable lytic pore. formation by C5b-9. Full platelet aggregation and activation by ATG also required the low affinity. Fc gamma receptor FcγRII. MV release, however, was FcγRII-independent. Platelet MV. expressed high prothrombinase activity. Moreover, blocking C5 inhibited ATG-induced thrombin. generation in platelet rich plasma. In 19 hematopoietic stem cell and kidney transplant patients,. ATG treatment resulted in thrombopenia and increased plasma levels of d-dimer and thrombin-anti-. thrombin-complexes. Flow cytometric analysis of complement ...