scispace - formally typeset
Search or ask a question

Which tablet is best for platelets? 

Platelet
Thrombin
Platelet-rich plasma
Hemostatic function
Platelet activation

Answers from top 11 papers

More filters
Papers (11)Insight
Journal Article•DOI
Precise patterning of the SEBS surface by UV lithography to evaluate the platelet function through single platelet adhesion
Wei Ye, Qiang Shi, Shing Chung Josh Wong, Jianwen Hou, Xiaodong Xu, Jinghua Yin 
29 Jul 2014-Biomaterials Science
19 Citations
The SPA assay methodology has the potential to enable a rapid, accurate point-of-care platform suitable for evaluation of platelet function, detection of dysfunctional platelets, and assay of drug effects on platelets in cancer patients.
Journal Article•DOI
Flow cytometric analysis of agonist-induced annexin V, factor Va and factor Xa binding to human platelets.
D. Dormann, J. Kardoeus, R. E. Zimmermann, Beate E. Kehrel 
01 Jan 1998-Platelets
20 Citations
The methodology might be of use for the study of platelets from patients with bleeding disorders.
Journal Article•DOI
Plasmin-induced platelet aggregation is accompanied by cleavage of aggregin and indirectly mediated by calpain
Rajinder N. Puri, Fengxin Zhou, Roberta F. Colman, Robert W. Colman 
01 Dec 1990-American Journal of Physiology-cell Physiology
21 Citations
We found that the rate of plasmin-induced aggregation of washed intact platelets and that of platelets modified by 5'-p-fluorosulfonylbenzoyladenosine (FSBA, an affinity analogue of ADP, which covalently modifies aggregin) were similar, indicating that the aggregation is independent of the ADP effect.
Open access•Book Chapter•DOI
Isolation and proteomic analysis of platelets by SELDI-TOF MS.
Sean R. Downing, Giannoula Klement 
01 Jan 2012-Methods of Molecular Biology
Thus, platelets may provide a much more biologically relevant analyte for biomarker discovery.
Open access•Journal Article•DOI
Hemostatic Function, Survival, and Membrane Glycoprotein Changes in Young versus Old Rabbit Platelets
Morris A. Blajchman, A F Senyi, Jack Hirsh, Edward Genton, James N. George 
01 Nov 1981-Journal of Clinical Investigation
99 Citations
These results demonstrate that young platelets are hemostatically more effective in vivo than old platelets.
Open access•Journal Article•DOI
Enhanced flow cytometric method for counting very low numbers of white cells in platelet products
L.J. Dumont, D.F. Dumont 
15 Dec 1996-Cytometry
30 Citations
This method has good linearity and reproducibility from 10-5,000 WBC/mL for platelets.
Journal Article•DOI
Comparison of three different preparations of platelet concentrates for growth factor enrichment
Thorsten Appel, Bernd Pötzsch, Jens Müller, Jens-Jörg von Lindern, Stefaan Bergé, Rudolf H. Reich 
01 Oct 2002-Clinical Oral Implants Research
102 Citations
The two systems for intraoperative use are similar in their effects on the platelets.
Journal Article•DOI
Production of functional platelets by differentiated embryonic stem (ES) cells in vitro
Tetsuro-Takahiro Fujimoto, Satoshi Kohata, Hidenori Suzuki, Hiroshi Miyazaki, Kingo Fujimura 
01 Dec 2003-Blood
138 Citations
These results show the potential utility of ES-derived platelets for clinical applications.
Journal Article•DOI
Hyperreactivity by an enhancement of the arachidonate pathway of platelets treated with cholesterol-rich phospholipid-dispersions.
Peter Wörner, Heinrich Patscheke 
01 May 1980-Thrombosis Research
26 Citations
The platelets treated with cholesterol-rich lipid dispersions can be used as an in vitro model for human platelets in various diseased states which are hyperre-active due to an enhanced prostaglandin synthesis.
Journal Article•DOI
Aspirin fails to inhibit platelet aggregation in sheep.
Hristos G. Spanos
01 Nov 1993-Thrombosis Research
18 Citations
This is the first report in which aspirin (ASA) has failed to inhibit aggregation of mammalian platelets.
Open access•Journal Article•DOI
Platelet dysfunction during trauma involves diverse signaling pathways and an inhibitory activity in patient-derived plasma.
Christopher C. Verni, Antonio Davila, Steve Balian, Carrie A. Sims, Scott L. Diamond 
01 Feb 2019-Journal of Trauma-injury Infection and Critical Care
40 Citations
Furthermore, the inhibitor effect of patient plasma on healthy platelets suggests that soluble plasma species may downregulate endogenous or transfused platelets during trauma.

Related Questions

Is ORS good for platelets?3 answers
Is Ragi good for platelets?5 answers
Is dates good for platelets?12 answers
Which Kiwi is best for platelets?5 answers
Which dry fruit is good for platelets?7 answers
Which tablet is best for increase platelets?7 answers

See what other people are reading

How does CRC risk factors contribute to chronic inflammation, a known mediator in carcinogenesis?
4 answers
Colorectal cancer (CRC) risk factors contribute to chronic inflammation, a well-established mediator in carcinogenesis, through various mechanisms. Chronic inflammation is a critical component in the malignant transformation of several cancers, including CRC, where it plays a significant role in tumor development and progression. The inflammatory tumor microenvironment (TME), characterized by the presence of pro-inflammatory cells, cytokines, and other mediators, fosters conditions conducive to cancer development. Specifically, chronic inflammation in CRC is driven by genetic mutations, DNA promoter methylation, and dysregulated metabolic pathways, which are influenced by lifestyle and dietary factors. Inflammatory bowel disease (IBD), including ulcerative colitis (UC), is a prime example of how chronic inflammation predisposes to CRC, with inflammation-related gene pathways dysregulated in both conditions. The chronic inflammatory state in IBD and sporadic CRC involves the upregulation of key glycolytic enzymes through the STAT3/c-Myc signaling pathway, indicating a metabolic reprogramming induced by long-term inflammatory signals. This reprogramming supports the progression from chronic inflammation to CRC. Moreover, chronic inflammation's role in carcinogenesis extends beyond the local TME to systemic effects. For instance, diet and lifestyle factors contribute to systemic inflammation, which in turn is associated with an increased risk of CRC. The production of inflammatory cytokines, chemokines, and genotoxic substances by infiltrated immune cells in the TME not only induces DNA damage and methylation but also promotes an immunosuppressive environment that facilitates tumor growth and progression. Additionally, epigenetic mechanisms, such as DNA methylation changes induced by inflammatory signals, play a crucial role in silencing genes involved in gastrointestinal homeostasis and injury response, further linking chronic inflammation to CRC. The complex interplay between chronic stress, inflammation, and CRC also highlights the systemic nature of inflammation's role in carcinogenesis, where stress-related neuropeptides and receptors regulate chronic inflammation and, consequently, CRC development. In summary, CRC risk factors contribute to chronic inflammation through genetic, metabolic, lifestyle, and systemic mechanisms, establishing a conducive environment for carcinogenesis.What endpoints for assessing pain do studies treating pain due to osteoarthritis of the knee use?
4 answers
Studies treating pain due to osteoarthritis of the knee commonly use endpoints such as total knee replacement (TKR) and composite endpoints that combine TKR with conservative thresholds of patient-reported outcomes (PROs) of pain and function. These endpoints are crucial in evaluating the effectiveness of therapies for knee osteoarthritis, as they directly capture clinical benefit and provide a reliable measure of treatment success. By utilizing these endpoints, researchers can assess the impact of interventions on pain relief and functional improvement in patients with knee osteoarthritis, ultimately aiming to enhance their quality of life and mobility. Additionally, the use of composite endpoints has been shown to reduce sample sizes required for studies, making the evaluation process more feasible and efficient.What are the effects lps has on the rat spleen analyzed with pcr?
4 answers
Lipopolysaccharide (LPS) administration in rats has been shown to have significant effects on the spleen. Studies have revealed that LPS exposure can lead to alterations in gene expression profiles related to innate and adaptive immunity in the spleen, affecting pathways associated with immune responses. Additionally, LPS-induced endotoxemia has been found to impact membrane phospholipids in the spleen, specifically altering major phospholipids and fatty acid composition, potentially leading to immune impairment. Furthermore, LPS exposure can result in the spleen serving as a reservoir of inflammatory myeloid cells that are released into the blood and brain, influencing neuroinflammation and cognitive deficits. These findings collectively highlight the intricate relationship between LPS exposure and the spleen, showcasing the diverse effects on immune responses and inflammatory processes in rats.How do Megakaryocytes perform endomtiosis and platelet production?
5 answers
Megakaryocytes undergo endomitosis, a unique process where they replicate their DNA without subsequent cell division, leading to polyploidization. This results in the formation of large, multinucleated cells with increased cytoplasmic mass, essential for platelet production. The maturation of megakaryocytes involves the development of an internal membrane system and the formation of proplatelet processes, from which platelets are shed into vascular sinusoids. These platelets are released into the bloodstream, while the remaining nuclear remnants are phagocytosed by marrow macrophages. Additionally, studies have shown that the absence of large cytoplasmic megakaryocytes, which are high-ploidy cells, can lead to increased hematopoietic stem cells and severe thrombocytopenia. Overall, the process of endomitosis and cytoplasmic maturation in megakaryocytes is crucial for efficient platelet production.What is the different between EVs derive from various cell source?
4 answers
Extracellular vesicles (EVs) derived from various cell sources exhibit differences in their composition and functions. Studies have shown that EVs carry a variety of biomolecules, including DNA, microRNAs, messenger RNA, lipids, and proteins, impacting different physiological processes in target cells. EVs from mesenchymal stromal cells (MSCs) have been highlighted for their therapeutic potential in regenerative medicine, with variations observed based on the conditioning period during isolation. Platelet-derived EVs (PEVs) are rich in diverse cargo and play a crucial role in coagulation, inflammation, and cell communication, showcasing their unique pathophysiological functions. Furthermore, EVs from MSCs of different sources have distinct functions and therapeutic effects, emphasizing the importance of understanding these variations for potential clinical applications. High-resolution analyses have revealed differences in protein and lipid composition between exosomes and microvesicles derived from different cell types, indicating unique characteristics based on their cellular origin.What is the molecular mechanism underlying the role of neutrophils in thrombus formation in atherosclerosis?
5 answers
Neutrophils play a crucial role in thrombus formation in atherosclerosis through the process of neutrophil extracellular trap (NET) formation. NETs are composed of DNA strands released by activated or dying neutrophils, decorated with various proteins, which act as solid-state reactors at the interface of blood with diseased arteries, contributing to inflammation, innate immunity, and thrombosis. These NETs can localize in atherosclerotic plaques and promote thrombus formation. Neutrophils release NETs through a process called NETosis, where DNA from nuclei or mitochondria forms a mesh-like structure that can trap pathogens but also contribute to chronic inflammatory diseases like atherosclerosis. The release of NETs by neutrophils, along with the expression of tissue factor and protein disulfide isomerase, further enhances their involvement in thrombus formation in atherosclerosis.How do the sequences of S. aureus alpha hemolysin and PVL compare?
5 answers
The sequences of Staphylococcus aureus alpha-hemolysin and Panton-Valentine leukocidin (PVL) exhibit differences in their effects on platelets and virulence. Alpha-hemolysin activates platelets initially but induces platelet alterations and apoptosis, impairing thrombus formation in systemic S. aureus infections. On the other hand, PVL is associated with severe staphylococcal pneumonia and skin infections, prolonging fever duration in bacteremic S. aureus cases without affecting clinical outcomes significantly. Additionally, variations in PVL expression were observed in different clones of S. aureus strain ATCC25923, with differences attributed to the insertion of a transposable element leading to altered gene transcription and increased PVL expression. These findings highlight the distinct mechanisms and impacts of alpha-hemolysin and PVL in S. aureus infections.Is there a change in the MDL of antithrombin？?
5 answers
Yes, there is a change in the molecular design and activity of antithrombin. MDL 28,050, a decapeptide antithrombin agent, has been developed through structural optimization of a functional domain of hirudin, a leech anticoagulant. Additionally, antithrombin can undergo conformational alterations induced by proteolysis or temperature changes, leading to the acquisition of antiangiogenic properties. This transition from an active to an inactive form is crucial, as latent antithrombin can constitute around 10% of plasma antithrombin and is affected by factors like temperature variations and conformational instability, which can impact its efficacy and lead to thromboembolic episodes. Therefore, changes in the molecular structure and function of antithrombin, including the development of new agents like MDL 28,050, play a significant role in its therapeutic potential and biological activity.Can a genetic predisposition explain why some patients develop cancer cachexia?
5 answers
A genetic predisposition may indeed play a role in the development of cancer cachexia. Studies have identified specific single nucleotide polymorphisms (SNPs) associated with weight loss and low skeletal muscle index in cancer patients. These SNPs are found in genes related to inflammation, muscle wasting, and appetite regulation, highlighting the genetic complexity underlying cachexia. Additionally, the expression profile of cachexia-inducing factors (CIFs) in tumors varies among different cancer types, potentially influencing the prevalence and severity of cachexia. Understanding the genetic basis of cachexia could lead to personalized risk assessment and targeted therapies, emphasizing the importance of genetic factors in the multifactorial syndrome of cancer cachexia.What are research articles that show aged bone marrow rejuvenation has beneficial effects for multiple organs?
5 answers
Research articles have demonstrated that rejuvenating aged bone marrow can have beneficial effects on multiple organs. Alibhai and Li's study showed that transplanting young bone marrow stem cells into aged recipients improved tissue repair responses in the heart, skeletal muscle, brain, and retina. Eroglu et al. found that photobiomodulation therapy effectively reversed aging in mouse bone marrow mesenchymal stem cells, enhancing their regenerative potential. Guo et al. highlighted that platelet-rich plasma rejuvenated aged human bone marrow stem cells, leading to improved outcomes in treating ischemic heart disease. Li et al. proposed using triboelectric stimulation to rejuvenate senescent bone marrow mesenchymal stromal cells, enhancing their proliferation and differentiation capacity. Lastly, Li et al. showed that reconstituting old mice with young bone marrow cells improved cardiac tissue regeneration, emphasizing the role of specific stem cell subsets in rejuvenating aged organs.Whole blood, facs, pma
5 answers
Whole blood samples can be utilized for flow cytometry assays involving phorbol 12-myristate 13-acetate (PMA) stimulation, as demonstrated by the successful benchmarking of lyophilized reagents for equivalent stimulation in healthy volunteers. Additionally, whole blood samples have been validated for the determination of circulating forms of prostate-specific antigen (PSA), showing stable concentrations of PSA forms immediately after venipuncture, making them suitable for point-of-care testing. Furthermore, whole blood luminol-dependent chemiluminescence has been used to detect increased reactive oxygen metabolite production in patients with bronchial hyperreactivity, indicating its potential as a systemic inflammatory marker in pulmonary inflammatory conditions. These findings collectively highlight the utility and reliability of whole blood samples in various clinical assays involving different biomarkers and stimulants.