Core and shell platelets of a thrombus: A new microfluidic assay to study mechanics and biochemistry
Research and Practice in Thrombosis and Haemostasis, ISSN: 2475-0379, Vol: 4, Issue: 7, Page: 1158-1166
2020
- 12Citations
- 37Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef8
- Captures37
- Readers37
- 37
Article Description
Hemostatic clots have a P‐selectin positive platelet core covered with a shell of P‐selectin negative platelets. To develop a new human blood microfluidic assay to interrogate core/shell mechanics. A 2‐stage assay perfused whole blood over collagen/± tissue factor (TF) for 180 seconds at 100 s −1 wall shear rate, followed by buffer perfusion at either 100 s −1 (venous) or 1000 s −1 (arterial). This microfluidic assay used an extended channel height (120 µm), allowing buffer perfusion well before occlusion. Clot growth on collagen stopped immediately with buffer exchange, revealing ~10% reduction in platelet fluorescence intensity (at 100 s −1 ) and ~30% (at 1000 s −1 ) by 1200 seconds. Thrombin generation (on collagen/TF) reduced erosion at either buffer flow rate. P‐selectin–positive platelets were stable (no erosion) against 1000 s −1, in contrast to P‐selectin negative platelets. Thrombin inhibition (with D‐Phe‐Pro‐Arg‐CMK) reduced the number of P‐selectin‐positive platelets and lowered thrombus stability through the reduction of P‐selectin–positive platelets. Interestingly, fibrin inhibition (with H‐Gly‐Pro‐Arg‐Pro‐OH acetate salt) increased the number of P‐selectin–positive platelets but did not lower stability, suggesting that fibrin was only in the core region. Thromboxane inhibition reduced P‐selectin–positive platelets and caused a nearly 60% reduction of the clot at arterial buffer flow. P2Y1 antagonism reduced clot size and the number of P‐selectin–positive platelets and reduced the stability of P‐selectin–negative platelets. The 2‐stage assay (extended channel height plus buffer exchange) interrogated platelet stability using human blood. Under all conditions, P‐selectin–positive platelets never left the clot.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2475037922020799; http://dx.doi.org/10.1002/rth2.12405; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85106541441&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/33134782; https://linkinghub.elsevier.com/retrieve/pii/S2475037922020799; https://dx.doi.org/10.1002/rth2.12405
Elsevier BV
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