scholarly journals A shear gradient-activated microfluidic device for automated monitoring of whole blood haemostasis and platelet function

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Abhishek Jain ◽  
Amanda Graveline ◽  
Anna Waterhouse ◽  
Andyna Vernet ◽  
Robert Flaumenhaft ◽  
...  
2007 ◽  
Vol 98 (12) ◽  
pp. 1266-1275 ◽  
Author(s):  
Ruben Xavier ◽  
Ann White ◽  
Susan Fox ◽  
Robert Wilcox ◽  
Stan Heptinstall

SummaryThe effects on platelet function of temperatures attained during hypothermia used in cardiac surgery are controversial. Here we have performed studies on platelet aggregation in whole blood and platelet-rich plasma after stimulation with a range of concentrations of ADP, TRAP, U46619 and PAF at both 28°C and 37°C. Spontaneous aggregation was also measured after addition of saline alone. In citrated blood, spontaneous aggregation was markedly enhanced at 28°C compared with 37°C. Aggregation induced by ADP was also enhanced. Similar results were obtained in hirudinised blood. There was no spontaneous aggregation in PRP but ADP-induced aggregation was enhanced at 28°C. The P2Y12 antagonist AR-C69931 inhibited all spontaneous aggregation at 28°C and reduced all ADP-induced aggregation responses to small, reversible responses. Aspirin had no effect. Aggregation was also enhanced at 28°C compared with 37°C with low but not high concentrations of TRAP and U46619. PAF-induced aggregation was maximal at all concentrations when measured at 28°C, but reversal of aggregation was seen at 37°C. Baseline levels of platelet CD62P and CD63 were significantly enhanced at 28°C compared with 37°C. Expression was significantly increased at 28°C after stimulation with ADP, PAF and TRAP but not after stimulation with U46619. Overall, our results demonstrate an enhancement of platelet function at 28°C compared with 37°C, particularly in the presence of ADP.


Lab on a Chip ◽  
2019 ◽  
Vol 19 (20) ◽  
pp. 3427-3437 ◽  
Author(s):  
Chia-Heng Chu ◽  
Ruxiu Liu ◽  
Tevhide Ozkaya-Ahmadov ◽  
Mert Boya ◽  
Brandi E. Swain ◽  
...  

A monolithic 3D-printed microfluidic device integrated with stacked layers of functionalized leukodepletion channels and microfiltration for the negative enrichment of circulating tumor cells directly from clinically relevant volumes of whole blood.


2019 ◽  
Vol 11 (15) ◽  
pp. 2057-2063 ◽  
Author(s):  
Syrena C. Fernandes ◽  
Keith R. Baillargeon ◽  
Charles R. Mace

We demonstrate device design considerations that enable the scaling of a paper-based microfluidic device to measure the hematocrit of whole blood using only 10 μL of sample.


Nanoscale ◽  
2020 ◽  
Vol 12 (42) ◽  
pp. 21788-21797
Author(s):  
Tharagan Kumar ◽  
Ruben R. G. Soares ◽  
Leyla Ali Dholey ◽  
Harisha Ramachandraiah ◽  
Negar Abbasi Aval ◽  
...  

A microfluidic device modified with a layer-by-layer assembly of cellulose nanofibrils allows efficient capture and enzymatic release of tumor cells.


Lab on a Chip ◽  
2015 ◽  
Vol 15 (6) ◽  
pp. 1533-1544 ◽  
Author(s):  
John Nguyen ◽  
Yuan Wei ◽  
Yi Zheng ◽  
Chen Wang ◽  
Yu Sun

We present a monolithic microfluidic device capable of on-chip sample preparation for both RBC and WBC measurements from whole blood.


1990 ◽  
Vol 4 ◽  
pp. 103
Author(s):  
L. Badreddine ◽  
E. Pellissier ◽  
S. Castel ◽  
S. Bourezak ◽  
F. Meriane

Transfusion ◽  
2015 ◽  
Vol 56 (3) ◽  
pp. 596-604 ◽  
Author(s):  
Mark H. Yazer ◽  
Emily M. Glackin ◽  
Darrell J. Triulzi ◽  
Louis H. Alarcon ◽  
Alan Murdock ◽  
...  

2001 ◽  
Vol 95 (5) ◽  
pp. 1220-1225 ◽  
Author(s):  
Nicola A. Horn ◽  
Lothar de Rossi ◽  
Tilo Robitzsch ◽  
Klaus E. Hecker ◽  
Gabriele Hutschenreuter ◽  
...  

Background Previous studies have reported conflicting results about the effect of sevoflurane on platelet aggregation. To clarify this point, we investigated the effects of sevoflurane on platelet antigen expression and function in vitro. Methods Human whole blood was incubated for 1 h with 0.5 and 1 minimum alveolar concentration sevoflurane, 21% O(2), and 5% CO(2). A control sample was kept at the same conditions without sevoflurane. After stimulation with adenosine diphosphate or thrombin receptor agonist peptide 6, samples were stained with fluorochrome conjugated antibodies, and the expression of platelet glycoproteins GPIIb/IIIa, GPIb, and P-selectin, as well as activated GPIIb/IIIa, were measured with two-color flow cytometry. In addition, platelet function was assessed by means of thromboelastography and using the platelet function analyzer 100. Results Already in subanesthetic concentrations, sevoflurane inhibits unstimulated and agonist-induced GPIIb/IIIa surface expression and activated GPIIb/IIIa expression on platelets in whole blood. The agonist-induced redistribution of GPIb into the open canalicular system was also impaired by sevoflurane, whereas no effect on P-selectin expression in activated platelets could be found. Sevoflurane significantly reduced the maximum thromboelastographic amplitude. Furthermore, platelet function analyzer 100 closure times were significantly prolonged. Conclusion The results show that sevoflurane significantly impairs platelet antigen expression in vitro. It is especially the inhibition of GPIIb/IIIa expression and activation that impairs bleeding time as reflected in thromboelastographic measurements and platelet function analyzer 100 closure times. The exact inhibitory mechanism remains unclear.


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