scholarly journals Microfluidic Immiscible Phase Filtration System for the Isolation of Small Numbers of Cells from Whole Blood

2019 ◽  
Vol 95 (8) ◽  
pp. 885-897
Author(s):  
Ileana Pirozzi ◽  
Adam Snider ◽  
Morey Kraus ◽  
E. Ralf Schönbrunner ◽  
Anubhav Tripathi
2000 ◽  
Vol 46 (6) ◽  
pp. 521-531 ◽  
Author(s):  
Mitsuaki Akino ◽  
Sadamitsu Yamamoto ◽  
Satoshi Saikawa ◽  
Masako Satoh ◽  
Kimiko Segawa ◽  
...  

2016 ◽  
Vol 115 (02) ◽  
pp. 333-343 ◽  
Author(s):  
Stefania Momi ◽  
Philip G. de Groot ◽  
Monica Battiston ◽  
Luigi de Marco ◽  
Emanuela Falcinelli ◽  
...  

SummaryPlatelets contain and release matrix metalloproteinase-2 (MMP-2) that in turn potentiates platelet aggregation. Platelet deposition on a damaged vascular wall is the first, crucial, step leading to thrombosis. Little is known about the effects of MMP-2 on platelet activation and adhesion under flow conditions. We studied the effect of MMP-2 on shear-dependent platelet activation using the O’Brien filtration system, and on platelet deposition using a parallel-plate perfusion chamber. Preincubation of human whole blood with active MMP-2 (50 ng/ml, i. e. 0.78 nM) shortened filter closure time (from 51.8 ± 3.6 sec to 40 ± 2.7 sec, p< 0.05) and increased retained platelets (from 72.3 ± 2.3 % to 81.1 ± 1.8 %, p< 0.05) in the O’Brien system, an effect prevented by a specific MMP-2 inhibitor. High shear stress induced the release of MMP-2 from platelets, while TIMP-2 levels were not significantly reduced, therefore, the MMP-2/TIMP-2 ratio increased significantly showing enhanced MMP-2 activity. Preincubation of whole blood with active MMP-2 (0.5 to 50 ng/ml, i.e 0.0078 to 0.78 nM) increased dose-dependently human platelet deposition on collagen under high shear-rate flow conditions (3000 sec-1) (maximum +47.0 ± 11.9 %, p< 0.05, with 50 ng/ml), while pre-incubation with a MMP-2 inhibitor reduced platelet deposition. In real-time microscopy studies, increased deposition of platelets on collagen induced by MMP-2 started 85 sec from the beginning of perfusion, and was abolished by a GPIIb/IIIa antagonist, while MMP-2 had no effect on platelet deposition on fibrinogen or VWF. Confocal microscopy showed that MMP-2 enhances thrombus volume (+20.0 ± 3.0 % vs control) rather than adhesion. In conclusion, we show that MMP-2 potentiates shear-induced platelet activation by enhancing thrombus formation.Supplementary Material to this article is available online at www.thrombosis-online.com.


Transfusion ◽  
2010 ◽  
Vol 50 (10) ◽  
pp. 2145-2151 ◽  
Author(s):  
Edward L. Snyder ◽  
Pamela Whitley ◽  
Tracy Kingsbury ◽  
Jeffrey Miripol ◽  
Christopher A. Tormey

The Analyst ◽  
2019 ◽  
Vol 144 (14) ◽  
pp. 4162-4174 ◽  
Author(s):  
Fei Hu ◽  
Juan Li ◽  
Niancai Peng ◽  
Zheng Li ◽  
Zengming Zhang ◽  
...  

The C-IFAST device enabled the rapid isolation of cfDNA, from 4 ml whole blood to 50 μl elution, within 15 min.


Vox Sanguinis ◽  
2005 ◽  
Vol 89 (2) ◽  
pp. 81-85 ◽  
Author(s):  
V. S. Hornsey ◽  
K. McColl ◽  
O. Drummond ◽  
C. V. Prowse

Author(s):  
W. H. Zucker ◽  
R. G. Mason

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.


Author(s):  
E. T. O'Toole ◽  
R. R. Hantgan ◽  
J. C. Lewis

Thrombocytes (TC), the avian equivalent of blood platelets, support hemostasis by aggregating at sites of injury. Studies in our lab suggested that fibrinogen (fib) is a requisite cofactor for TC aggregation but operates by an undefined mechanism. To study the interaction of fib with TC and to identify fib receptors on cells, fib was purified from pigeon plasma, conjugated to colloidal gold and used both to facilitate aggregation and as a receptor probe. Described is the application of computer assisted reconstruction and stereo whole mount microscopy to visualize the 3-D organization of fib receptors at sites of cell contact in TC aggregates and on adherent cells.Pigeon TC were obtained from citrated whole blood by differential centrifugation, washed with Ca++ free Hank's balanced salts containing 0.3% EDTA (pH 6.5) and resuspended in Ca++ free Hank's. Pigeon fib was isolated by precipitation with PEG-1000 and the purity assessed by SDS-PAGE. Fib was conjugated to 25nm colloidal gold by vortexing and the conjugates used as the ligand to identify fib receptors.


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