scholarly journals IgA and IgM protein primarily drive plasma corona-induced adhesion reduction of PLGA nanoparticles in human blood flow

2017 ◽  
Vol 2 (2) ◽  
pp. 180-190 ◽  
Author(s):  
Daniel J. Sobczynski ◽  
Omolola Eniola-Adefeso
2017 ◽  
Vol 102 (2) ◽  
pp. 228-244 ◽  
Author(s):  
Kameljit K. Kalsi ◽  
Scott T. Chiesa ◽  
Steven J. Trangmar ◽  
Leena Ali ◽  
Makrand D. Lotlikar ◽  
...  

2021 ◽  
Vol 8 (2) ◽  
pp. 20218207
Author(s):  
Akram Jassim Jawad ◽  
Auda J. Braihi

A new attempt to use Polyvinylpyrrolidone (PVP) as a bio-drag reducing polymer agent for human blood flow has been studied. PVP was added at 0, 500, 750 and 1000 part per million (ppm) and mixed with human blood at room temperature for 2 minutes. Then, a cone on plate rheometer was used to investigate the effectiveness of PVP agent on blood rheological properties. The results showed significant effecting of PVP on blood fluidity characteristics, where the viscosity decreased as the PVP content increased or as a shear rate increased. For a certain shear rate, the shear stress decreased as PVP content increased. These changes will lead to increased mixing efficiency within the capillaries, increased oxygen transportation, increased tissue perfusion, modified red blood cells (RBCs) distribution, reduced pressure drop gradients, enhanced turbulent flow tendency, enhanced viscoelasticity nature of the blood and its strengthened non-Newtonian pattern. Also, the results showed that the viscosity-shear stress relationships become more linear at higher PVP concentrations. PVP addition caused no shifting in UV-absorbing positions and only moderate intensity changing. Atomic force microscopy (AFM) parameters provide other indicators about the role of PVP as a drag reduction agent for blood flow, where all of the amplitude, hybrid and special parameters decreased significantly.


Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 958-958
Author(s):  
Prithu Sundd ◽  
Maritza Ann Jimenez ◽  
Margaret F. Bennewitz ◽  
Tomasz Brzoska ◽  
Egemen Tutuncuoglu ◽  
...  

Abstract Background: Acute chest syndrome (ACS) is a type of acute lung injury and the leading cause of mortality in Sickle Cell Disease (SCD). Current treatments for ACS are primarily supportive, and there is a critical need for rescue therapies. ACS is often a sequela of acute systemic vaso-occlusive crisis and preceded by thrombocytopenia. However, the role of platelets in the pathogenesis of ACS remains largely unknown. Methods: We used our validated model of vaso-occlusive crisis in transgenic, humanized SCD mice, which is triggered by intravenous challenge with nanogram levels of the TLR4 ligand, lipopolysaccharide (LPS). Platelet-neutrophil aggregates and blood flow in the lung microcirculation was visualized in real time in vivo, using multi-photon-excitation microscopy of intact lung in live SCD mice. SCD or control human blood was perfused through microfluidic channels in vitro and neutrophil-platelet aggregation was visualized using fluorescence microscopy. Platelet derived extracellular vesicles were characterized using nanoparticle tracking and biochemical approaches. Results: We have made a novel finding that the arrest of blood flow and injury in the lung is secondary to blockade of pulmonary arterioles by platelet-neutrophil aggregates. Using in vitro microfluidic studies, we confirmed that platelet-neutrophil aggregation is higher in LPS-treated SCD patient blood compared with healthy controls, and this correlates with increased numbers of platelet-derived extracellular vesicles (EVs) that express IL-1β. Our studies also reveal that platelet-neutrophil aggregation in pulmonary arterioles of SCD mice is associated with an increase in peripheral blood levels of platelet-derived EVs containing IL-1β. Remarkably, inhibition of TLR4 or TLR4/NLRP3-inflammasome activated caspase-1, or inhibition of IL-1β signaling, attenuated release of platelet EVs and platelet-neutrophil aggregation in the lung arterioles of SCD mice in vivo and SCD human blood in vitro . Conclusions: TLR4 and NLRP3-inflammasome-mediated caspase-1 activation in platelets during vaso-occlusive crisis leads to release of IL-1β-containing EVs into the circulation. These circulating platelet EVs promote platelet-neutrophil aggregation in pulmonary arterioles, which results in arrest of blood flow in the lung, leading to ACS. Therapeutic inhibition of TLR4/NLRP3-caspase-1 signaling in platelets or IL-1β signaling is a potential therapy for ACS in SCD patients. Acknowledgments: This study was supported by 1R01HL128297-01 (P.S.) and VMI startup funds (P.S.). Disclosures No relevant conflicts of interest to declare.


Small ◽  
2020 ◽  
Vol 16 (33) ◽  
pp. 2002861 ◽  
Author(s):  
Mai N. Vu ◽  
Hannah G. Kelly ◽  
Adam K. Wheatley ◽  
Scott Peng ◽  
Emily H. Pilkington ◽  
...  

1982 ◽  
Vol 96 (1) ◽  
pp. 209-220
Author(s):  
G. M. Hughes ◽  
Y. Kikuchi ◽  
H. Watari

The blood of a carangid fish, the yellowtail (Seriola quinqueradiata) has been studied with particular reference to the deformability properties of the red blood cells. The rate at which blood flows through a Nuclepore filter containing 5 micrometers pores has been determined under the same conditions that have been used with human blood. Marked differences were found in the flow of yellowtail blood which depended on the particular way in which the blood had been sampled. Such differences seem to be due to a sensitivity of fish red blood cells to their environmental conditions. Blood flow through filters is temperature-dependent, the rate increasing with a rise in temperature. Measurements made at 37 degrees C gave values which were similar to those normally obtained for human red blood cells, in spite of their greater dimensions (10.4 × 6.8 × 3.4 micrometers), and nucleated nature. It was also found that the blood flow rate of human blood was slower than that of yellowtail blood when measured at the normal environmental temperatures (15 degrees C) for these fish.


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