Deformability of red blood cells from different species studied by resistive pulse shape analysis technique

Ok, Baskurt

doi:10.1016/0006-355x(96)00014-5

Cited by 34 publications

(26 citation statements)

References 13 publications

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“…Indeed, pharmacologic agents or hemoglobin, cytoskeletal, metabolic or lipid abnormalities that impair the deformability of the RBC will give rise to the premature clearance of the cell and, potentially, anemia. Because of the crucial biological importance of RBC deformability, numerous methodologies have been devised to measure both cellular and membrane deformability [3,[26][27][28][29][30][31][32][33]. These approaches include ektacytometry, micropore transit analyses, and micropipette aspiration.…”

Section: Discussionmentioning

confidence: 99%

“…To understand the pathophysiology of disease, previous investigators have used techniques such as ektacytometry and the cell transit analyzer to measure cellular deformability [3,[26][27][28][29][30][31][32][33]. Ektacytometry measures deformability by subjecting RBC suspended in a viscous solution to rotational shear stress such that the normal cells form ellipsoids.…”

Section: Introductionmentioning

confidence: 99%

“…However, the sensitivity of this method may vary with cell size (smaller cells pass through with less resistance) and RBC concentration in suspension. The abnormally large or rigid cells, which are clinically important, would also block the micropore and be excluded from analysis [3,28,34]. Moreover, these traditional deformability assays are relatively large devices that require expensive instrumentation and are labor-intensive and time-consuming procedures that are ill-suited for rapidly screening donor blood prior to transfusion or for screening individuals (or entire villages) for the red cell abnormalities such as SCD or thalassemias.…”

Section: Introductionmentioning

confidence: 99%

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Microfluidic analysis of cellular deformability of normal and oxidatively damaged red blood cells

et al. 2013

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Microfluidic analysis of blood has potential clinical value for determining normal and abnormal erythrocyte deformability. To determine if a microfluidic device could reliably measure intra-and inter-personal variations of normal and oxidized human red blood cell (RBC), venous blood samples were collected from repeat donors over time. RBC deformability was defined by the cortical tension (pN/mm), as determined from the threshold pressure required to deform RBC through 2-2.5 lm funnel-shaped constrictions. Oxidized RBC were prepared by treatment with phenazine methosulphate (PMS; 50 mM). Analysis of the control and oxidized RBC demonstrated that the microfluidic device could clearly differentiate between normal and mildly oxidized (20.13 6 1.47 versus 27.51 6 3.64 pN/mm) RBC. In vivo murine studies further established that the PMS-mediated loss of deformability correlated with premature clearance. Deformability variation within an individual over three independent samplings (over 21 days) demonstrated minimal changes in the mean pN/mm. Moreover, inter-individual variation in mean control RBC deformability was similarly small (range: 19.37-21.40 pN/mm). In contrast, PMS-oxidized cells demonstrated a greater inter-individual range (range: 25.97-29.90 pN/mm) reflecting the differential oxidant sensitivity of an individual's RBC. Importantly, similar deformability profiles (mean and distribution width; 20.49 6 1.67 pN/mm) were obtained from whole blood via finger prick sampling. These studies demonstrated that a low cost microfluidic device could be used to reproducibly discriminate between normal and oxidized RBC. Advanced microfluidic devices could be of clinical value in analyzing populations for hemoglobinopathies or in evaluating donor RBC products post-storage to assess transfusion suitability. Am. J. Hematol. 88:682-689,

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Microfluidic analysis of cellular deformability of normal and oxidatively damaged red blood cells

et al. 2013

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“…That steeper negative slope is caused by a reduced cardiac output (CO) secondary to progressively increased peripheral resistance, the latter resulting from elevated blood viscosity. [74][75][76] Canine RBCs, although smaller than human cells, have the same area-to-volume ratio 77 and mean corpuscular hemoglobin concentration 78 and, hence, similar deformability 79,80 and internal viscosity. Therefore, hypothetical human red cell curves can be plotted on the same graph ( Figure 6 curves A and C).…”

Section: The Viscosity Paradoxmentioning

confidence: 99%

Sickle cell disease and stroke

Verduzco

Nathan

2009

Blood

167

121

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Twenty-four percent of sickle cell disease (SCD) patients have a stroke by the age of 45 years. Blood transfusions decrease stroke risk in patients deemed high risk by transcranial Doppler. However, transcranial Doppler has poor specificity, and transfusions are limited by alloimmunization and iron overload. Transfusion withdrawal may be associated with an increased rebound stroke risk. Extended blood typing decreases alloimmunization in SCD but is not universally adopted. Transfusions for thalassemia begun in early childhood are associated with lower rates of alloimmunization than are seen in SCD, suggesting immune tolerance. Optimal oxygen transport efficiency occurs at a relatively low hematocrit for SCD patients because of hyperviscosity. Consequently, exchange rather than simple transfusions are more effective in improving oxygen transport efficiency, but the former are technically more demanding and require more blood units. IntroductionSickle cell disease (SCD) is a protean disorder caused by elevations of intraerythrocyte and total blood viscosity. Hypoxiainduced gelation of hemoglobin S (HbS) deforms the erythrocyte and its membrane and causes massive cation loss as well as increased erythrocyte surface expression of adhesion molecule receptors. The concomitant lack of deformability and enhanced stickiness lead to obstructive adhesion of sickle cells to each other and to vascular endothelium. 1 The result is ischemia reperfusion injury and endothelial cell damage with leakage of von Willebrand factor, platelet clumping, cytokine release, and attraction of granulocytes, macrophages, T cells, and invariant natural killer T (iNKT) cells to areas that become both infarcted and inflamed. 2,3 The obstruction and inflammation in turn cause further hypoxia and acidosis and, consequently, further sickling, the so-called vicious cycle of SCD.Of the many severe consequences of SCD, acute stroke and chronic cerebral ischemia are among the most disabling. 4 The fragile cerebral vessels of young children are particularly vulnerable: crippling strokes may blight a child's life even before the age of 2 years. The terrible consequences of SCD-induced stroke have prompted multiple approaches to prevention of this pernicious complication.Stroke in SCD was initially noted in 1923, 5 13 years after the first description of the disease. 6 A landmark angiographic case study in 1972 demonstrated the particular vulnerability of the internal carotid artery and circle of Willis 7 with consequent formation of fragile collaterals. This can lead to Moyamoya syndrome, a characteristic finding on cerebral angiograms consisting of multiple small collateral vessels around the circle of Willis that give a "puff of smoke" appearance.In this review, we offer a brief discussion of the natural history and prevention of stroke in SCD. We first discuss secondary prevention studies because they have led to landmark trials of primary prevention strategies. The review then highlights the potential pitfalls of nonspecific imaging modalities to sc...

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“…CELL mechanical properties are a label-free biomarker indicative of cell health (1)(2)(3); for example, in cases such as malaria (1)(2)(3)(4), sickle cell anemia (5), and sepsis (6), cells stiffen with onset of disease. Also, in breast (7,8) and oral (9) cancers, changes in deformability are sufficient to differentiate between cells of varying metastatic potential.…”

Section: Introductionmentioning

confidence: 99%

High‐throughput linear optical stretcher for mechanical characterization of blood cells

et al. 2015

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This study describes a linear optical stretcher as a high-throughput mechanical property cytometer. Custom, inexpensive, and scalable optics image a linear diode bar source into a microfluidic channel, where cells are hydrodynamically focused into the optical stretcher. Upon entering the stretching region, antipodal optical forces generated by the refraction of tightly focused laser light at the cell membrane deform each cell in flow. Each cell relaxes as it flows out of the trap and is compared to the stretched state to determine deformation. The deformation response of untreated red blood cells and neutrophils were compared to chemically treated cells. Statistically significant differences were observed between normal, diamide-treated, and glutaraldehyde-treated red blood cells, as well as between normal and cytochalasin D-treated neutrophils. Based on the behavior of the pure, untreated populations of red cells and neutrophils, a mixed population of these cells was tested and the discrete populations were identified by deformability. V C 2015 International Society for Advancement of Cytometry

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Deformability of red blood cells from different species studied by resistive pulse shape analysis technique

Cited by 34 publications

References 13 publications

Microfluidic analysis of cellular deformability of normal and oxidatively damaged red blood cells

Microfluidic analysis of cellular deformability of normal and oxidatively damaged red blood cells

Sickle cell disease and stroke

High‐throughput linear optical stretcher for mechanical characterization of blood cells

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