scholarly journals Erratum: “Red Cell Motion and Deformation in the Microcirculation” (Journal of Biomechanical Engineering, 1978, 100, pp. 139–148)

1979 ◽  
Vol 101 (1) ◽  
pp. 52-52 ◽  
Author(s):  
S. P. Sutera
Keyword(s):  
Red Cell ◽  
Biomechanical Engineering ◽  
Cell Motion

Rheological factors in platelet — vessel wall interactions

1981 ◽  
Vol 294 (1072) ◽  
pp. 251-266 ◽  
Keyword(s):  
Vessel Wall ◽  
Thrombus Formation ◽  
Reaction Rates ◽  
Red Cell ◽  
Speed Of Response ◽  
Artificial Surfaces ◽  
Platelet Thrombus ◽  
Cell Motion ◽  
Wall Interactions ◽  
Cell Cell

Rheological aspects of platelet-vessel wall interactions involve cell-cell encounters, platelet - vessel wall encounters and platelet-thrombus interactions. The cell-cell encounters are usually caused by convection of cells in shear flows rather than by Brownian motion; this is important in aggregation and in the enhancement of the diffusion of platelets by red cell motion. Platelet - vessel wall interactions can involve transient adhesion (lasting from a fraction of a second to a few minutes) as well as more permanent adhesion. Reaction rates between platelets and walls are generally very small except on damaged vessels and some artificial surfaces. Ultrafiltration through the vessel wall affects cell-wall interactions. Rheological analyses of thrombus formation have been made and show interesting relations to experimental observations. Some experimental results have indicated that platelets are capable of reacting within a small fraction of a second. Red cells may act as mechanoreceptors for increases in shear rate and facilitate the speed of response of platelets. Surface geometrical forms such as bumps and cavities tend to prolong residence times and facilitate thrombus formation.

Red Cell Motion and Deformation in the Microcirculation

1978 ◽  
Vol 100 (3) ◽  
pp. 139-148 ◽  
Author(s):  
S. P. Sutera
Keyword(s):  
Large Scale ◽  
Plug Flow ◽  
Red Cells ◽  
Internal Diameter ◽  
Red Cell ◽  
Cell Dynamics ◽  
Small Vessels ◽  
Dimensionless Correlations ◽  
Cell Motion ◽  
The Relationship

The human microcirculation is taken to include all vessels with internal diameter less than 500 μm. In these small vessels the heterogeneous nature of the blood suspension becomes apparent in the external characteristics of the flow, which signifies that a continuum model of blood flow in this regime is inadequate. The motion and deformation of red cells in the capillaries is discussed in detail with emphasis on the relationship between red cell dynamics and apparent viscosity. Large scale hydraulic models of red cell motion in capillaries have yielded dimensionless correlations applicable to the microscopic prototypes. In the larger vessels the distribution of red cells across the vessel lumen is generally nonuniform and axial velocity profiles reveal the occurrence of partial plug flow. Red cells traveling near the vessel wall where the shear rate is highest may exhibit a transition to liquid droplike behavior.

A mathematical model for red cell motion in narrow capillary surrounded by tissue

2008 ◽  
Vol 196 (1) ◽  
pp. 193-199 ◽  
Author(s):  
Rekha Bali ◽  
Swati Mishra ◽  
Shraddhya Dubey
Keyword(s):  
Mathematical Model ◽  
Red Cell ◽  
Narrow Capillary ◽  
Cell Motion

The orientation of sickle hemoglobin fibers within fascicles

1988 ◽  
Vol 46 ◽  
pp. 400-401
Author(s):  
Christopher A. Miller ◽  
Bridget Carragher ◽  
William A. McDade ◽  
Robert Josephs
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Relative Orientation ◽  
Unit Cell ◽  
Red Cell ◽  
High Ph ◽  
Sickle Hemoglobin ◽  
Polar Crystal ◽  
Helical Configuration

Highly ordered bundles of deoxyhemoglobin S (HbS) fibers, termed fascicles, are intermediates in the high pH crystallization pathway of HbS. These fibers consist of 7 Wishner-Love double strands in a helical configuration. Since each double strand has a polarity, the odd number of double strands in the fiber imparts a net polarity to the structure. HbS crystals have a unit cell containing two double strands, one of each polarity, resulting in a net polarity of zero. Therefore a rearrangement of the double strands must occur to form a non-polar crystal from the polar fibers. To determine the role of fascicles as an intermediate in the crystallization pathway it is important to understand the relative orientation of fibers within fascicles. Furthermore, an understanding of fascicle structure may have implications for the design of potential sickling inhibitors, since it is bundles of fibers which cause the red cell distortion responsible for the vaso-occlusive complications characteristic of sickle cell anemia.

Erythrophagocytosis in the Liver in Hemolytic Anemias

1968 ◽  
Vol 26 ◽  
pp. 184-185
Author(s):  
O. T. Minick ◽  
E. Orfei ◽  
F. Volini ◽  
G. Kent
Keyword(s):  
Acid Phosphatase ◽  
Oxidative Damage ◽  
Phosphatase Activity ◽  
Kupffer Cells ◽  
Acid Phosphatase Activity ◽  
Common Type ◽  
Red Cell ◽  
Cell Fragments ◽  
Reticulo Endothelial System ◽  
Important Site

Hemolytic anemias were produced in rats by administering phenylhydrazine or anti-erythrocytic (rooster) serum, the latter having agglutinin and hemolysin titers exceeding 1:1000.Following administration of phenylhydrazine, the erythrocytes undergo oxidative damage and are removed from the circulation by the cells of the reticulo-endothelial system, predominantly by the spleen. With increasing dosage or if animals are splenectomized, the Kupffer cells become an important site of sequestration and are greatly hypertrophied. Whole red cells are the most common type engulfed; they are broken down in digestive vacuoles, as shown by the presence of acid phosphatase activity (Fig. 1). Heinz body material and membranes persist longer than native hemoglobin. With larger doses of phenylhydrazine, erythrocytes undergo intravascular fragmentation, and the particles phagocytized are now mainly red cell fragments of varying sizes (Fig. 2).

Pure red cell aplasia

2000 ◽  
Vol 111 (4) ◽  
pp. 1010-1022 ◽  
Author(s):  
Paul Fisch ◽  
Rupert Handgretinger ◽  
Hans-Eckart Schaefer
Keyword(s):  
Pure Red Cell Aplasia ◽  
Red Cell ◽  
Red Cell Aplasia
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