What is the reason can be as describe margination
Answers
Answer:
Margination” refers to the movement of particles in flow toward the walls of a channel. The term was first coined in physiology for describing the behavior of white blood cells (WBCs) and platelets in blood flow.
Explanation:
hope it helps you buddy
PLEASE MARK THIS AS BRAINLIEST ANSWER
FOLLOW ME
Answer:
What causes Margination?
When the gap size between the cell surface and the wall becomes larger than the thickness of RBCs, margination is caused by overtaken or overtaking events.
Explanation:
Naturally occurring hemodynamic phenomena found in microcirculatory systems, such as Zweifach-Fung (bifurcation law), margination and plasma skimming, has been mimicked for designing microfluidic devices for blood cell separation and enrichment (Kersaudy-Kerhoas et al., 2010). RBCs tend to concentrate at the centre of a blood vessel under flow, which has two consequences: (1) plasma skimming between two asymmetrical daughter vessels reduces RBC fraction in one vessel, and (2) leukocyte margination to the vessel sidewalls as a result of RBC and leukocyte collisions. This biomimetic approach of margination was demonstrated in a microfluidic system for leukocyte enrichment from blood, resulting in a 34-fold enrichment (Shevkoplyas et al., 2005), while the use of multiple triangular expansions upstream (Fig. 8.10) mimicking postcapillary venules for nucleated cell margination from RBC gave a 45.75-fold enrichment (Jain and Munn, 2011). A recent demonstration of this technique was based on the blood condition sepsis where E. coli and S. cerevisiae, along with inflammatory cellular components, were removed from blood in a two stage single pass device at ~ 1 mL/h per channel, with realistic potential for multiplexing or parallelisation for higher throughput (Hou et al., 2012).
Sign in to download full-size image
8.10. Design of nucleated cell separation unit. (a) Schematic of the separation device. The device is made using PDMS soft lithography. (b) Illustration of working principle. Whole blood enters the device at the inlet port. Nucleated cell margination is encouraged in the pre-extraction stage of the device. With the NCs segregated near the wall, they can then be collected into the extraction channels. Pure RBCs are also collected through the central drain channel. (c) A snapshot of the extraction region of the device. Labelled NCs can be seen entering the extraction channels at top and bottom.
(Source: Reproduced from Jain and Munn, 2011, with permission of The Royal Society of Chemistry.)
Immunologic Mechanisms of Vasculitis
J. Charles Jennette, Ronald J. Falk, in Seldin and Giebisch's The Kidney (Fourth Edition), 2008
SELECTIN-MEDIATED ROLLING
The first step in the exit of leukocyte from the unimpeded flow of blood cells within vessel lumens is margination adjacent to the endothelial surface. This is characterized by leukocyte “rolling” along the endothelial surface and is mediated primarily by selectins, which have lectin-like N-terminal domains that mediate transient adhesion to their ligands so that leukocytes can resist the sheer forces of the flowing blood enough to roll along the endothelial surface but not enough to remain tethered at one spot (44). At sites of small-vessel vasculitis, increased expression of P-selectin and E-selectin on endothelial cells is induced by inflammatory mediators. This induces leukocyte rolling that allows the binding of integrins on leukocytes to counter-receptors on endothelial cells. The three categories of selectins are L-selectin, E-selectin, and P-selectin. L-selectin is constitutively expressed on all circulating leukocytes except for a minor subpopulation of lymphocytes. Synthesis and surface expression of E-selectin are induced in endothelial cells by inflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) (10). Because RNA and protein synthesis are required, expression of E-selectin is delayed for several hours after an inflammatory stimulus is received. This differs from the more rapid release of preformed P-selectin that is stored in cytoplasmic granules of both platelets and endothelial cells (Weible-Palade bodies) and is rapidly expressed at the surface of these cells by mediators released at site of acute inflammation, such as histamine and thrombin (70). The ligands (counterreceptors) for selectins are carbohydrate domains on elongated mucin-like molecules that project outward from cell surfaces. Ligation of selectins on leukocytes and endothelial cells with counterreceptors on endothelial cells and leukocytes, respectively, is transient and mediates the “rolling” of leukocytes along the endothelium in the direction of blood flow (64). The additive ligation of more than one class of selectins to ligands is required for efficient tethering of leukocytes to endothelial cells so that they can engage integrins and begin diapedesis (112). This is especially true at sites of vascular inflammation that do not involve postcapillary venules because there is less constitutive expression of adhesion molecules at these sites and often higher flow rates and thus greater sheer force.
HOPE THIS HELPS