Congested Corpuscles

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Science  14 Dec 2007:
Vol. 318, Issue 5857, pp. 1699
DOI: 10.1126/science.318.5857.1699a

Sickle cell disease results from a mutation in the gene encoding the β chain of hemoglobin; the mutant protein tends to polymerize, especially so in its deoxygenated form. The extended polymers (HbS) forcibly alter the elasticity of the red blood cell, changing it from a biconcave disc into the sickle shape that gives the condition its name. One outcome is a logjam of corpuscles (known as a vascular occlusion) in small blood vessels. Although there is a clear link between occlusion and the irregular shape of the sickle red blood cell, other factors are likely to influence the process as well. To test for the minimal requirements for occlusion events in the absence of inflammation or coagulation, Higgins et al. have developed a microfluidic device that allows independent control of geometry (channel size), physics (applied hydrostatic pressure), and chemistry (oxygen tension) under conditions of steady flow. The times to occlusion and resolution (de-occlusion) were measured and used to generate a phase-space representation, revealing that the capacity of blood cells to flow through capillaries was determined by the mechanical properties of the cell and by geometric and hydrodynamic factors. The device was also used to quantitate the improvement in blood flow in samples taken from a patient before and after infusion of (normal) HbA-containing erythrocytes. — SJS

Proc. Natl. Acad. Sci. U.S.A. 104, 10.1073/pnas.0707122104 (2007).

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