Static normal human blood possesses a distinctive yield stress. When the yield stress is exceeded, the same blood has a stress-shear rate function under creeping flow conditions closely following Casson's model, which implies reversible aggregation of red cells in rouleaux and flow dominated by movement of rouleaux. The yield stress is essentially independent of temperature and its cube root varies linearly with hematocrit value. The dynamic rheological properties in the creeping flow range are such that the relative viscosity of blood to water is almost independent of temperature. Questions raised by these data are discussed, including red cell aggregation promoted by elements in the plasma.
A 55-year-old woman with common variable immunodeficiency and mild chronic obstructive lung disease received 3 units of plasma as immunoglobulin replacement therapy. During the administration of the final unit, her temperature rose 1°C, with no other observable symptoms. Fifteen minutes later she developed shortness of breath without nausea, vomiting, rash, or pruritus. In 30 min she lost consciousness, was breathless, and cyanotic. Resuscitative efforts failed. Autopsy failed to pinpoint a cause of death. There was no evidence of ABO or Rh incompatibility, bacterial contamination, or hemolysis. There were no neutrophil, platelet or IgA antibodies detectable in the patient or the 3 plasma donors. There were no lymphocytotoxic HLA antibodies in the patient or two of the plasma donors. The third donor had HLA-B35 lymphocytotoxic antibodies that did not agglutinate or aggregate neutrophils. The patient’s HLA type was A2, A3; B35, B40. Lymphocytotoxic crossmatches using lymphocytes of the patient were positive with plasma from the third donor but negative with the other two. An eluate prepared from post-mortem lung parenchymal tissue was cytotoxic to 7 of 8 panel lymphocytes positive for the HLA-B35 antigen but not with cells lacking B35. The implicated plasma donor was healthy with a history of 6 pregnancies. This case report illustrates the potential hazard of transfusion of plasma containing HLA antibodies.
SynopsisThe reaction product of 4-hydroxyacetanilide and 1,2-epoxy-3-phenoxypropane, when added at 19 wt % to a conventional epoxy-resin-curing agent mixture, increases the tensile strength of the cured system from 82 MPa to 123 MPa and increases the shear modulus (20°C, 1 Hz) from 970 MPa to 1560 MPa. As well as showing increased strength, the tentile-test specimens also fail in a ductile fashion, i.e., the slope of the stress-strain curve is negative a t failure, with appreciable localized deformation occurring during fracture. For notched samples (compact tension specimens), the fracture properties are strongly strain-rate-dependent. At low strain rates the additive-containing sample has a fracture energy (!?I~, critical strain energy release rate) about twice that of the additive-free control, but a t higher strain rates 91, falls to about 65% of the control value. The critical stress for crack propagation is also strain-rate-dependent and is about 50% higher than the control a t low strain rates and about 10% less than the control a t higher strain rates. Dynamic mechanical analysis and dielectric loss measurements indicate that the additive causes a decrease in the TR and a suppression of the &relaxation. Chemically, the additive accelerates the cure process but does not significantly alter the final extent of reaction of the epoxy resin. After curing, the additive is almost totally extractable by solvent indicating that it is not chemically bound to the polymer. These observations are discussed in terms of the concept of antiplasticization.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.