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Olive Drummond

Publications and source records attributed to Olive Drummond.

5 recordsLinked to original sources
PubMed2006

The effects of leukodepletion on the generation and removal of microvesicles and prion protein in blood components.

BACKGROUND: Universal leukodepletion (LD) has been implemented in the United Kingdom to reduce the risk of transfusion-transmitted variant Creutzfeldt-Jakob disease. If LD causes microvesiculation of blood cells, however, potentially infectious membrane-associated prion could reach the final products. STUDY DESIGN AND METHODS: We have measured microvesicles (MV) derived from red cells (RBC-MV), platelets (PLT-MV), and white blood cells (WBC-MV) and cellular prion protein (PrP(c)) in blood components produced by four whole-blood, five RBC, three PLT, and two plasma LD filters and three plateletpheresis techniques. RESULTS: RBC-MV and PLT-MV were either unaltered or reduced by all processes, with PLT-MV reduced 10-fold by RBC LD and greater than 300-fold by plasma LD. WBC-MV were reduced or unchanged by RBC and PLT LD and reduced by plasma LD. Whole-blood filtration appeared to increase MVs derived from granulocytes, but the load in the final components was comparable to that in processed RBCs in additive solution. PrP(c) was reduced by whole-blood, RBC, and plasma LD and unchanged by PLT techniques. There were differences between various filters and techniques, which were generally minor compared to the overall effects. CONCLUSION: These findings suggest no detrimental effects of LD processes in terms of generation of MVs or PrP(c) release.

Blood Component Transfusion↗
PubMed2003

The effect of methylene blue photoinactivation and methylene blue removal on the quality of fresh-frozen plasma.

BACKGROUND: T: he effects of using fresh or frozen-thawed plasma, WBC reduction of plasma before freezing, and the use of two different methylene blue (MB) removal filters on the quality of MB-treated plasma were compared. STUDY DESIGN AND METHODS: In a paired study (n = 11/arm) plasma was frozen within 8 hours of collection, thawed, MB photoinactivated, and then filtered using one of two MB removal filters. Fresh plasma (n = 16) and plasma WBC reduced before freezing (n = 19) were MB inactivated. RESULTS: Freeze-thawing resulted in loss of activity of FXII and VWF of 0.06 and 0.04 units per mL, respectively, but no significant loss of activity of factors II through XI or fibrinogen. Further loss of activity occurred after MB treatment: FII (0.07 IU/mL), FV (0.11 U/mL), FVII (0.08 IU/mL), FVIII (0.28 IU/mL), F IX (0.12 IU/mL), FX (0.16 IU/mL), FXI (0.28 U/mL), FXII (0.15 U/mL), VWF antigen (0.05 IU/mL), VWF activity (0.06 U/mL), and fibrinogen (0.79 g/L). Losses due to this step were significantly (5-10%) lower in fresh plasma compared to frozen-thawed plasma. Neither MB removal filter resulted in significant loss of activity of any factor studied. CONCLUSION: MB removal, by either of the available filters, has little impact on the coagulation factor content of plasma, but freezing of plasma before MB treatment results in a small additional loss.

Blood Coagulation↗
PubMed2002

The expression of prion protein by endothelial cells: a source of the plasma form of prion protein?

The neuronal prion protein (PrPC) is also expressed within peripheral tissues including human blood. The majority of blood PrPC is found within the plasma fraction. We hypothesized that the vascular endothelium could be a source of this PrPC. Reverse transcription polymerase chain reaction demonstrated that both human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1) expressed PrPC mRNA. Flow cytometry confirmed PrPC expression on HMEC-1s and HUVECs (120900 +/- 15058 and 58327 +/- 4577 molecules PrPC/cell respectively), with no upregulation following cellular activation. Confocal immunofluorescence microscopy confirmed that HMEC-1s and HUVECs were positive for PrPC on the plasma membrane. Time-resolved dissociation-enhanced fluoroimmunoassay (DELFIA) analysis of cell culture medium demonstrated a slow constitutive release of soluble PrPC not associated with activation. In contrast to von Willebrand factor antigen, PrPC plasma levels in vivo decrease following desmopressin therapy in patients with von Willebrand disease. Measurement of PrPC plasma levels in patients with varying blood counts demonstrated no association between cell count and PrPC concentration. However, there was a higher level of PrPC in plasma from patients with end-stage renal failure. In conclusion, endothelial cells of both macrovascular and microvascular origin expressed high levels of PrPC which can be constitutively released into the cell culture medium.

Blood Cell Count↗