PubMed · 7157140
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R Castillo, F J Casals, S Maragall, J Rodés, A Ordinas. 1982. [Changes in platelet function in liver diseases].. https://pubmed.ncbi.nlm.nih.gov/7157140/
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Phospholipid (PL) scramblase is a plasma membrane protein that mediates accelerated transbilayer migration of PLs upon binding Ca2+, facilitating rapid mobilization of phosphatidylserine to the cell surface upon elevation of internal Ca2+. In patients with Scott syndrome, a congenital bleeding disorder related to defective expression of membrane coagulant activity, circulating blood cells show decreased cell surface exposure of phosphatidylserine at elevated cytosolic [Ca2+], implying an underlying defect or deficiency of PL scramblase. To gain insight into the molecular basis of this disorder, we compared PL scramblase in Scott erythrocyte membranes to those of normal controls. Whereas membranes of Scott cells were unresponsive to Ca2+-induced activation of PL scramblase at neutral pH, apparently normal PL scramblase activity was induced at pH < 6.0. After extraction with octylglucoside, a membrane protein was isolated from the Scott cells which exhibited normal PL scramblase activity when reconstituted in vesicles with exogenous PLs. Like PL scramblase from normal erythrocytes, PL scramblase from Scott erythrocytes was maximally activated either by addition of Ca2+ (at pH 7.4) or by acidification to pH < 6.0, and similar apparent affinities for Ca2+ and rates of transbilayer transfer of PLs were observed. This suggests that the defect in Scott syndrome is related to an altered interaction of Ca2+ with PL scramblase on the endofacial surface of the cell membrane, due either to an intrinsic constraint upon the protein preventing interaction with Ca2+ in situ, or due to an unidentified inhibitor or cofactor in the Scott cell that is dissociated by detergent.
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In order to develop decentralized anticoagulant care by off-site blood sampling and transport of samples to a centralized laboratory for International Normalized Ratio (INR) determination we have performed a direct comparative study of INR stability. Analysis was performed daily for 5 d using nine thromboplastins. The overall mean difference of INR after 3d was only 0.05 INR units for samples with a therapeutic INR. After 5 d there was a mean difference of 0.11 INR units with 'non-Manchester' reagents and 0.44 INR units with 'Manchester' reagents. With over-anticoagulated samples mean differences of 0.55-0.72 INR units were observed after 3 d and 1.16-2.46 INR units after 5 d. Although there was some variation in stability of results with different thromboplastins, the difference over time with each thromboplastin was much less than the difference between thromboplastins. In conclusion, there is no clinically significant change in INR when analysis is delayed for up to 3 d. Off-site blood sampling can accommodate a large increase in patient workload without a major revenue increase in primary care and with continued total quality management and central expert advice.