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Biomedical subjects

J R Storry

Publications and source records attributed to J R Storry.

7 recordsLinked to original sources

NOR polyagglutination and Sta glycophorin in one family: relation of NOR polyagglutination to terminal alpha-galactose residues and abnormal glycolipids.

BACKGROUND: This report describes the characterization of polyagglutinable red cells (RBCs), identified in two generations of a Polish family. CASE REPORT: Untreated and modified RBCs of the proposita (TS) were tested by serologic methods, using human sera, antibodies, lectins, and inhibitors of agglutination. Moreover, glycophorins were characterized by sodium docecyl sulfate-polyacrylamide gel electrophoresis and Western blotting, and glycolipids were purified, fractionated by thin-layer chromatography, and detected with Ricinus communis agglutinin I (RCA-I, specific for galactose residues) and Griffonia simplicifolia IB4 lectin (GSL-IB4, specific for Gal alpha1-3Gal- structure). Some of the experiments were also performed on RBCs of members of TS's family. RESULTS: Polyagglutination, found in four members of TS's family, was identified as the second case of an earlier described NOR polyagglutination. The polyagglutination was decreased by treating the RBCs with alpha-galactosidase and was inhibited by a neutral glycolipid fraction from NOR+ RBCs. Detection of neutral glycolipids of TS's RBCs on the thin-layer plate by RCA-I and GSL-IB4 revealed the presence of components that were not detectable in control RBCs. Moreover, Western blotting of RBC membranes from five family members with glycophorin monoclonal antibodies and agglutination assays with anti-St(a) and anti-Dantu sera identified the presence of St(a) glycophorin in four members of the family, two of whom were NOR+ and two NOR-. CONCLUSION: Our results showed that two rare features of TS's RBCs, NOR polyagglutination and St(a) glycophorin, are inherited independently, and that NOR+ RBCs contain neutral glycolipids with an abnormal oligosaccharide structure, most likely terminated with alpha-galactosyl residues.

Adult

Rh haplotypes that make e but not hrB usually make VS.

BACKGROUND AND OBJECTIVES: The Rh phenotypes hrB- and VS+ are both rare in Whites but more common in Blacks. The high-incidence antigen hrB is present on most red cells that are e+. The presence of VS on red cells is associated with an aberrant expression of e, often called eS. MATERIALS AND METHODS: Using conventional serologic methods, including a monoclonal anti-hrB-like antibody, we studied 65 e+ samples that were apparently hrB-. RESULTS: Of the 65, we found that 59 (91%) were VS+. Recent findings have indicated that in VS+ persons a change from leucine to valine occurs at amino acid 245 of the RHCE-encoded polypeptide. While this residue is predicted to lie within the red cell membrane bilayer, the change presumably affects alanine 226 (that is present when e is expressed) in such a way that eS is seen. CONCLUSIONS: Our findings suggest that the change from e to eS may result in nonexpression or marked depression of expression of hrB that is, perhaps, an epitope of e. While the molecular basis of the hrB-phenotype is not known, it is unlikely that the leucine-to-valine change at residue 245, resulting in the aberrant from of e, explains all hrB-samples. First, hrB-VS+ and hrB- VS- samples must differ. Second, some hrB- VS+ samples are C+, some are C-. Presumably diverse molecular bases are involved in hrB-phenotypes.

Black People

Characterization of antibodies produced by S-s- individuals.

BACKGROUND: Historically, classification of U- and U variant (U+var) individuals has been made by hemagglutination and adsorption and elution studies performed with polyclonal U antisera. Molecular studies and serologic tests with a potent monoclonal anti-He have shown that U+var red cells, some of which are He+, possess an altered form of glycophorin B. STUDY DESIGN AND METHODS: Seventeen sera, previously determined to contain anti-U, were tested with a panel of red cells of common and rare MNS types. RESULTS: Five sera contained anti-U only, and 12 sera contained broadly reactive antibodies with apparent, but inseparable, anti-U,He or anti-U,N,He specificities. CONCLUSION: The majority of antibodies produced by S-s-U- individuals are anti-U plus anti-glycophorin B and are analogous to the broadly reactive antibodies produced by En(a-) individuals whose red cells lack glycophorin A or have altered glycophorin A. To avoid further immunization of patients with anti-U, sera used for classification of S-s-U- donors should be selected to detect S-s- red cells that possess altered forms of glycophorin B.

Antibody Specificity

Expression and quantitative variation of the low-incidence blood group antigen He on some S-s-red cells.

BACKGROUND: Red cells devoid of glycophorin B (GPB)-borne S, s, and U antigens are classified as an S-s-U- or S-s-U variant (U+var) and can arise from deletion and nondeletion genetic backgrounds. In nondeletion forms of S-s-U-, little information is available on whether the altered GPB gene (GYPB) is expressed in red cells. STUDY DESIGN AND METHODS: Red cells classified as S-s-U- or S-s-U+var were tested with anti-U, anti-U/GPB, anti-He, and anti-N by hemagglutination. Selected samples were tested by flow cytometry, immunoblotting, and polymerase chain reaction amplification using allele-specific primers. RESULTS: He (MNS6) was found on 23 percent (20/87) of samples. These and another 21 of the 87 samples were agglutinated by an anti-U/GPB reagent; this indicated that approximately 50 percent of S-s-samples possessed GPB variants. The strength of He varied among the samples. Genomic polymerase chain reaction with allele-specific primers showed the presence of expected DNA GPB-like products encoding He. Immunoblotting showed that He was carried on a membrane component with a relative molecular mass indistinguishable from that of GPB. CONCLUSION: The finding of He on S-s- red cells provides direct evidence for the presence of an altered form of GPB in red cells previously thought to be devoid of this glycophorin. Quantitative variation in He antigen expression was observed in a subset of S-s- red cells.

Animals

Red cell alterations associated with virucidal methylene blue phototreatment.

Several red cell storage properties were evaluated following phototreatment with methylene blue (MB) under conditions that inactivated > or = 6 log10 of added vesicular stomatitis virus. Red cell 2,3 DPG levels were similar to untreated controls throughout conventional 42-day storage at 4 degrees C. Plasma hemoglobin levels were elevated approximately twofold in MB-phototreated samples, and morphology scores were 5 percent lower after 42-day storage. ATP levels declined 30 percent in phototreated samples and in a control sample containing MB and not exposed to light. Lipid peroxidation was not observed in treated or control cells, nor were differences observed in sodium dodecyl sulfate-polyacrylamide gel electrophoresis of ghost membranes derived from phototreated and control samples. Phototreated cells exhibited enhanced ion permeability; sodium and potassium levels approached equilibrium with the suspending medium within 4 to 7 days after treatment. Direct agglutination tests using rabbit anti-human IgG or rabbit anti-human serum albumin on MB-phototreated cells indicated that serum proteins had absorbed to the surface of treated red cells. Plasma depletion by washing red cells prior to phototreatment did not prevent protein binding upon subsequent addition of untreated autologous or group AB plasma. To a much smaller extent, phototreatment of plasma resulted in IgG association with untreated red cells. The addition of glutathione to red cell suspensions prevented IgG binding to phototreated red cells but did not prevent enhanced ion permeability. Taken together, these data suggest that the red cell surface is altered by virucidal MB phototreatment of vesicular stomatitis virus.

2,3-Diphosphoglycerate