E.R. Giblett

Enolase: human tissue distribution and evidence for three different loci.

Four different cellogel electrophoretic patterns of enolase were found in human tissue extracts. They consisted cf:

Phenotyping human leukemic T-Cell lines: Enzyme markers; surface antigens, and cytogenetics

We have compared phenotypic markers for a series of established human leukemic T-cell lines collected from different laboratories. Cell lines were tested first for genetic markers using polymorphic enzymes and then for expression of T lymphoid cell surface differentiation antigens using monoclonal antibodies. Chromosomal analysis was used as an additional method for identification of selected cell lines. On the basis of enzyme markers, it was possible to assign each of the cell lines examined to one of nine different groups. With two exceptions, surface antigen phenotypes for each of 12 cell lines were clearly distinctive. Thus, some groups of cell lines indistinguishable by enzyme markers could be further subdivided by surface antigen phenotyping. However, significant quantitative variation in expression of individual antigens was observed. In addition, surface antigen expression was not uniform in different subcultures of one cell line studied in detail. These results indicate that leukemic T-cell lines cannot be used generally as simple models of surface antigen expression in normal T-cell differentiation.

The position of the Radin blood group locus in relation to other chromosome 1 loci

Data are presented which indicate that the Radin blood group antigen is governed by a locus, for the present called Rd, which is located between PGM1 and αFUC Rh, and is either very closely linked to or identical with Sc.

Adenosine deaminase and nucleoside phosphorylase activity in patients with immunodeficiency syndromes.

Abstract Red cell adenosine deaminase (ADA) and nucleoside phosphorylase (NP) activities were measured in 62 patients with various immunodeficiency syndromes and in 67 adult and 37 infant controls. NP activity was found to be within the normal range (1206 ± 144 U/gHb in adults, 1266 ± 270 U/gHb in infants) in all but 4 patients who had NP deficiency and abnormal T-cell but normal B-cell function. The mean ADA activity was 36 U/gHb (with 95% confidence interval of 22.5 – 58.1 U/gHb) for normal adult controls ( n = 67) and 35 U/gHb (95% confidence interval 21.6 – 60.8 U/gHb) for infant controls ( n = 37). Red blood cell ADA activity of the patients showed great variability: Normal activity was found in patients with X-linked agammaglobulinemia, ataxia telangiectasia, and Wiskott-Aldrich syndrome. Six of 17 patients with combined immunodeficiency syndrome (CID) had ADA deficiency, and 7 CID patients had significantly elevated red cell ADA activity. Two identical twins with common-variable immunodeficiency showed red cell ADA activity of five to six times that of the normal controls; however, ADA activity of white cells and cultured skin fibroblasts was normal. Family members of these twin sisters had normal red cell ADA activity. It is not known if the elevated ADA activity observed in some patients with immune deficiency is directly related to the abnormal immune function.

Polymorphism of the sixth component of complement (C6) in the dog

Isoelectric focusing was used to identify five alleles at the locus determining the production of the sixth component of complement (C6) in the dog. Four of these alleles, C61, C62, C64,and C65,were studied in family pedigrees and shown to be inherited in a codominant autosomal fashion. All alleles except for C64occurred commonly in the multiple breeds tested.

Analysis of linkage relationships of Co, Jk and K with each other and with chromosome 2 loci ACP1 and Km.

Linkage analyses of locus pairs involving ACPI, Co, Jk, K and Km indicate: probable linkage between Co and Jk (ẑ=+3.80 at θ= 0.29); possible linkage between Jk and Km (z =+1.93 at θ= 1.30); a mild hint of linkage between Co and K 9z=+1.01 at θ= 0.30); inadequate information for Co: Km linkage for K: Jk, K: Km, ACPI: Jk, ACPI: K and ACPI: Km. The compiled information does not allow assignment of Co, Jk or K to chromosome 2.