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Biomedical subjects

E Solomon

Publications and source records attributed to E Solomon.

At least 217 records · Page 12Linked to original sources
PubMed1979

Assignment of the human acid alpha-glucosidase gene (alphaGLU) to chromosome 17 using somatic cell hybrids.

Hybrid clones (MOGs) were made between the mouse line RAG and a primary fibroblast line from an individual of the rare alphaGLU 2 phenotype. Fifteen independent primary clones and 32 subclones were tested for the presence of human alphaGLU after separation of the human and rodent enzymes by starch gel electrophoresis. Twenty-three other human-mouse hybrids from six different crosses were analysed for the presence of human alphaGLU by exploiting a difference in the thermostability of the human and mouse enzymes. The hybrids were also analysed for up to 25 other enzymes which were used as markers for different human chromosomes. Two of the MOG hybrids were karyotyped and karyotype data were already available for a number of the other hybrids. The combined results demonstrate that alphaGLU is located on chromosome 17, and probably on 17q.

Animals↗
PubMed1979

The clinical assessment of the normal and abnormal foot during locomotion.

The clinical assessment of the weight-bearing foot during locomotion is normally based on subjective judgement rather than on quantitative measurement. Although anatomical abnormalities are often apparent at examination, the accurate assessment of an abnormality of function is more difficult to assess particularly if the abnormality is only apparent under dynamic loading conditions. The many drawbacks in previous methods proposed for the clinical assessment of gait have led to the development of a novel system which allows an immediate quantitative visualization of the magnitude and point of application of the forces applied to the plantar surface of the foot during locomotion. This paper describes the technique and presents visual data on normal locomotion, on abnormal locomotion and the changes induced into a patient's abnormal gait by corrective surgery.

Biomechanical Phenomena↗
PubMed1978

The genetic control of HLA-A and B antigens in somatic cell hybrids: requirement for beta2 microglobulin.

The lymphoblastoid cell line Daudi lacks both HLA-A and B antigens and beta2 microglobulin. Somatic cell hybrids derived from a fusion between this line and D98/AH--2 were shown to express four HLA antigens not detectable on either parent cell, A1, A10(Aw26), Bw16(Bw38, Bw17. The initial definition by direct cytotoxicity assay was confirmed by absorption of reactions against target T lymphocytes, thus avoiding problems due to contaminating Ia antibodies, and by blocking the reactions by pretreatment with a chicken anti-human beta2 microglobulin serum. That the new specificities were due to the Daudi HLA region was confirmed by the finding that interspecific hybrids between Daudi and A9L, containing a single human chromosome 6, expressed A10 and Bw17. This also defined the haplotypes of Daudi as A10(Aw26), Bw17 and A1, Bw16(Bw38). The re-expression of the Daudi HLA-A and B antigens in two independent sets of hybrids indicates that it does not carry a mutation in the HLA region. It has previously been reported that somatic cell hybrids with Daudi, which contain chromosome 15, do not express human beta2 microglobulin. These results suggest that the reason for the lack of HLA-A and B antigens on Daudi is a secondary effect due to the mutation(s) in the beta2 microglobulin gene.

Beta-Globulins↗
PubMed1977

Biosynthesis of the first component of complement by human fibroblasts.

1. Haemolytic activity corresponding to that of the first component of complement (C1) was synthesized and secreted by all nine human fibroblast cell lines examined. No activity was found in the culture media of a variety of other human cell lines. 2. The component-C1 haemolytic activity secreted by the fibroblast lines behaved in an identical manner, in most respects, with that of the component-C1 haemolytic activity of human serum. The component-C1 haemolytic activity secreted by fibroblasts, however, was less susceptible to inhibition by rabbit fragment F(ab')(2) anti-(human subcomponent C1q) than was the component-C1 haemolytic activity of human serum. 3. Biosynthesis of fibroblast component-C1 haemolytic activity was inhibited by the presence of cycloheximide and regained on its removal. 4. Incorporation of radioactivity into proteins secreted by the fibroblasts and release of component-C1 haemolytic activity by the fibroblasts both increased in a linear manner until several days after the cultures had reached a state of confluent growth. 5. Radioactivity was incorporated into subcomponents C1q, C1r and C1s, as judged by the formation of specific immunoprecipitates and by absorption with immune aggregates. 6. The immunoprecipitates formed by using antisera against subcomponents C1r and C1s were run on polyacrylamide gels in sodium dodecyl sulphate, and this provided convincing physiochemical evidence for the biosynthesis of these subcomponents de novo. 7. The results obtained with immunoprecipitates formed by using anti-(subcomponent C1q) suggest that subcomponent C1q may be synthesized and secreted by fibroblast cell lines in vitro, in a form with a higher molecular weight than that of subcomponent C1q which is isolated by conventional techniques of protein fractionation from fresh serum.

Cell Line↗
PubMed1977

Assignment of the DIA1 locus to chromosome 22.

Human/rodent hybrid cell cultures were examined for the presence of DIA1 and other marker enzymes. Many of these hybrids were also analysed for human chromosomes. Complete concordance was found only with chromosome 22.

Animals↗
PubMed1977

Immunochemical analysis of the N-acetyl hexosaminidases in human-mouse hybrids made using a double selective system.

A human-mouse hybrid, DUR 4 (Solomon et al., 1976), containing a human X/15 translocation chromosome and also chromosome 5, among other human chromosomes, was used in a double selection system to obtain hybrids of four different types: X/15+ 5+, X/15- 5+, X/15+, 5-. Standard positive and negative selection systems were used for the X chromosome, and negative selection for chromosome 5 was done with diphtheria toxin. The assignment of HEXB and presently only when both the X/15 chromosome and chromosome 5 were present. A "HEXA-like" band segregated with chromosome 15 (or X/15) but independently of chromosome 5. This component, unlike HEXA, does not contain human HEXbeta antigen.

Animals↗
PubMed1976

Human gene mapping using an X/autosome translocation.

Human fibroblasts containing a translocation between the X chromosome and chromosome 15 were fused with the 6-thioguanine-resistant mouse cell line, IR. Resulting hybrids, selected in HAT medium, retained the X/15 chromosome. Hybrids which were counterselected in 6-thioguanine lost this chromosome. The X-linked markers glucose-6-phosphate dehydrogenase (G6PD), phosphoglycerate kinase (PGK), and hypoxanthine phosphoribosyl transferase (HPRT), and the non-X-linked markers pyruvate kinase (PKM2) mannose phosphate isomerase (MPI), N-acetyl hexosaminidase A (HEXA) and beta2-microglubulin (beta2-m) all segregated in concordance with the X/15 translocation chromosome. The latter markers have been assigned to chromosome 15. Selection against the X/15 chromosome was done using antihuman beta2-m serum. Electrophoretic and immunochemical analyses of the N-acetyl hexosaminidases A and B in these hybrids were performed.

Acetylglucosaminidase↗