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Biomedical subjects

M J Hobart

Publications and source records attributed to M J Hobart.

16 recordsLinked to original sources
PubMed1992

A cleavable biotinylating agent and its use in protein electroblots.

A direct method for the synthesis of N-biotinyl penicillamine is described. It has been shown to be a convenient biotinylating agent for antibodies which have been previously coupled with SPDP. The biotinylated antibodies can be used to detect antigens on protein electroblots using 125I-labelled streptavidin and radioautography. The biotin and its attached streptavidin and radiolabel can be removed under mild conditions and the blot reprobed with a different antibody using an identical protocol.

Antibodies, Monoclonal↗
PubMed1990

C7 reference typing and nomenclature recommendations.

The results of reference typing for C7 are presented and discussed. It appears that the present literature is using consistent nomenclature except that it was not possible to distinguish between the European C7-3 allele and Japanese C7-6. Oriental populations have both a higher frequency of variants and a greater variety of variants than Caucasian populations. Some samples with complex patterns defied classification, and it is speculated that these may be from persons with duplicated C7 genes. It is recommended that no change to the present system of nomenclature be made before a more detailed molecular understanding of the system is achieved.

Complement C7↗
PubMed1988

Allotypes of mouse complement component C6 in inbred strains and some wild populations.

This collaborative work was undertaken to resolve discrepancies in reports of the number of forms of complement component C6 present in the circulation of mice from various inbred strains. Plasma C6 was analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and by isoelectric focusing (IEF), and C6 band patterns were developed by electroblotting and immunoprobing. Results of C6 allotyping of mice from 36 strains confirmed that while 20 strains (prototype strain BALB/c) possessed only one relative mass (Mr) for which typed C6A1 on IEF, the other 16 strains all possessed more than one C6 Mr form. Moreover, IEF analysis demonstrated additional polymorphic differences; among these 16 strains, 11 typed C6A1B1 like the prototype strain CBA, the AKR and RF/J strains typed C6A2B2, and the Japanese MOM strain as well as the C57BR/cdJ and C57L/J strains possessed two forms with IEF mobilities intermediate between C6A1B1 and C6A2B2. These will now be referred to as C6A3B3. Thus, a total of four different mouse C6 haplotypes have been identified. Testing C6 allotypes in a limited number of wild mice revealed that haplotypes found in inbred strains of Western or Eastern origin tend to reflect haplotypes of the wild mice from Europe or Japan, respectively.

Animals↗
PubMed1979

Linkage studies in hereditary angio-oedema.

The locus for hereditary angio-oedema must lie well outside the limits of the HLA complex. Linkage tests with 16 marker loci gave no hint of linkage. In particular, close linkage is excluded for C6, PGM1 MNSs, Gm, Rh, Km, Hp, and ABO.

Angioedema↗
PubMed1978

Combined genetic deficiency of C6 and C7 in man.

By routine screening of sera, a subject was discovered who showed a sub-total deficiency of C6 and C7. No clinical disease was associated with this deficiency which was transmitted through the subject's family as a single genetic characteristic, the C6 deficiency being associated with a silent allele at the structural locus. The propositus was found to have low quantities of an abnormal C6 which was both antigenically deficient and smaller in size than normal C6 (110,000 daltons compared with 140,000 daltons) and small quantities of apparently normal C7. It is concluded that the most likely explanation for this defect is that the subject has a structural mutation in his C6 gene which produces hyopsynthesis not only of C6 but also of the closely linked gene for C7. These findings suggest the possibility that C6 and C7 may function as a single genetic unit and that the primary transcript copied from the genome includes information for both proteins.

Aged↗
PubMed1977

C6: synthesis by the liver in vivo.

The allotype of the sixth component of complement was determined in a patient before and after liver transplantation. The C6 phenotype changed from A before transplantation to B (the donor phenotype) within 10 days of the transplant and remained wholly of the donor phenotype at 17 wk. This demonstrates that the liver is the exclusive or predominant site of C6 synthesis in vivo in man.

Blood Transfusion↗
PubMed1977

Linkage studies with C6.

The common structural variants of C6 have been used to study the linkage relations of the locus in human pedigrees. Linkage between C6 and RH, Fy, ACP1, MNSS, Jk, HLA, ABO, ESD, Hp, ADA, GPT, Gc, Pi, Gm and Km has been excluded at recombination fractions at least as great as 0-1 in the male.

Alleles↗
PubMed1976

Role of complement components on cells and in cell interactions.

The complement system, though complex, is relatively easy to study both in terms of its reaction pathways, its distribution and its genetics. There is reason to believe that the complement system is involved in cell surface events and interactions at a variety of levels and we may hope that the knowledge of the system in the blood plasma will provide relatively easy insights into the more difficult areas with cells.

Antigen-Antibody Reactions↗
PubMedDate not supplied

The genetics of the complement system.

It is suggested that the classical and alternative pathways of C3 activation and the terminal complement reaction pathway represent three replicates formed by gene duplication. It seems likely that the precursor system was what is now the alternative pathway and that its original function was a positive feedback loop for amplifying inflammatory reactions. These views are supported by physicochemical data on the complement components; by genetic data; and by similarities in the reaction patterns. Study of subjects with isolated complement component deficiencies provides information on the function of complement in vivo. It has been found that complement component deficiency is associated with bacterial infection, particularly with Neisseria; and even more so with immune complex disease. This second, rather surprising, association is likely to be the result of a requirement for complement in the catabolism of immune complexes on the one hand, and the need for an intact complement system to eliminate low virulence infectious organisms on the other.

Biological Evolution↗