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Biomedical subjects

A Svejgaard

Publications and source records attributed to A Svejgaard.

At least 343 records · Page 19Linked to original sources
PubMed1975

The HL-A7 histocompatibility antigen in sarcoidosis in relation to tuberculin sensitivity.

Eighty cases of sarcoidosis have been investigated. In all except eight patients a histological verification of the diagnosis was obtained by mediastinoscopy or liver biopsy. The HL-A7 antigen was not increased in the entire group. However, in the group of patients with a negative sensitivity to tuberculin after the appearance of the disease there was a significant increase compared with controls. In the patients with a positive reaction, there was a complete absence of HL-A7. The HL-A system therefore does not seem to influence the liability to contract sarcoidosis, but once this condition has developed HL-A7 positives are more likely to lose cellular immunity to tuberculin and to reveal symptoms.

Adolescent↗
PubMed1975

HL-A antigen, gene, and haplotype frequencies in Denmark.

Between 426 and 1,967 unrelated Danes have been HL-A typed for most presently known HL-A antigens of the LA (first), FOUR (second), and AJ (third) segregant series. Antigen, gene and haplotype frequencies with delta values are given. AJ series antigens are most strongly associated with some of the FOUR series antigens, and except for one case, the linkage disequilibrium between AJ and FOUR does not seem to be influenced by the LA series; the exception concerns HL-A9, RH-315, and 12: the RH-315 determinant is significantly more frequent on HL-A9, 12 haplotypes and on other HL-A12 carrying haplotypes. The term "superhaplotype" is suggested for gene constellations such as the HL-A9, RH-315, 12 "haplotype". It is suggested that the associations between cross-reacting antigens from one series with the same antigen from another series may reflect recent evolutionary divergence of the cross-reacting antigens.

Chromosome Mapping↗
PubMed1975

Amylo-1,60glucosidase deficiency (glycogenosis type III) in the Faroe Islands.

Seven cases of glycogenosis type III (amylo-1,6-glucosidase deficiency) in two probably related families from the Faroe Islands are presented. The group of patients comprised two pairs of sibs. In a total of 78 members of the two families case histories were obtained and clinical examinations, analyses of amylo-1,6-glycosidase activity in erythrocytes and leucocytes, determinations of red cell, serum and enzyme groups as well as HL-A types were performed. In addition, all patients were subjected to studies of liver function. The distribution patients in these families supports the assumption of autosomal recessive inheritance. Heterozygotes could not be diagnosed with certainty by the methods of enzyme activity analysis employed. The incidence of glycogenosis type III with amylo-1,6-glucosidase deficiency was found to be high in the Faroe Islands.

Adolescent↗
PubMed1975

Reiter's disease and the histocompatibility antigen, HL-A 27.

HL-A27 were found in 31 of 48 patients with Reiter's disease (65%) as compared with 8% of 2 103 health controls. It is suggested that HL-A27 is closely related to the inheritance of a special immune response leading to an increased susceptibility to a special type of reactive arthritis which Reiter's disease has in common with ankylosing spondylitis and a certain type of psoriatic arthritis.

Arthritis, Infectious↗
PubMed1974

Two separate genes controlling stimulation in mixed lymphocyte reaction in man.

The genetic control of strong stimulation in the mixed lymphocyte culture reaction is determined by a separate gene (MLR-S) closely linked to the FOUR-locus of the HL-A chromosomal region. Three additional examples of siblings with recombination between FOUR-locus and MLR-S locus are presented which confirms the independent genetic control of mixed lymphocyte reaction from the control of HL-A antigens. The occurrence of two recombinant children in one family with four other children representing all possible HL-A haplotype-combinations, strongly supports the genetic mapping of the MLR-S determinants outside the HL-A chromosomal region. The experiments presented show that additional genes located within the HL-A region itself contribute with a weak stimulation of allogenic mixtures. These data are discussed in relation to the marginal stimulation of the mixed lymphocyte culture reaction which can be seen between unrelated individuals. It seems that a group of relatively histocompatible individuals can be defined by identity of the MLR-S locus but with differences on the weak MLC-determinants, and that this group for the purpose of clinical transplantation behaves as histocompatible individuals.

Adult↗