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Biomedical subjects

A Kaakinen

Publications and source records attributed to A Kaakinen.

14 recordsLinked to original sources
PubMed1981

HLA-B27 frequency and MLC reactions in acute anterior uveitis.

HLA-A and B antigens were determined in 37 unrelated patients with acute non-granulomatous anterior uveitis (AAU) and in 114 control subjects. HLA-B27 was identified in 31 patients with AAU (83.8%) and in 15 control subjects (13.2%). Fifteen patients (40.5%) had associated rheumatic diseases and all of them (100%) had HLA-B27. Of the 22 patients without any associated disease, 16 (72.7%) had HLA-B277. To study the HLA-D composition MLC tests were done as one-way microcultures between members of four groups consisting of 10, 10, 8, 8 patients with AAU and two or three healthy controls in each test group. No difference between patient-to-patient reactions as compared with the control reactions could be observed. The results show that AAU is very closely associated with HLA-B27 but not with any of the HLA-D antigens.

Adult↗
PubMed1977

HLA antigens in malignant melanoma.

HLA-A, -B, -C and -D typing was performed on 54 Norwegian patients with microscopically verified malignant melanoma. A slight, but non-significant increase in the frequency of HLA-B27 and LD 108 was demonstrated among the patients compared with healthy Norwegian controls.

HLA Antigens↗
PubMed1977

Stimulation of human lymphocytes by allogenic macrophages in vitro.

Macrophages were obtained from human peripheral blood by incubating mononuclear cells in plastic tissue culture flasks. After 1-14 days, the cells were used in mixed lymphocyte macrophage cultures. Macrophages could not, themselves, be stimulated to proliferation by allogenic cells, but stimulated allogenic lymphocytes. By the use of responding cells and stimulating macrophages from HLA-D homozygous individuals, the HLA-D determinants could be shown to be responsible for the stimulation of allogenic lymphocytes.

Cells, Cultured↗
PubMed1977

Hereditary angioneurotic edema (HANE): Lack of close linkage between HLA haplotypes and C1 esterase inhibitor deficiency.

The HLA haplotypes were defined in a series including 11 patients with hereditary angioneurotic edema (HANE), five symptom-free subjects with pathological laboratory findings characteristic of HANE, and their 33 healthy kinsmen. The subjects belonged to two Finnish families representing the more common form of HANE which is recognized by the immunochemically observed decrease of the inhibitor (C1-INH) blocking the esterase activity of the first complement component. No linkage between HANE and the HLA system was found.

Adolescent↗
PubMed1977

HLA antigens in malignant melanoma.

HLA-A, -B, -C, and -D typing was performed on 54 Norwegian patients with microscopically verified malignant melanoma. A slight, but nonsignificant, increase in the frequency of HLA-B27 and LD 108 was demonstrated among the patients, compared with healthy Norwegian controls.

Antigens, Neoplasm↗
PubMed1976

Typing for HLA-D determinants. comparison of typing results using homozygous stimulating cells and primed cultures.

Typing for HLA-D determinants, using primed lymphocyte typing (PLT), has been compared to the results obtained using conventional homozygous stimulating cell primary MLC tests. The HLA-Dwl, -Dw2 and -Dw3 specificities were studied. Preliminary results indicate that these two methods essentially type for the HLA-D determinants and that reproducible results can be obtained employing the PLT technique after 24 hours of incubation in the secondary cultures.

Epitopes↗
PubMed1975

Identification of five lymphocyte activating determinants in man.

Eleven putative LD-1 locus homozygous cell donors were found by MLC tests in non-consanguineous families. Lymphocytes from each of them were used as stimulating typing cells in MLC tests together with responding cells from the other homozygous cell donors and from 45 random unrelated individuals. Four of the stimulating typing cells were found to identify a determinant in non-random association with HL-A7; LD-7a, three other cells typed for a determinant non-randomly associated with HL-A8; LD-8a, and one cell seems to identify LD-W5 in non-random association with W5. Two possible additional LD-1 determinants, LD-oh and LD-om, were less well defined with two of the cells. The combined gene frequency of the five possible LD-1 determinants is approximately 0.45 among Norwegians.

Alleles↗
PubMed1975

LD antigens associated with HL-A8 and myasthenia gravis.

The finding that the SD antigen HL-A8 is associated with myasthenia gravis has raised the question as to whether or not there is also an association between some specific LD antigen and myasthenia gravis and/or HL-A8. MLC technique was used to study LD antigens in 33 myasthenic patients. The cells of a myasthenic patient who was homozygous for both HL-A and LD products were used in MLC tests as stimulators with HL-A8 bearing cells from 24 myasthenics, their 17 relatives and 16 controls and to non-HL-A8 cells from nine myasthenics and 16 controls. At least three different LD genes were found to be associated with HL-A8. One of them, called LDm' was present in 17 (63 %) of the 27 HL-A8-bearing haplotypes of myasthenics, and in nine (47 %) of the 19 HL-A8-bearing haplotypes of controls. In our study LDm was not found in the 84 haplotypes devoid of HL-A8. LDm is strongly associated with HL-A8 and through this also with myasthenia. Calculated from phenotype frequencies for HL-A8 and its association to LDm' the LDm frequencies are 9 % in the control population, 30 % in myasthenics and 48 % in young females with onset of myasthenia below 35 years. LDm had no indendent correlation with any of the clinical parameters of myasthenia gravis, even though is was found more often in HL-A8+ females with the onset of myasthenia before 35 years than in the whole myasthenic group. LDm appears to be similar to LD8a antigen.

Age Factors↗