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Biomedical subjects

E Gyódi

Publications and source records attributed to E Gyódi.

12 recordsLinked to original sources
PubMed1992

Clinical and family studies in Hungarian patients with gout.

In this study we examined 22 Hungarian male probands with gout and 105 of their first degree relatives. This was the first family study in Hungary in which the characteristics of distribution of gout and hyperuricaemia among patients with gout and their first degree relatives, as well as the possible correlation between the prevalence of the disease and MHC class I antigens was investigated. Our gout patients showed the following characteristics: (1) There was a typical onset after age 40, benign oligoarticular form of arthritis, underexcretion of uric acid, moderate hypertension without evidence of reduced renal function, and a relatively high frequency of hyperostosis. (2) The prevalence of hyperuricaemia and gout exceeded the general population level in the first degree relatives of our gout patients. (3) The distribution of MHC class I antigens among the first degree relatives of our patients with gout showed no characteristic patterns. (4) There was no correlation between HLA B27 antigens and prevalence of gout or hyperostosis in family sibling studies. (5) The high frequency of gout and hyperuricaemia, as well as the lack of characteristic HLA patterns among the first degree relatives of gout patients in our family studies, point to the possible cumulative effect of several genes and environmental factors in the etiopathogenesis of this disease.

Adult↗
PubMed1979

The natural killer activity (cytotoxicity) of lymphocytes.

The authors' own investigations into the spontaneous lymphocyte-mediated cytotoxicity (SLMC) have been reviewed and discussed in th light of literary data. It is suggested that SLMC is a resultant of complex effects contributed by antibodies present in the human serum and those attached to the surface of lymphocytes as well as by spontaneous (sui generis) functions of effector cells. The lymphocytes eliciting SLMC belong to the "O" subpopulation, bear Fc receptors and are presumably, identical with "K" lymphocytes. In animal experiments, the authors have shown that the SLMC reaction directed againt a virus-induced tumour is under polygenetic control primarily governed by gene(s0 linked to the histocompatibility region. In man, similarly as in the mouse, SLMC was found to be a genetically-controlled lymphocyte function in which gene(s) linked to the HLA-A2 B12 or the HLA-A3 B7 haplotype may play a determining role. The authors' clinical observations indicate that LSMC represents an important part of the defense mechanism against malignancies and autoimmune diseases. Estimation and follow-up of SLMC may be useful in monitoring the clinical course.

Animals↗
PubMed1978

Studies of the HLA--D determinants in the Hungarian population.

A Hungarian random population sample was tested for six well-known and two new HLA--D specificities. HLA--D antigen and gene frequencies in the studied population agree with the frequencies observed in pooled random Caucasians, only HLA--Dw3 being significantly elevated. The incidences of Dw1 and Dw4 are, however, lower while the incidences of the Dw5 and Dw6 alleles seem to be higher in our population sample without reaching statistical significance. As for the two new specificities, the IVAD-1 specificity has a low frequency, while IVAD-3 occurs quite frequently. HLA--B and HLA--D associations seem to be different in our population sample as compared to others. In spite of the high incidence of the HLA--Bw35 antigen, no HLA--D association was found. The two new HLA--D specificities did not show association with any of the established HLA--B antigens.

Epitopes↗
PubMed1977

Cytotoxic effect of anti-H-2 and anti-Ia antisera on human B and T cells.

Anti-H-2 and anti-Ia alloimmune mouse antisera were tested by the microcytotoxicity test on human peripheral blood B- and T-cell preparations. Anti-H-2 antisera react by a higher titer and/or cytotoxicity scoring grade on B cels than on T cells. Anti-Ia antisera react practically only with B cells. It was assumed that anti-H-2 antisera contain two components. One component reacts specifically with certain HLA-A- or -B-locus antigens or other closley linked gene products. The other component reacts predominantly or only with B-cell determinants; the specificity of the latter component has not yet been studied in sufficient detail.

Animals↗
PubMed1977

Cell-mediated immunity in subjects immunized with HLA antigens.

Production of cellular immune reaction in subjects immunized against HLA antigens was studied by the capillary migration inhibition test in vitro and by the skin test in vivo. The majority of the immunized subjects (10 out of 13) developed a cell-mediated immunity to the donor antigens. Production of HLA antibodies was demonstrable in a smaller proportion of the cases. The complementary nature of humoral and cellular responsiveness was borne out by the present observations. The result of the skin test performed simultaneously with the migration inhibition test correlated well with the result in vitro.

Blood Transfusion↗
PubMed1977

HLA antigens in patients with adrenocortical hyperfunction.

The HLA antigen frequencies in 100 Caucasian patients with adrenocortical hyperfunction were compared with those found in 352 healthy unrelated subjects. Fourteen antigens on the HLA--A locus, seventeen antigens on the HLA--B locus and three antigens on the HLA--C locus were determined using the standard NIH microlymphocytotoxicity test. The frequency of HLA--A1 antigen in the patient group was 49% as compared with 28% in the controls (pcorr less than 0.01). An increased frequency of HLA--B8 and HLA-BW35 antigens was also found, but the difference was not significant. Increased A1--B8 and A1--BW35 haplotype frequencies were observed. The relationship between the HLA system and various endogenous and exogenous factors eliciting hypercorticism, together with complementary family studies indicate that the HLA system may be a useful genetic marker of the disease susceptibility gene.

Adrenocortical Hyperfunction↗