Search PubMed⌕ Search

Biomedical subjects

I E Petrichenko

Publications and source records attributed to I E Petrichenko.

9 recordsLinked to original sources
PubMed1991

[Endocrine status changes in children with bronchial asthma].

A study was made of adrenocortical function by measuring blood plasma cortisol concentration and amount of glucocorticoid receptors in lymphocytes as well as thyroid function by measuring blood plasma triidothyronine and thyroxine concentration in 58 bronchial asthma children aged 1 to 14 years. The authors revealed alterations in the functional activity of the indicated endocrine glands depending on the intensity of bronchial patency disorders and the nature of the therapeutic measures carried out.

Adolescent↗
PubMed1991

[Regulation of intracellular cholesterol synthesis in hypercholesterolemia by glucocorticoids].

The rate of endogenous cholesterol synthesis in blood lymphocytes and skin fibroblasts from patients with type IIa hyperlipidemia was found to be increased in comparison with healthy donors. The cells of hyperlipidemic patients had lowered levels of glucocorticoid receptors concomitantly with a partial loss of their sensitivity to glucocorticoids. In fibroblasts from patients with hereditary hypercholesteremia of homozygous type the number of glucocorticoid receptors did not exceed 10% of their content in normal cells. The decrease of the number of glucocorticoid receptors in patients with type IIa hyperlipidemia seems to be a compensatory response of cells culminating in activation of endogenous cholesterol synthesis.

Acetates↗
PubMed1989

Number of glucocorticoid receptors in lymphocytes and their sensitivity to hormone action.

The study demonstrated a decreased level of glucocorticoid receptors (GR) in peripheral blood lymphocytes from hypercholesterolemic subjects, and an elevated level in patients with acute myocardial infarction. In the lymphocytes with a high GR number, dexamethasone inhibited [3H]-thymidine and [3H]-acetate incorporation into DNA and cholesterol, respectively, in the same manner as in the control cells. On the other hand, a decreased GR number resulted in a less efficient dexamethasone inhibition of the incorporation of labeled compounds. These data showed that the sensitivity of lymphocytes to glucocorticoids changed only with a decrease of GR level.

Adult↗
PubMed1989

[Reduced cell sensitivity to glucocorticoid hormones in hypercholesterolemia].

The number of 3H-dexamethasone binding sites in lymphocytes of subjects with hypercholesterolemia (HCS) was found to be decreased as compared to the receptor level in normolipidemic patients (N). In HCS-lymphocytes, the dexamethasone-induced inhibition of 3H-thymidine and 14C-acetate incorporation was less pronounced (by 20% and 22%, respectively) than in control cells, which is suggestive of the decreased sensitivity of HCS-lymphocytes to the hormone. An addition of 5-25% HCS blood sera to human skin fibroblast cultures caused a 10-50% decrease in the number of 3H-dexamethasone binding sites and diminished the Kd values 2-3 times. Lipid-depleted HCS-sera had no effect on the glucocorticoid reception in fibroblasts, whereas very low (VLDL) and low (LDL) density lipoproteins inhibited the 3H-dexamethasone binding to the cells. The most potent inhibiting effect was exerted by VLDL (both N-VLDL and HCS-VLDL). HCS-VLDL were more effective than N-LDL. HCS-HDL and N-HDL did not effect the 3H-dexamethasone binding to fibroblasts. In cells preincubated with VLDL dexamethasone inhibited the incorporation of 3H-thymidine and 14C-acetate less intensively (by 27% and 20%, respectively) than in control fibroblasts. The experimental results are suggestive of a decreased sensitivity of peripheral HCS-cells to glucocorticoids, which may shed some light on the mechanism of hypercholesterolemia realization into coronary heart disease and atherosclerosis.

Adult↗
PubMed1989

Reduced sensitivity of peripheral cells to glucocorticoids in hypercholesterolemia.

It has been found that lymphocytes of hypercholesterolemic (HCh) subjects are characterized by a reduced number of glucocorticoid receptors (GcR) as compared with the cells of normolipidemics (N). Addition of HCh-sera or very low density lipoproteins, or low density lipoproteins isolated both from HCh-sera and N-sera to cultured human skin fibroblasts brought about a fall in the number of GcR in the cells. High density lipoproteins had no effect on GcR level. Dexamethasone was less effective in inhibiting cholesterol synthesis from [14C]acetate in the lymphocytes and fibroblasts with a reduced number of GcR. In the presence of dexamethasone (I x 10(-8)M) in fibroblast growth medium, reduced number of GcR (due to preincubation with very low density lipoproteins) led to a substantial increase in cholesterol synthesis. These findings indicate that the sensitivity of peripheral cells to glucocorticoids is decreased in HCh which might be one of the trigger mechanisms of atherogenesis.

Cells, Cultured↗
PubMed1986

[Changes in the characteristics of glucocorticoid hormone binding in human peripheral blood lymphocytes during myocardial infarct].

Competitive binding was used to determine the number of binding sites to glucocorticoid hormones in peripheral blood leukocytes of normal subjects, patients with unstable angina pectoris and patients with myocardial infarction. A sharp (2-3-fold) increase in the number of binding sites was observed in patients with myocardial infarction during the first 24 hours after the onset of the disease.

Adult↗
PubMedDate not supplied

[Mechanism of activating the lymphocyte glucocorticoid receptor in acute myocardial infarct].

Dose-dependent increase in content of highly specific binding sites for glucocorticoids (receptors), but without alteration in their affinity to the hormone, was observed after incubation during 2 hrs of healthy donor lymphocytes with blood serum of patients with acute myocardial infarction. The similar effects exhibited protein extracts of necrotized and normal parts of human myocardium (heart antigens) as well as the autologous blood serum and human blood serum albumin treated with UV-irradiation. Number of receptors was not altered in human skin fibroblasts incubated both with the patients blood serum and with the UV-treated blood serum. Antigenic effects of protein components, developed in blood serum after acute myocardial infarction, on cells of the lymphoid system appear to be responsible for the increase in number of binding sites for glucocorticoids in lymphocytes of patients with acute myocardial infarction or in lymphocytes of healthy donors incubated with the patients blood serum.

Adult↗