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Biomedical subjects

G Csaba

Publications and source records attributed to G Csaba.

At least 307 records · Page 17Linked to original sources
PubMed1986

Studies into disturbing receptor 'memory' in a unicellular (Tetrahymena) model system: changes in the imprinting potential on exposure to combinations of related and unrelated hormones.

Signal molecules (hormones) can induce a hormonal imprinting in the unicellular Tetrahymena, as judged from an increase in binding capacity on reexposure in the subsequent generations. Structurally unrelated polypeptide hormones (insulin, FSH) neutralize each other's effect, whereas related hormones (TSH-FSH) may amplify or depress it. The non-signal polypeptide molecule BSA prevents hormonal imprinting on combined exposure. The glucocorticoid hormone enhances binding capacity for insulin (as in mammals) and increases its imprinting potential, whereas on TSH and FSH it has no similar effects. The amino acid hormone serotonin increases the binding capacity for TSH and FSH in non-pretreated cells, but depresses rather than stimulates the imprinting potential of these hormones, measured in the case of the second encounter.

Animals↗
PubMed1986

Influence of interference with the cyclic AMP-adenylcyclase-phosphodiesterase system on TSH-induced hormonal imprinting in the Tetrahymena.

Primary interaction of TSH with the unicellular Tetrahymena accounted for an increase in TSH binding capacity on reexposure, i.e. for a regular hormonal imprinting. TSH in itself did not give rise to a faulty imprinting (for insulin). Combination of TSH with dibutyryl cAMP reduced the intensity of imprinting, whereas theophylline or lithium ions not only reduced the efficacy of normal imprinting, but also gave rise to faulty imprinting (for insulin instead of TSH).

Adenylyl Cyclases↗
PubMed1986

Age of the cell culture: a factor influencing hormonal imprinting of Tetrahymena.

Insulin imprinting of Tetrahymena pyriformis in different growth phases had been investigated. Cells formed in the early logarithmic phase (18-hour culture) showed enhanced hormone binding at the second encounter with the hormone proving that imprinting had developed. This phenomenon was not observed in cells formed in the late logarithmic phase (42-hour culture) or in the stationary phase (66-hour culture). Lipid transformation processes, alteration of the guanyl cyclase activity and enhanced cell division may be responsible for this effect. Cell-growth phase G1 was especially favourable for development of imprinting.

Animals↗
PubMed1986

Can neonatal treatment with a related hormone adapt the receptor for itself?

Treatment of rats with endotoxin immediately after birth caused destruction of the cell membrane, resulting in depression of the thyroxin level and of the response to thyrotropin in adulthood. The thyroid gland of the rats treated neonatally with endotoxin failed to differentiate TSH from gonadotropin. Neonatal treatment (imprinting) with thyrotropin or gonadotropin after preexposure to the endotoxin improved the adult response to the exogenous hormone presented for imprinting after endotoxin. It appears that during the reconstruction stage following upon membrane perturbation in the critical period of receptor maturation, the adequate hormone or a related molecule can equally adapt the receptor for itself, but neither can fully compensate the perinatal membrane injury, nor the consequent diminution of receptor activity.

Adaptation, Physiological↗
PubMed1986

Influence of neonatal steroid (diethylstilbestrol, allylestrenol) treatment on the sexual behaviour of the adult rat.

A single neonatal treatment with diethylstilbestrol (DES) or allylestrenol (AE) considerably depressed the sexual activity of male rats in adulthood. DES had a stronger depressive effect than AE. Though the adult sexual activity of intact female rats was also reduced by DES it was not influenced by AE. Ovariectomized females that had been hormone-treated before experimental mating showed reduced sexual activity under the influence of neonatal DES-treatment but increased sexual activity when treated neonatally with AE.

Allylestrenol↗
PubMed1986

Influence of deciliation and ciliary regeneration on hormonal imprinting in Tetrahymena. Observations on the 'localization' of imprinting.

Imprinting induced in Tetrahymena with insulin is not abolished by deciliation. No imprinting occurred in deciliated cells exposed to insulin at 1 or 2 h of regeneration. However, imprinting did occur if Tetrahymena was exposed to insulin after 3 h of regeneration. It appears that while presence of cilia is a prerequisite of imprinting, the pertinent information is not, or not exclusively stored in the cilia.

Animals↗
PubMed1986

Digoxin effect and imprinting in the unicellular Tetrahymena.

Treatment with digoxin increased, whereas treatment with ouabain decreased, the growth rate of Tetrahymena, but the progeny generations showed an increased mitotic rate after both treatments. A single exposure to digoxin or ouabain accounted for a more than twofold increase in the incorporation (binding) of the cardiac glycosides in the progeny generations.

Autoradiography↗
PubMed1986

Influence of the neonatal (clomiphene) inhibition of estradiol imprinting on gonadal development and gonadal and thyroid hormone production later in life.

Treatment of newborn rats with clomiphene citrate during the first 5 days of life gave rise to a marked decrease in body mass and to a still greater decrease in gonadal mass. A decrease was also observed in the testicular diameter of the males. The females showed a 43% increase in their estradiol levels over the control and an increase in the sensitivity to gonadotropins. Thyroxine level, which was also determined in view of the known gonadotropin-thyrotropin overlap, showed no change 6 weeks after pretreatment with clomiphene, while the thyroid gland responded to gonadotropin in the same manner as to thyrotropin.

Animals↗
PubMed1986

Effect of diphtheria and tetanus toxoids on the growth of, and imprinting developed in, Tetrahymena.

The growth of Tetrahymena was influenced by both diphtheria and tetanus toxoids; depression occurred at a high and stimulation at a low concentration. Pretreatment with the stimulating concentration of diphtheria toxoid caused a lasting modification of growth rate and development of imprinting that resulted in an enhanced response of the cell at reexposure to the toxoid. Tetanus toxoid failed to induce either switch over of cell function or imprinting.

Animals↗
PubMed1986

Changes of free histones in chick testicular and ovarian cells after embryonic and/or neonatal treatment with diethylstilbestrol (DES) or allyloestrenol (AE).

DES and AE when injected into the yolk sac of chick embryos on the 9th day of incubation decreased the neonatal weight of the testis and the PMB-reaction of spermatogonia whereas they increased the neonatal weight and granulosa cell PMB-reaction of the ovary. In the ovary, embryonic treatment increased the efficiency of post-hatching hormone treatments.

Age Factors↗
PubMed1986

Free histones in the cells of the rat uterus after neonatal treatment with diethylstilbestrol or allylestrenol.

Neonatal diethylstilbestrol and allylestrenol treatments resulted in a prompt release of free histones that could be demonstrated histochemically by the phosphomolybdic-acid-benzidine reaction. This effect could not be observed in the uterus of 6-10-week old rats but reappeared between 11-14 weeks in the myometrium and uterine epithelium without any repeated treatment. This may be due to the increased production of endogenous steroids. The finding suggest caution when applying steroids to pregnants and neonates.

Allylestrenol↗
PubMed1986

Late effects of embryonic allylestrenol treatment in chicken.

Allylestrenol when applied to chick embryos on the 9th day of incubation or on the 9th day of incubation and at hatching brought about a severe purulent inflammation of the oviduct at 6 weeks of age in 50% of the animals. Treatment at hatching only had no effect whatsoever. The findings suggest that allylestrenol must be applied with caution during pregnancy.

Allylestrenol↗
PubMed1986

Overlapping imprinting of thyrotropic (TSH) and gonadotropic (FSH, LH) hormones in cultures of newborn rat testicles and ovaries.

Cultured gonadal cells of male and female newborn rats increase their hormone-binding capacity after the first treatment with gonadotropin. The imprinting effect of thyrotropin, similar in structure to gonadotropin and binding to its receptors, was found more pronounced in testicular than in ovarial cells. In the latter a negative imprinting with TSH was observed. Results corroborate the view that hormone receptors are present in early stages of ontogenesis and prove the development of imprinting also in cultured target cells.

Animals↗
PubMed1986

Detection of localization and internalization of membrane DNA in the Tetrahymena by the lactoferrin--colloidal gold technique.

It is known that lactoferrin binds to DNA. In the present study a lactoferrin-gold complex bound initially to the ciliary membrane, then appeared in coated pits and intracytoplasmic vesicles. On treatment for 1 h, the gold particles could be detected near to the nucleus. The lactoferrin-gold complex neither bound to the surface, nor appeared in the cytoplasm of those cells which had been exposed to DNAse for pretreatment.

Animals↗