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O M Efremov

Publications and source records attributed to O M Efremov.

At least 19 recordsLinked to original sources
PubMed2006

[Effect of vilon on neuroendocrine status and sexual function of old male rats].

The hypogonadal status of hemigonadectomised male rats has been choseh as a model of age-related sexual function decline in animals. The effect of dipeptide Vilon on parameters of sexual function and neuroendocrine status was studied. The results showed that regular introduction of Vilon in a dose of 50 microg per rat activates sexual function in old male rats. The obtained data confirm that Vilon significantly affects neuroendocrine status of animals, as well as the level of LH, prolactin and ACTH and changes the content of neurotransmitters in hypothalamus. We consider the changes in sexual function caused by Vilon not relate to change in one parameter only, but are mediated by a set of neuroendocrine and neuromediatorial factors. Significant decrease in prolactin content in blood is worthy of notice, as age-related hypersecretion of this hormone is one of the main factors leading to age-related sexual function decline.

Adrenocorticotropic Hormone↗
PubMed2001

[Interleukin-1beta and depressive states].

Administration of Interleukin-1 beta (IL-1 beta) in pyrogenic and subpyrogenic doses induced a depression of social and exploratory behaviour in rats. A reduction in locomotor activity only occurred with pyrogenic doses of the IL-1 beta. The low dose induced the reduction whereas the high dose the increase of anxiety in elevated plus maze. The opposite effects of two doses of IL-1 beta were observed also in a test with saccharine.

Animals↗
PubMed1994

Pyrogenic activity of human native and human recombinant interleukins-1 beta: stabilization with albumin enhances the pyrogenic action of recombinant IL-1 beta delivered into the rabbit brain.

The pyrogenic potential of natural and recombinant human IL-1 beta in rabbits was found to be very similar when the substances were given intravenously. Under these conditions, stabilization of rIL-1 beta with human serum albumin (HSA) failed to affect the pyrogenic activity of recombinant IL-1 beta. When the two preparations were administered directly into the PO/AH area of the brain, recombinant IL-1 beta was less pyrogenic than its natural counterpart. This lower pyrogenicity of recombinant IL-1 beta was corrected if the injected material contained HSA, which is known to stabilize in vitro the biological activities of IL-1 beta against slow degradation. The possibility is now considered that the central and peripheral systems for IL-1 inactivation are different. The existence of an intrabrain IL-1 pool is suggested and its significance for neuroimmunomodulation is stressed.

Animals↗
PubMed1993

[The pyrogenic activity of native and recombinant human interleukin-1 beta].

Comparative doses (100-180 ng/kg) of highly purified human native interleukin-1 beta (nIL-1 beta) and human recombinant IL-1 beta (rIL-1 beta) intravenously injected were found to cause similar changes in body temperature in rabbits. Under these conditions, stabilization of rIL-1 beta by human serum albumin (HSA) fails to affect rIL-1 beta pyrogenic activity. nIL-1 beta, 0.05-2.0 ng, injected into the PO/AH region of the brain causes dose-dependent fever in the animals. With intrahypothalamic nIL-1 beta (versus i.v. injection), the pyrogenic activity of rIl-1 beta is much lower than that of nIL-1 beta. Moreover, pyrogenicity appears to be dependent on the type of rIL-1 beta, namely on free or stabilized by HSA. The former has about 100-fold and the latter a 25-fold lower activity than the native cytokine (in terms of a dose-pyrogenic effect relationship). The findings are discussed in the light of the existence of various interleukin IL-1 beta pools.

Animals↗
PubMed1991

Fever produced by intrahypothalamic injection of interleukin-1 and interleukin-6.

Pure human interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6), both of natural origin, were found to cause fever in rabbits when injected into the PO/AH region of the brain. The threshold dose required for this effect was between 0.4 and 4 U, equivalent to 0.04 to 0.4 ng for IL-1 beta, and around 50 U, equivalent to 0.05 ng for IL-6. From this it was estimated that this area of the brain responds to a local concentration of approximately 1 ng/ml of these cytokines, a level which can easily be reached after intravenous administration of threshold pyrogenic doses of either cytokine. The observation supports the view that fever induced by systemic endogenous production of IL-1 and IL-6 is due to a direct effect on the thermoregulatory center and may not require production of mediators, such as prostaglandins, at sites distant from the center.

Animals↗
PubMed1981

[Role of cAMP in the mechanism of the fever reaction].

It has been shown that accumulation of endogenous cAMP caused by theophylline increases the body sensitivity to the minimum doses of leukocytic and bacterial pyrogens and to prostaglandin E1. The increasing effect of theophylline was abolished by administering the higher doses of the pyrogenic agents. Repeated daily administration of bacterial pyrogen in conjunction with theophylline does not induce the development of tolerance. The possible reasons for enhanced fever in response to the minimum doses of the pyrogenic agents during accumulation of endogenous cAMP are discussed.

Animals↗
PubMed1980

[Conditions favoring production and mechanism of action of macrophage pyrogen].

Activation of mononuclear phagocytes by staphylococci in vitro results in the production of endogenous pyrogen. Macrophage pyrogen does not posses species pyrogenic specificity. Intracisternal injection increases pyrogen susceptibility more than 100-fold as compared to intravenous injection. Still more abrupt increase in pyrogen susceptibility was observed in the animals in the presence of elevated body cAMP concentration induced by theophylline preinjection.

Animals↗
PubMed1978

[Endogenous pyrogen formation by bone marrow cells].

The cells of the rabbit bone marrow produced endogenous pyrogen in response to stimulation with bacterial lipopolysaccharide. Incubation of the cells in medium No 199 containing a 15% homologous serum is optimal for the release of pyrogen. It is supposed that the cells of the bone marrow take part in the formation of endgenous pyrogen and in the mechanism of pyrexia in the organism.

Animals↗
PubMed1976

[Effect of cytostatic drugs on fever development following administration of bacterial pyrogen].

A study was made of the development of pyretic reaction to the administration of a bacterial lipopolysaccharide (pyrogenal) after preliminary treatment of rabbits with actinomycin D and cortisone. Such treatment failed to change the reactivity of thermoregulating centres to the endogenous pyrogen. Intravenous injection of bacterial pyrogen was followed by marked shortening of pyretic reaction; the reaction was markedly inhibited in response to its intracysternal administration. An important role played by polymorphonuclear leukocytes in the formation of endogenous pyrogens in the mechanism of pyrexia induced by bacterial pyrogens was shown in this work.

Animals↗
PubMedDate not supplied

[Effect of some imidazole-4,5-dicarboxylic acid derivatives on the activity of N-methyl-D-aspartate (NMDA) receptors].

The results of experiments on mice showed that some imidazole-4,5-dicarboxylic acid derivatives injected into lateral cerebral ventricles produce a dose-dependent convulsant or anticonvulsant effects, that is, possess the properties of partial NMDA receptor agonists. The most promising partial NMDA receptor agonist selected for further investigation is 2-propylimidazole-4,5-dicarboxylic acid.

Animals↗