[Compensatory adjustment of hemopoietic stem cell pool of CBA mice after acute intake of 90Sr].

It was investigated the functional status of stem cell pool (CFUs) of bone marrow, spleen and peripheral blood in mice (CBA) in early (1-30 days) and late (180-360 days) period after acute intake of 90Sr (29.6 kBq/g). Cumulative dose in red bone marrow due to incorporated 90Sr was 0.98-87.7 Gy. The kinetics, proliferative and differentiative potential of stem hemopoietic cells (CFUs) and productivity of hemopoietic tissues were significantly influenced by dose rate, absorbed dose and degree of suppresssion of bone marrow functions. The obtained results indicated that the sarcomogenous doses of 90Sr (29.6 kBq/g) resulted in realization of compensatory reactions in hemopoietic stem cell pool to support the life ability of irradiated animals: higher proliferative potential of CFUs and its repopulation, redistribution of cell subpopulations during differentiation and activation of spleens hemopoiesis.

[Physico-chemical bases of the mechanism of thermal inactivation of the foot-and-mouth disease virus]. / Fiziko-khimicheskie osnovy mekhanizma termoinaktivatsii virusa iashchura.

Experiments demonstrated that the effect of water activity on the solvate complex of virions underlies the mechanism of thermal inactivation of the foot and mouth disease virus in suspension; changes in the structure of the complex impair the electrophysical balance of the RNA-protein relations and hence, destroy the virus. Heating of virus-containing suspensions at moderate positive temperatures leads to destruction of the noninfectious part of virus population of 146S particles, thus decreasing the infectious activity of the virus.

[Mechanism of retaining stability of foot-and-mouth disease virus during manufacturing dried concentrated preparations]. / Mekhanizm sokhraneniia ustoichivosti virusa iashchura pri poluchenii sukhikh kontsentrirovannykh preparatov.

Removal of moisture from concentrated virus suspensions in a sequential manner using ultrafiltration, active ventilation and vacuum dehydration of concentrated powders enables us to obtain preparations with a residual content of moisture less than 1%, while the structure and properties of FMD virus are retained. Mechanism of inactivation of FMD virus in drying is attributed to electrophysical processes associated with development of electric potentials in evaporated objects due to directional movement of charged water molecules. Having reached certain values, outer electric potential induces charge exchange in virions that leads to the break of energy balance in the structure of virus particles and to their disruption when rehydrating in buffer solution.

[The electrophysiological properties of the structural polypeptides of the foot-and-mouth-disease virus]. / Elektrofiziologicheskie svoistva strukturnykh polipeptidov virusa iashchura.

The methodological approaches of isolation of preparations of FMDV structural polypeptides to analyse them by the electrophoresis and electro-focussing methods are presented. The value of isoelectric points of protein coat of FMDV structural polypeptides and corresponding them values of electric potential are determined. The similarity and differences of FMDV serotypes, characterized by the value of relative surface, falling on separate polypeptides, are determined for the virion structure on the basis of superposition principle. FMDV has been shown to possess the summarized negative charge of different values. The charge depends on the virus type and it is a determining condition for viruses resistance in environment. A graphical model of FMDV is suggested on the basis of systemic approach and it reflects the dipole character of electric charge distribution in virion structure and agrees with the virus model, built on the basis of icosahedron symmetry.

The functional role of the noradrenergic neurons in the thermoregulatory circuits in mice.

Intracerebroventricular (i.c.v.) treatment of mice with 6-hydroxydopamine (6-OHDA; 20--50 micrograms per mouse), which depletes brain noradrenaline (NA) and DA, completely prevents or significantly diminishes the hypothermic effect of various classes of drugs: dopaminomimetics--apomorphine (0.5--10 mg/kg), piribedil (40--100 mg/kg), bromocriptine (3 to 10 mg/kg), CM 29-712 (2--10 mg/kg), d, l-amphetamine (1--2 mg/kg), and L-DOPA (10--100 mg/kg) in combination with Ro 4-4602 (5--40 mg/kg); cholinomimetics--oxotremorine (0.04--0.05 mg/kg), arecoline (5--10 mg/kg) and pilocarpine (2--3 mg/kg); neuroleptics--chlorpromazine, promazine, perphenazine, chlorprothixene, haloperidol, fluanisone (5--10 mg/kg); central alpha-adrenoblocker aceperone (20--40 mg/kg); inhibitor of tyrosine-hydroxylase alpha-methyltyrosine (200--300 mg/kg); inhibitor of dopamine-beta-hydroxylase--disulfiram (150--250 mg/kg) and FLA-63 (15--25 mg/kg). This antihypothermic effect was demonstrated up to 3 months after administration of 6-OHDA for DA-mimetics and neuroleptics and up to 3 weeks for cholinomimetics. The hypothermic effect of presumable GABA-mimetics Phenybut (100--150 mg/kg) and Lioresal (10--25 mg/kg) was enhanced by a prior 6-OHDA treatment. Pretreatment of mice with desipramine (25 to 30 mg/kg i.p.), protriptyline (20 mg/kg) or AW 15(1)1129 (15--20 mg/kg) 20--45 min before 6-OHDA administration protects the central NA-ergic neurons from a destructive effect of 6-OHDA and partially or completely counteracts the antihypothermic as well as prohypothermic (in the case of GABA-mimetics) effect of 6-OHDA. In rats desipramine counteracted antihypothermic effect of 6-OHDA in the case of piribedil, but not of apomorphine. Intracerebroventricular treatment of mice with a low (15 microgram) dose of 5, 6-dihydroxytryptamine (5, 6-DHT) enhanced the hypothermic effects of DA-mimetics; higher doses of 5, 6-DHT (26 and 30 micrograms) and 5, 7-DHT (40 and 46 micrograms) diminished the hypothermic effects; the antihypothermic effect of 6-OHDA was stronger than that of equimolar doses of 5, 6- or 5,7-DHT; desipramine pretreatment counteracted antihypothermic effects of 5, 6-DHT and 5, 7-DHT as well as depletion of brain NA they produce. The data presented reveal the key position for NA-ergic neurons in a temperature regulation and, particularly, in effects of various drugs on body temperature in mice. The tentative fragment of the neuronal thermoregulatory circuit is proposed in attempt to account for the presented an other known data concerning drug action (and interactions) on core temperature in mice.

[Functional role of noradrenergic neurons in the hypothermic effect of apomorphine and other dopaminomimetics]. / Funktsional'naia rol' noradrenergicheskikh neironov v gipotermicheskom éffekte apomorfina i drugikh dofaminomimetikov.

Administration of 6-hydroxydopamine hydrobromide (20-50 mg) into the cerebral ventricles of mice products the depletion of noradrenaline and dopamine in the brain and counteracts the hypothermic effect of dopaminomimetic drugs of direct (apomorphine, piribedil, bromocryptin, CM29-712) and indirect (d, l-amphetamine, L-DOPA) type of action. Pretreatment of animals with the blockers of catecholamines noradrenergic neuronal uptake (desipramine, protryptyline and AW15(1)II29) counteracts both the depletion of noradrenaline in the brain and the antihypothermic effect of 6-hydroxydopamine. The experimental data support the noradrenergic involvement in the hypothermic effect of dopaminomimetics in mice.