Biomedical subjects

O P Sakharova

Publications and source records attributed to O P Sakharova.

14 recordsLinked to original sources

PubMed1990

[Primary disability due to tuberculosis].

The social and clinical background of 1,043 tuberculosis patients newly recognized as disabled was studied. A complex study of the interrelation between tuberculosis-induced disability and medical and social factors was undertaken. Ineffective treatment proved to be the leading cause of disability, associating with untimely detection of the disease in 19.4% of the cases, irregular chemotherapy in 51.2%, concurrent chronic alcohol abuse in 31.4% as well as with insufficient use of surgical interventions and disruptions in the treatment continuity at its different stages. An important role in establishing the disability belongs to a low qualification level of the patients, their ++counter-indicated occupational conditions and the associated difficulties in their employment. A possible drop in the disability extent depends upon a number of issues dealing with preventive, diagnostic, therapeutic and social activities.

Adult↗

PubMed1982

[Tetanus toxin disturbance of 3H-GABA transport in the synaptosomes].

Synaptosomes isolated from the rat brain cortex were made use of to study the effect of tetanus toxin (TT) in doses of 1000-1200 MTD/ml (for rats) on 3H-GABA uptake and GABA and 3H-GABA release. After 15 minutes of incubating synaptosomes with TT, partial suppression of 3H-GABA release induced by K+-depolarization (30 and 40 mMK+) was discovered. TT did not suppress GABA release from synaptosomes (35-minute incubation), induced by ouabain (0.5 mM). Incubation of synaptosomes with TT in a Ca2+-containing medium for 2.5 h led to a noticeable (40%) suppression of their ability to accumulate 3H-GABA. Tetrodotoxin (10(-6)-10(-7)lg/1) increased 3H-GABA uptake but did not eliminate differences in the mediator uptake by poisoned and control synaptosomes. Incubation of synaptosomes with TT in media containing no Ca2+ was not followed by suppression of 3H-GABA uptake. The amount of 3H-GABA released during K+-depolarization by synaptosomes incubated with TT for 2.5 h was found to be less (with regard to the absolute magnitudes and proportion of 3H-GABA taken up) than in control.

Animals↗

PubMed1982

[Increase in glutamate decarboxylase activity in the synaptosomes after treatment with tetanus toxin].

The tetanus toxin (TT) action on crude glutamic acid decarboxylase (GAD) preparation and GAD activity of synaptosomes were studied. TT was not found to affect GAD, but the GAD activity of synaptosomes isolated from the rat brain cortex increased by 46% after 15 min of incubation in the presence of a dose of 0.1 DLM TT. In some experiments, the GAD activity of a crude synaptosomal fraction isolated from TT affected lumbar segments of the rat spinal cord 48 hours after 0.2 DLM TT injection into the m. gastrocnemius was higher than in the control. If the GAD activity was evaluated in the presence of saturating concentrations of pyridoxal-5-phosphate, the difference in the GAD activities between the control and TT-affected synaptosomes (in vivo and in vitro) was not revealed. These findings allow the suggestion that the TT influences on GABA synthesis are mediated by membrane processes and that they occur at the level of the cofactor and apoenzyme interaction.

Animals↗

PubMed1982

[Effect of tetanus toxin on K+ and Na+ concentration in synaptosomes].

A study was made of the effect of tetanus toxin (TT) in doses of 20-1000 MLD (for rats) on synaptosomes isolated from the rat brain cortex. TT produced a decrease in K+ content in synaptosomes. The effect depended on the dose of TT (I50=22 MLD). The content of Na+ remained unchanged. The action of TT depended on the time and the maximal effect was seen upon 60 minutes of incubation. TT inactivated by boiling or by antitoxin did not affect K+ content in synaptosomes. An increase of K+ concentration up to 17 mM in an incubation medium led to an increase in K+ content in TT-poisoned synaptosomes but not in the control ones. Possible changes in membrane electrogenesis in nerve terminals caused by TT are discussed.

Animals↗

PubMed1980

[Functional characteristics of nerve endings isolated from brain by the Hajos method].

A study was made of the functional potentialities of synaptosomes isolated from the brain cortex and lumbar enlargement of the spinal cord. The yield of synaptosomes from the brain cortex amounted to 10 mg (with reference to protein) from 1 g of wet tissue, and that of synaptosomes from the spinal cord was equal to 1/3 of the yield from the brain, with the preparation being strongly contaminated with myelin scraps. Brain synaptosomes were marked by high level of respiration whose magnitude was affected by the agents (ouabain, high concentrations of K+ and benzylpenicillin) that change ion membrane transport. Synaptosomes maintained higher GABA gradient across the plasmatic membrane. Ouabain and potassium depolarization produced a considerable release of GABA and 3H-GABA into the incubation medium. A conclusion is made that the method of Hajos should be rather used for rapid isolation of the synaptosomal fraction from the rat brain cortex.

Animals↗

PubMed1978

[Activity of Na, K-ATPase and the enzymes of intermediate metabolism in the brains of rats exposed to electroshock].

Activity of Na, K -ATPase, acetylcholinesterase (AChE) and glutamic acid decarboxylase (GAD) in the fractions of the rat brain and spinal cord tissue were studied in rats during a single electroshock (ES) and 5 and 30 minutes after it. GAD activity of the synaptosome fraction was shown to decrease insignificantly, but activity of AChE, Na, K -ATPase and possibly of proteolytic enzymes increased 5 minutes after electroshock and became normal in 30 minutes. It is supposed that the revealed inhibition of Na, K -ATPase activity in the "synaptosomes" of the rat brain cortex could be of pathogenetic significance in the origination of the convulsive process.

Acetylcholinesterase↗

PubMed1977

[Tyrosine hydroxylase activation upon electric stimulation of isolated hypothalamic nerve endings in rats].

The effect of electrical stimulation on the membrane-bound tyrosine hydroxylasectivity of the rat hypothalamus synaptosomes was studied. The electrical stimulation caused an elevation of O2 consumption and the elevation of glycolysis indicating synaptosome excitation. The membrane-bound tyrosine hydroxylase activity increased under these conditions. The KM value for tyrosine decreased from 0.091 to 0.026 mM. Noradrenaline inhibition of the enzymatic activity diminished. It is assumed that the effect of depolarization on the catecholamine synthesis velocity in the nerve endings involves tyrosine hydroxylase modification.

Animals↗

PubMed1975

[Changes in the protein composition of the synaptic structures of the brain of rats in tetanus intoxication].

As shown by the method of electrophoresis on polyacrylamide gel, the number of proteins with low electrophoretic mobility proved to be increased in the triton extract fractions of synaptic structures isolated from spinal cord of rats with local tetanus; no changes in the protein spectrum were revealed in the dodecyl-sulphate extract. In vitro tetanus toxin stimulated the lysin-H3 incorporation into the total proteins of synaptosomes of rat brain cortex.

Animals↗

PubMed1975

[Oxidative phosphorylation in rat spinal cord mitochondria in tetanus].

The mitochondria isolated from the spinal cord of rats with local tetanus utilized oxygen and inorganic phosphate more intensive than the mitochondria of normal animals. Ratios of P/O were similar. In experiments in vitro purified tetanus toxin in doses 5 X 10(2) = 1 X 10(5) MLD (for mice) did not effect on oxidation of intact mitochondria.

Animals↗

PubMed1975