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Biomedical subjects

E V Liubimova

Publications and source records attributed to E V Liubimova.

12 recordsLinked to original sources
PubMed1989

[The role of thrombocyte prostanoids and products secreted by dense granules in the platelet attachment, spreading and aggregation on collagen substrates].

The role of platelet prostanoids and substances released from dense bodies (ADP and serotonin) in the initial attachment, spreading and aggregation of platelets on surfaces coated with I, III, IV and V genetic types of collagen was investigated. A positive linear correlation was found to exist between thrombi-like aggregate formation on collagen substrates and platelet prostanoid synthesis. No correlation was established between platelet aggregate formation and 14C-serotonin release. The cyclooxygenase inhibitor indomethacin and the antagonists of PG endoperoxides and TXA2 (13-APA and BM 13.177) completely block thrombi-like aggregate formation. Neither 13-APA nor BM 13.177 affect platelet spreading, while indomethacin inhibits this process by 25%. The ADP-scavenger CP/CPK inhibits platelet aggregation and spreading by 25-30%. The inhibitors of cyclooxygenase and CP/CPK do not influence the initial attachment of platelets. The data obtained suggest that thrombi-like aggregate formation on collagen substrates is mediated by the synthesis of PG endoperoxides and TXA2; however, in platelet spreading this synthesis plays a limited role. Spreading and aggregation of platelets on collagen substrates is only partly mediated by ADP and serotonin. Initial attachment of platelets does not depend on ADP and serotonin release and PG endoperoxide/TXA2 synthesis.

Adenosine Diphosphate↗
PubMed1989

[Stimulation of spreading and aggregation of platelets on immobilized type V collagen: mechanisms depending on Ca2+ and protein kinase C].

The effects of phorbol ester (PMA) and stable prostaglandin endoperoxide analog (U46619) on platelet interaction with a surface coated with monomeric type V collagen (CV substrate) and free Ca2+ concentration in platelet cytoplasm ([Ca2+]in) have been studied. In the absence of PMA and U46619, the discoid and spherical platelets from suspension are attached to CV substrate but are incapable of spreading and aggregation on the substrate. An addition of PMA (0.15-1.5 nM) or U46619 (1.5 microM) to the reaction mixture stimulates platelet spreading and the formation of multilayer (thrombi-like) aggregates on CV substrate. Using the fluorescent probe Quin 2, it was found that U46619 (0.1 microM) increases [Ca2+]in from the basal level (100-120 mM) to 600 nM. PMA (0.75-15 nM) exerts only a slight effect increasing [Ca2+]in by 30-40 nM. The data obtained suggest that the PMA-induced spreading and aggregation of platelets on CV substrate can occur via activation of protein kinase C at relatively low [Ca2+]in values. These results also testify to the existence of a substrate-independent mechanism of spreading of platelets activated in suspensions by soluble inducers.

Aminoquinolines↗
PubMed1989

[Interaction of thrombocytes with immobilized collagen in the vascular wall (a model for step-by-step study of formation of parietal thrombi)].

Scanning electron microscopy was used to examine the interaction of platelets with types I, III, IV, and V human collagens (CI, CIII, CIV, and CV substrates) immobilized on the surface of cultural plates. Basic differences were found in the activity of collagen substrates against platelets. On the CV substrate, virtually all the adhesive platelets were in a non-spreading++ state, i.e. at the stage of initial attachment to the spread. The CIV substrate showed initial attachment, spreading, and attachment of platelets from the suspension to the spread platelets. In addition to the processes occurring at the CIV substrate, the CI and CIII substrates produced multilayer platelet aggregates on the strata of spreading platelets (thromboid aggregates). The surfaces covered with various types of collagens are an adequate model for quantitative step-by-step study of the formation of parietal thrombocytic thrombi and of mechanisms of this process control.

Blood Vessels↗
PubMed1981

[Model system for studying thrombocyte interaction with the reconstructed vascular wall].

A new model system is suggested which is a partial reconstruction of normal, locally and vastly injured vessel walls on the basis of fibrillar collagen grown cultures of endothelial cells. The kinetic curve of adhesion on collagen of gel-filtered human platelets reaches saturation within 40 min. During adhesion the shape of collagen bound platelets changes. Acetyl-salicylic acid and platelet free serum inhibit adhesion. Endothelial cells are nonadhesive to platelets; they do not affect the platelet adhesion to the intercellular areas covered with fibrillar collagen.

Animals↗
PubMed1979

[Content of thyroglobulin polyribosomes in normal and pathological thyroid cells].

The content of individual thyreoglobulin (TG) polyribosomes in human thyroid gland was studied in healthy persons and in patients with thyroid pathology. The content of TG polyribosomes makes up to 16.2% in normal thyroid tissue and is found to decrease down to 7.8% and 7% under nodal euthyroid goiter and toxic adenoma, respectively. This content is decreased to 12.5% under diffuse toxic goiter and is intermediate between nodal and diffuse toxic goiter under mixed goiter (9.4%).

Goiter↗
PubMed1978

[Albumin mRNA from rat liver cells. Analysis of immunoadsorption of individual polyribosomes].

The analysis of albumin polyribosomes immunoadsorption is carried out using "sandwich" immunoadsorbents prepared on the basis of two aminobenzylcelluloses: commercial (paraaminobenzylcellulose) and synthesised (methaaminobenzyloxymethylcellulose). A method is worked out which is good for the estimation of the adaptibility of different aminobenzylcellulose preparations as an insoluble basis for the immunoadsorbent. Major properties of the "sandwich" sorbent (the accessible capacity and specificity) and the percent of isolated individual polyribosomes are found to be interrelated and determined by conditions of the immunoadsorption reaction. The increase of polyribosomes and sorbent concentrations and their ratio in the incubation medium results in the increase of the sorbent accessible capacity and the decrease in the inspecific adsorption but at the same time the percent of adsorbed polyribosomes decrease too. The "excess" of adsorbent with respect to polyribosomes, participating in the binding reaction, is necessary for the quantitative isolation of individual polyribosomes.

Albumins↗
PubMedDate not supplied

[Metabolism of mRNA in regenerating mouse liver: acceleration of the processing and decay of mRNA].

The kinetics of accumulation of poly(A+)mRNA in polyribosomes and the ratio: poly(A+)mRNA/(poly A-)mRNA were studied in regenerating mouse liver. It has been found, that the ratio: (poly A+)mRNA/(poly A-)mRNA was associated with the function of the cells: (poly A+)mRNA fraction has been decreased to 7% at 7 hours after partial hepatectomy and then reached the original value (25%) at 30-40 hours. The kinetics of accumulation of (poly A+)mRNA in polyribosomes during the transition from resting to growing state has revealed that both the lifetime and the presumable time of processing of the mRNAs of free and membranebound polyribosomes were decreased as compared to resting liver cells.

Animals↗