[The immunodiagnosis of thrombocyte membrane glycoprotein deficiencies: Glanzmann's thrombasthenia, Bernard-Soulier syndrome and GMP-140 protein deficiency]. / Immunodiagnostika defitsitov membrannykh glikoproteinov trombotsitov: trombastenii Glantsmanna, sindroma Bernara--Sul'e i defitsita belka GMP-140.

Immunological methods were developed for the diagnosis of platelet membrane glycoprotein (GP) deficiencies. The number of membrane GP on platelet surface was determined as the binding of 125I-labeled monoclonal antibodies (mAB) directed against individual platelet GP. Total amount of GP in platelet lysate was assessed by immunoblotting with specific polyclonal antibodies. Methods were applied for patients with different thrombocytopathies. Binding of mAB VM16a, directed against GP IIb-IIIa was strongly decreased in patients with Glanzmann's thrombasthenia (0.5-14.5% of normal) and binding of anti-GP Ib mAB VM16d--in patient with Bernard-Soulier syndrome (0.5% of control) indicating the deficiencies of corresponding GP. In patient with gray platelet syndrome binding of both antibodies was not decreased but even increased. It was shown by immunoblotting that platelets from the patient with gray platelet syndrome contained normal amount of GP IIa, but strongly decreased amount of GMP-140 (14.5% of control)--membrane GP of platelet--granules.

[Inhibition of Fc-receptor dependent platelet aggregation by monoclonal antibodies against the glycoprotein IIb-IIIa complex]. / Ingibirovanie Fc-retseptorzavisimoi agregatsii trombotsitov monoklonal'nom antitelom protiv kompleksa glikoproteinov IIb-IIIa.

A murine monoclonal antibody (MoAb) VM16a specifically binding to human platelets has been produced. Approximately 56,000 molecules of VM16a bound per platelet at saturation (Kd = 7.9 nM) but no binding to platelets from Glanzmann's thrombasthenia patients was detected. VM16a precipitated two proteins with molecular masses corresponding to those of glycoproteins (GP) IIb and IIIa from solubilized surface-labelled platelets. However, after dissociation of the GPIIb--IIIa complex with EDTA VM16a did not bind to platelets and precipitated nothing from their lysate, thus evidencing that its determinant is complex-dependent. VM16a had no effect on ADP-, thrombin- and ristocetin-induced platelet aggregation but inhibited the aggregation induced by collagen. This inhibitory effect was more pronounced in the presence of plasma. VM16a completely blocked the Fc-receptor-mediated aggregation induced by aggregated human IgG, aggregated murine IgG1 and the previously described MoAb VM58. F(ab')2 fragments of VM16a were also able to inhibit this aggregation by decreasing the rate of aggregation induced by aggregated IgG and by extending the lag phase of VM58-induced aggregation. These results suggest that the platelet Fc-receptor may be topographically associated with the GPIIb-IIIa complex.

[The effect of pulp extirpation on the function of the hard dental tissues]. / Vliianie depul'pirovaniia na sostoianie tverdykh tkanei zuba.

The authors analyze the results of clinical and experimental studies of the status of hard dental tissues before and after pulp removal. The findings evidence that Ca and P levels reduce and O2 and oxide levels increase in the hard tissues of pulpless teeth, this probably resulting in changed color and friability of pulpless teeth. These data may be useful in dental surgery when forming carious cavities in pulpless teeth and in orthodontics to make pulp insertions with due consideration for the friability of pulpless teeth.

[Platelet adenosine desaminase in various hematological diseases]. / Adenozindezaminaza trombotsitov krovi pri razlichnykh gematologicheskikh zabolevaniiakh.

Activity of adenosine deaminase (EC 3.5.4.4) was studied in thrombocytes of donors and patients with various hematological diseases. The enzymatic activity was decreased in acute leukemia, chronic myeloleukemia, chronic leukemia and blast transformation myeloma, microspherocytic and hypoplastic anemias. Variable level of the activity was observed in chronic lympholeukemia and non-Hodgkin disease. In all the diseases studied functions of thrombocytes were altered after treatment with various aggregating agents (ADP, thrombin, collagen, adrenaline, ristomycin).