[Isolation and characteristics of ligand specificity of VLA-1 integrin from human smooth muscles]. / Vydelenie i kharakteristika ligandnoi spetsifichnosti VLA-1 integrina iz gladkikh myshts cheloveka.

Using affinity chromatography with immobilized monoclonal antibodies to the beta 1-subunit of human integrin, a total integrin fraction (subfamily beta 1) was isolated from the detergent extract of human smooth muscle (uterus). Immunoprecipitation and immunoblotting with specific antibodies revealed integrins VLA-1 and VLA-5. The former was isolated in a homogeneous state by chromatography on immobilized type I collagen in the presence of 1 mM Mn2+. The pure receptor yield was 2-4 mg per 400 g of smooth muscle tissue. Analysis of substrate specificity of VLA-1 in the liposome test revealed that this integrin possesses a broad spectrum of ligand specificity and can interact via a Ca2+, Mg(2+)-dependent mechanism with interstitial collagens of I, II and III types and with basal membrane proteins (type IV collagen and laminin). VLA-1 does not interact with fibronectin, thrombospondin or albumin. Denaturation of type I collagen decreases the liposome binding 5-7-fold. The peptide Gly-Arg-Gly-Asp-Ser-Pro added to the incubation mixture does not inhibit the liposome interaction with incorporated VLA-1 integrin, type I collagen and laminin.

[Effects of fibronectin instillation on reparative regeneration of the corneal tissue (an experimental study)]. / Vliianie instilliatsii fibronektina na reparativnuiu regeneratsiiu rogovichnoi tkani (éksperimental'noe issledovanie).

Comprehensive morphologic studies (including light microscopy, morphometry, autoradiography) of experimental rabbits have revealed a stimulating effect of fibronectin instillations on healing of central penetrating wounds of the cornea. A polypotent mechanism of the stimulating effect of fibronectin instillations during all the stages of the reparative process in the corneal tissue was proved.

[Apo B, fibrinogen-fibrin and fibronectin in the intima of the normal human aorta and large arteries and in atherosclerosis]. / Apo B, fibrinogen-fibrin i fibronektin v intime aorty i krupnykh arterii cheloveka v norme i pri ateroskleroze.

Apo B, fibrinogen/fibrin, fibronectin, thrombocytes, factor VIII of the blood coagulation and smooth muscle cells (SMC) were identified by the immunofluorescence method in the intima of aorta and big arteries under normal conditions and in atherosclerosis. Monoclonal antibodies (MCA) against C-end fragments of A alpha-fibrinogen chain were used in the study of fibrinogen/fibrin. MCA reacting with plasma fibronectin and those reacting with A-area of the polypeptide chain specific for the cell fibronectin were used for the identification of fibronectin. Small amount of fibrinogen/fibrin, no fibronectin in the extracellular matrix and the cell fibronectin around SMC were observed on the normal intima and lipid strip in spite of the presence of Apo B. The results indicate that fibrinogen/fibrin is accumulated in the plaques due to the incorporation of the wall thrombi, insudation from the blood plasma, intramural haemorrhages as well as around cells, presumably macrophages.

[Fibronectin and fibrinogen/fibrin at the focus of an experimental myocardial infarct]. / Fibronektin i fibrinogen/fibrin v ochage éksperimental'nogo infarkta miokarda.

The content of fibrinogen/fibrin, plasma and cellular fibronectin, the 1st type collagen, laminin and skeletal muscle myosin in the zone of experimental myocardial infarction was studied by the immunofluorescent method. The infiltration of the necrotized cardiomyocytes with fibrinogen/fibrin and plasma fibronectin was observed 3 hours and later after coronary artery ligation. Fibrinogen/fibrin and plasma fibronectin form a "primary matrix" of the granulation tissue in which the fibers of the 1st type collagen are being formed. Cellular fibronectin starts to be synthesized 3 days after the infarct development and its content in the extracellular matrix (ECM) of the granulation tissue increases 7-15 days after the infarction. The amount of the fibronectin in ECM of the scar tissue decreases 30 days after the infarct. Fibrinogen/fibrin is always found in the granulation tissue replacing the myocardial infarction but its content in ECM decreases during the scar formation.

[Comparative study of the binding of human blood plasma fibronectin with clinical strains of staphylococci]. / Sravnitel'noe izuchenie sviazyvaniia fibromnektina plazmy krovi cheloveka s klinicheskimi shtammami stafilokokkov.

The interaction of 62 S. aureus clinical strains and, respectively, 20 and 17 isolated S. epidermidis and S. saprophyticus strains with human blood plasma fibronectin (FN) has been studied. The specific interaction of FN with bacteria has been evaluated simultaneously by the binding of 125I with FN (method 1), the FN-mediated agglutination of staphylococci (method 2) and the character of colonies formed in 0.15% agar medium containing FN (method 3). The data obtained in this investigation indicated that all S. aureus strains under study react with FN to a different extent. When evaluating the binding of FN with bacteria, the most pronounced correlation was observed between methods 1 and 3. None of the methods used in this investigation has revealed interaction between FN and S. epidermidis and S. saprophyticus strains under study. The authors suggest that a preliminary inference on the capacity of the isolated clinical strains of staphylococci for reaction with FN may be made from the character of colonies formed in 0.15% agar medium containing FN.

[Effect of components of the extracellular matrix on the accumulation of lipids in human cells]. / Vliianie komponentov ékstratselliuliarnogo matriksa na nakoplenie lipidov v kletkakh cheloveka.

The effect of extracellular matrix components on cholesterol accumulation in different human cells was studied. Insoluble LDL-Heparin-Fibronectin-Gelatin complexes were incubated with human cells: fibroblasts, monocytes, peritoneal macrophages, cells of the aortic wall--endothelial, subendothelial intimal, medial; and total cholesterol content in these cells was determined. It has been demonstrated that components of extracellular matrix being complexed with LDL enhance total cholesterol accumulation in all cell types studied: the highest amount of cholesterol was accumulated by subendothelial intimal cells and peritoneal macrophages. It is suggested that components of extracellular matrix can play an important role in the development of lipid-laden foam cells that are accumulated in the arterial wall in atherosclerotic lesions.

[Quantitative immunoenzyme determination of fibronectin in biological fluids]. / Kolichestvennoe immunofermentnoe opredelenie fibronektina v biologicheskikh zhidkostiakh.

Quantitative immunoenzyme assay of fibronectin in blood plasma is developed. Isolation and purification of fibronectin from human blood plasma, harvesting of specific antibodies to fibronectin, production of the antibodies and peroxidase conjugates and step-by-step procedure of the immunoenzyme assay in a "sandwich" modification are described. The assay was applied for diagnostics of several infectious and somatic diseases.

[Immunomorphological study of fibronectin and collagen types I, III, IV and V in the myocardium in cardiosclerosis]. / Immunomorfologicheskoe issledovanie fibronektina i kollagena I, III, IV, V tipov v miokarde pri kardioskleroze.

Fibronectin and collagen, types I, III, IV and V, in the granulation tissue replacing the myocardial infarction, in the focal and diffuse cardiosclerosis were studied by means of the immunofluorescent method. The extracellular matrix in the granulation tissue contained fibronectin and collagen of the above types. Intracellular fibronectin was also found in the necrotized cardiomyocytes. Fibronectin and collagen of type IV were not detected in the postinfarction scars. The extracellular matrix consisted mainly of collagen, types III and V. Fibronectin and collagen, types I, III and V, are observed in the connective tissue in diffuse cardiosclerosis in the presence of the coronary arteries stenosis. No prevalence of the collagen of any type was found.

[Decreased effectiveness of cold-induced heparin precipitation of plasma fibronectin in infection]. / Snizhenie éffektivnosti kholodovoi geparinopretsipitatsii plazmennogo fibronektina pri sepsuse.

Plasma fibronectin (FN) is one of the major blood opsonins. The content of the glycoprotein reduces in sepsis which in turn may aggravate the course of the infection. FN is detectable in the content of cryoglobulins and cryofibrinogen. The formation of the heparin precipitate following plasma incubation in the cold in the presence of heparin is determined by FN involvement. Fibrinogen (FG) is another main component of the heparin precipitate. To determine the functional activity of plasma FN in sepsis and other pathological conditions, a study was made of the ability of FN and FG to go into the precipitate formed in blood plasma in the cold after its incubation with heparin. Unlike normal subjects in whom over 80% of FN on the average and about 20% of FG went into the heparin precipitate, in patients with hemoblastoses and aplastic anemia complicated by sepsis, less than 40% of FN on the average and about 7% of FG went into the precipitate. In some patients with sepsis, the heparin precipitate did not form. The reduction of FN ability to go into the heparin precipitate correlated with the gravity of the patients' condition. In uncomplicated hemoblastoses, cryoglobulinemia and cryofibrinogenemia and in immunocomplex pathology, the consumption of FN and FG during heparin precipitate formation did not significantly differ from the control. The data indicate that sepsis patients with blood system pathology may develop not only quantitative FN deficiency in the blood but also disorder of the functional activity of the opsonin.

[Fibronectin content of the intima of normal and atherosclerotic arteries]. / Soderzhanie fibronektina v intime arterii v norme i pri ateroskleroze.

An immunofluorescent study demonstrated the localization of fibronectin and collagen of types 1, 3, 4 and 5 in normal arterial intima and atherosclerotic patches. In the atherosclerotic patches, fibronectin is mostly grouped among cells of smooth-muscle origin together with collagen of type 4, while the fibrous tissue of the patches contains little fibronectin. It is assumed that changed extracellular matrix composition reflects the development of atherosclerotic patches, and fibronectin can be regarded as a marker of early stages of atherosclerosis.

[Plasma fibronectin level in patients with depression of hematopoiesis]. / Kontsentratsiia plazmennogo fibronektina u bol'nykh s depressiiami krovetvoreniia.

Plasma fibronectin is regarded to play an important part in a decrease of the resistance to infections. To specify the role of fibronectin in the pathogenesis of infectious complications in patients with depressions of hemopoiesis, the content of this opsonin was measured by ELISA in 113 patients with different patterns of hemoblastoses, lymphoproliferative diseases and with an aplastic syndrome. In 42 patients, the concentration of opsonin was measured in the presence of the superimposed infection of varying gravity. The fibronectin content was examined in 39 patients before, during and after completion of the cytostatic polychemotherapy. It turned out that in patients with paraproteinemic hemoblastoses, lymphogranulomatosis, aplastic anemia, chronic lympholeukemia, acute lympho- and myelo(mono)blastic leukemias, cyclic neutropenia, chronic myelosis and hematosarcomas, the concentration of fibronectin remained normal in the absence of infections. The computation of the linear correlation ratio did not reveal any association between the opsonin level and the concentration of neoplastic elements in the peripheral blood. Repeated measurements of the fibronectin level in patients whose underlying disease ran its course in association with marked neoplastic fever failed to detect any deficiency of the glycoprotein. The lowering of the fibronectin level was recorded in patients with a grave concomitant infection of the type of sepsis, necrotic enteropathy and lobar pneumonia. The degree of opsonin deficiency correlated with the patients' disease gravity. Prolonged reduction in the blood fibronectin level was of unfavourable prognostic importance. Cytostatic polychemotherapy, myelotoxic agranulocytosis as well as infectious complications of low gravity did not influence the concentration of fibronectin.(ABSTRACT TRUNCATED AT 250 WORDS)

[Immunomorphological study of fibronectin localization in a primary human aorta cell culture]. / Immunomorfologicheskoe issledovanie lokalizatsii fibronektina v pervichnoi kul'ture kletok aorty cheloveka.

Using indirect immunofluorescence, fibronectin localization in primary culture of human aortic cells was studied. Intimal and medical cultures obtained from normal and atherosclerotic zones were investigated. Four morphological cell types, previously described elsewhere, were found in these cultures. All the cell types were able to synthesise fibronectin and to form the extracellular matrix in culture. But the pattern and quantity of this matrix differs in different cell types. Elongate cells formed a fine network of fibronectin on their surface, but stellate, polygonal and asymmetric cells contained only several fibers of extracellular fibronectin. There was difference in the fibronectin localization pattern of the surface of cells, isolated from intima and media as well as from normal and atherosclerotic zones.

[Blood fibronectin level in experimental burn shock]. / Uroven' fibronektina v krovi pri èksperimental'nom ozhogovom shoke.

The blood fibronectin concentration in rats was measured by the ELISA during burn shock. Fifteen minutes after burn the fibronectin level was found to drop by 30% of the initial level on the average. Deep hypofibronectinemis lasted up to 24 h after burn. At the same time the clinical and pathomorphological picture of the shock was fairly pronounced. The survived animals demonstrated a progressive normalization of the fibronectin level. The fibronectin level completely returned to normal by the outcome of the second day after burn and then progressed to reactive hyperfibronectinemia by 70-72 h. The data obtained point to the involvement of fibronectin into the pathogenesis of burn shock, which is likely to be connected with the mechanism of reticuloendothelial system dysfunction.

[Changes in fibronectin concentration during therapeutic plasmapheresis. Therapeutic effectiveness of selective removal of fibronectin in immune complex pathology]. / Izmenenie kontsentratsii fibronektina v protsesse provedeniia lechebnogo plazmafereza. Terapevticheskaia èffektivnost' selektivnogo udaleniia fibronektina pri immunokompleksnoi patologii.

Variation in the concentration of plasma fibronectin (FN) seen during 65 sessions of therapeutic plasmapheresis was studied in 20 inpatients with the following diagnoses: acute leukemias (4), paraproteinemic hemoblastoses (5), Sjögren's syndrome (2), protracted septic endocarditis (1), systemic lupus erythematosus (17), acute polyradiculoneuritis (1), multiple sclerosis (3). The patients' age ranged within 19 to 64 years. There were 10 men and 10 women. The concentration of FN in 218 plasma samples was measured by the ELISA. It was discovered that plasma of healthy donors contained 200 to 400 micrograms/ml FN (M +/- 1.5 sigma). Prior to plasmapheresis the glycoprotein content in all the patients was on the average within normal (300 micrograms/ml). After the session the concentration of FN decreased almost two-fold (130 micrograms/ml); after 6 hours it was 175 micrograms/ml on the average, whereas after 24-48 hours it reached the initial level. Repeated plasmapheresis sessions carried out once every 3-4 days did not lead to the depletion of the FN pool, since its level reached the initial one over the first 24-48 hours. Such a mechanism was unchanged regardless of the initial level of FN recorded in the patients blood (high, normal or low). No relationship was found between FN deficiency which developed after plasmapheresis and infectious complications. It is assumed that FN deficiency per se cannot be responsible for the patients' decreased resistance to infection. Three patients received a series of selective plasmapheresis. Sjögren's syndrome and immune complex vasculitis was diagnosed in one female patient, hemorrhagic vasculitis due to chronic hepatitis in another female patient, the third female patient manifested gammapathy with cryoglobulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on the mechanism of translocation in ribosomes. IV. The role of ribisomal proteins S12 in translocation. / Izuchenie mekhanizma translokatsii v ribosomakh IV. Rol'ribosomnogo belka S12 v translokatsii

It is shown that ribosomes, the 30S subparticles of which are reconstituted without protein S12, read out poly(U) and synthesize polyphenylalanine in the absence of protein elongation factors (EF-T and EF-G) and GTP, i.e. perform "non-enzymatic" translation. On the contrary, ribosomes, the 30S subparticles of which are reconstituted with protein S12, do not display "non-enzymatic" translation without its activation with parachloromercuribenzoate. This means that a complete removal of protein S12 from the ribosome, as well as its damage with para-chloromercuribenzoate, leads to the unblocking of the potential ability of ribosomes for spontaneous ("non-enzymatic") translocation. The presence of intact protein S12 in the ribosome prevents spontaneous (EF-G-GTP-independent) translocation. A suggestion is made that the intact protein S12 forms an additional contact between the ribosomal subparticles and thus participates in the ribosomal mechanism of translocation by affecting the locking-unlocking of the subparticles.