Biomedical subjects
Publications and source records attributed to E A Kuznetsova.
A mathematical model of a new pontic design is developed. The final element analysis of the model proved the efficiency of the design. Effects on the denture length, abutment area cone angle, thread strain and height of location on abutment teeth, depending on the type and site of exercise, were studied.
Polymorphism of clinical manifestations in Toxoplasma infection and variegated disease patterns virtually rule out the diagnosis based solely on clinical symptoms, which makes modern laboratory tests particularly important. Amplification test system based on the polymerase chain reaction has been developed for the diagnosis of Toxoplasma infection. Computer analysis of nucleotide sequence of Toxoplasma gondii surface antigen gene P30 was analyzed, which helped choose and synthesize specific oligonucleotide primers. A method for biological material processing was selected, allowing sufficient DNA output. Optimal conditions for amplification reaction, ensuring absolute specificity and high (10-100 cells/sample) sensitivity, were determined.
Genetically programmed (apoptotic) cell death plays a key role in cell and tissue homeostasis and in pathogenesis of various diseases. However, the mechanisms involved in apoptotic cell death are poorly understood. At present, the role of proteases in key events of apoptosis is intensively studied and discussed and the involvement of various proteolytic enzymes in the induction and development of the cell death is well-recognized. Proteases of various classes participating in apoptosis have been identified as well as some substrates of these proteases whose cleavage is critical to cell viability; specific protease inhibitors which prevent the cell death have been synthesized. This review summarizes new data on proteolytic enzymes involved in apoptosis and considers the mechanisms of activation of proteases upon induction of apoptosis and the pathways of their involvement in the cell death. The participation of nuclear proteolytic enzymes in the destabilization of chromatin structure and regulation of DNA fragmentation by endonucleases in apoptotic cells is discussed.
Recent evidence suggests the existence of several endogenous Na+,K+-ATPase inhibitors in mammals. Previously, we have shown that the amphibian Na+,K+-ATPase inhibitor marinobufagenin (3,5-dihydroxy-14,15-epoxy bufodienolide) acts as a vasoconstrictor in isolated rat and human arteries. Mammalian plasma was shown to contain marinobufagenin-like immunoreactive material, which is responsive to saline volume expansion. The present study describes purification of a bufodienolide, which is similar to marinobufagenin, from the urine of patients after acute myocardial infarction with the use of thin-layer chromatography and reverse-phase high-performance liquid chromatography (HPLC). The purified substance cross-reacted with marinobufagenin antibody, demonstrated maximal UV absorbance at 300 nm characteristic of bufodienolides, and eluted from HPLC columns with the same retention time as marinobufagenin. Mass spectrometry of purified material revealed the presence of a substance indistinguishable from amphibian marinobufagenin and having molecular mass of 400 D. The present studies show that one of the human digitalis-like factors may have a bufodienolide structure and is likely to represent marinobufagenin or its isomer, and they suggest a role for this substance in the pathogenesis of myocardial ischemia.
The induction of structural lesions and repair in DNA of lymphoid cells from the peripheral blood, spleen and thymus of mice treated with natural mouse interferon alpha (IFN-alpha) 24 and 48 h prior to gamma irradiation were studied using the comet assay and apurinic-apyrimidinic (AP) site radiolabeling. It was demonstrated that the radiation-induced damage assessed by the comet assay in the DNA of peripheral blood lymphocytes (PBLs), splenocytes and thymocytes of mice treated with IFN-alpha before irradiation was considerably less and was repaired more easily in the postirradiation period than that in untreated mice. The DNA of PBLs and splenocytes from interferon-treated mice showed a decrease in the spontaneously occurring and radiation-induced AP sites, as determined immediately and 90 min after irradiation, compared to the level of AP sites in the DNA of untreated mice. The results lead us to assume that IFN-alpha activates the DNA repair systems in the cells of lymphoid tissue.
The main aim of the study was to test the hypotheses that (a) concentrations of endogenous digoxin-like factor (EDLF) are increased in the initial period after acute myocardial infarction (AMI) and (b) may contribute to the onset of ventricular arrhythmias. 54 patients of both sexes with a first transmural AMI were included in a retrospective study. Plasma concentrations of EDLF were measured repeatedly during days 1-14 after AMI using DELFIA digoxin fluoroimmunoassay. 16 male patients with unstable angina pectoris and suspected AMI as well as 8 healthy subjects of both sexes served as controls. Plasma concentrations of EDLF in patients during the first day of AMI were increased (1.25 + (-)0.26 ng/ml, digoxin equivalents, p < 0.05) as compared with both healthy controls (0.34 + (-)0.08 ng/ml) and patients with unstable angina pectoris (0.4 + (-)0.06 ng/ml). First day after AMI plasma levels of EDLF in 7 patients with primary ventricular fibrillation were higher (2.54 + (-)0.67 ng/ml, p < 0.03) than in 47 patients without ventricular fibrillation (1.05 + (-)0.27 ng/ml). In 14 patients with AMI and congestive heart failure (class III, Killip) plasma concentrations of EDLF were significantly lower (0.32 + (-)0.09 ng/ml, p < 0.03) than in 40 patients with AMI without congestive heart failure (1.51 + (-)0.32 ng/ml). Starting from the second day of AMI plasma EDLF decreased to the level of control and did not change during two weeks of observation. These results, being in agreement with our previous experimental data, show an increase of plasma EDLF after AMI and suggest that EDLF may be involved in myocardial ischemia-induced arrhythmogenesis and participate in pathogenesis of congestive heart failure after AMI.
OBJECTIVES: The aim of the study was to test the hypotheses that the concentrations of endogenous digoxin-like factor (EDLF) are (i) increased in the initial period after acute myocardial infarction (AMI) and (ii) may contribute to the genesis of ventricular arrhythmias. DESIGN: Consecutive sample study. SETTING: An 800-bed city teaching hospital, primary hospitalized care centre. SUBJECTS: Fifty-four consecutive patients of both sexes with a first transmural AMI, 16 male patients with unstable angina pectoris and eight healthy subjects. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Time-course of the changes of plasma concentrations of EDLF (DELFIA digoxin fluoroimmunoassay) in patients during days 1-14 after uncomplicated AMI and AMI complicated with ventricular fibrillation and congestive heart failure. RESULTS: Plasma concentrations of EDLF in patients on the 1st day after AMI were increased (1.25 +/- 0.26 ng ml-1 digoxin equivalents, P < 0.025) as compared with both healthy controls (0.34 +/- 0.06 ng ml-1) and patients with unstable angina pectoris (0.40 +/- 0.08 ng ml-1). On the 1st day after AMI the plasma levels of EDLF in seven patients with primary ventricular fibrillation were higher (2.54 +/- 0.67 ng ml-1, P < 0.05) than in 47 patients without ventricular fibrillation (1.05 +/- 0.27 ng ml-1). In 14 patients with AMI and congestive heart failure (class III, Killip), plasma concentrations of EDLF were significantly lower (0.32 +/- 0.09 ng ml-1, P < 0.01) than in 40 patients with AMI without congestive heart failure (1.51 +/- 0.32 ng ml-1). Starting from the 2nd day of AMI, plasma EDLF decreased to the level of the control values (0.35 +/- 0.04 ng ml-1) and did not change during a 2-week period of observation. CONCLUSIONS: The results show an increase of plasma EDLF during the 1st day after AMI, and that higher plasma EDLF may be associated with the development of ventricular arrhythmias.
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The activity of a neurospecific enzyme of tyrosine hydroxylase (TH) in monomolecular films formed onto solid surface was studied. The data obtained show that the formation of two-dimensional films onto negative-charge surfaces by the Langmuir-Schafer technology does not lead to the inactivation of the enzyme. Neuroleptic trifluoperazine increased the activity of TH. Monomolecular films of TH may be used as a sensitive element of biosensors for primary monitoring of neuroleptic-like compounds.
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The effect of mercaptoethylamine (MEA) on degradation of DNA in thermophilic bacteria Bac. stear. exposed to gamma-, UV-rays or methylnitrosourea (MNU) was studied. Using centrifugation on alkaline and neutral sucrose gradients, it was shown that MEA inhibits the accumulation of breaks in the DNA of Bac. stear. It also lowers the level of DNA degradation in toluene-treated cells of Bac. stear. under the action of the intrinsic nuclease, reduces the activity of the endonuclease specific for apurinic DNA, as well as that of S1-nuclease and DNase-I in vitro. The inhibition in the accumulation of DNA breaks is assumed to be due to a decrease of the endonuclease activity in the cells of thermophilic bacteria.
Experiments on rabbits anesthetized with urethane and chloralose were made to study the effect of microiontophoretically applied dopamine (DA) and immobilized DA connected with a polymer (DA-P) on extracellularly recorded activity of sensorimotor cortical neurons. Both DA-P and low-molecular DA reduced the frequency of spontaneous action potentials in the majority of the examined neurons in a dose-dependent manner. The inhibitory effect of DA-P was less powerful than that of DA under the same conditions of microiontophoretic application. Since low-molecular DA included in the structure of DA-P does not penetrate the neuron, it is concluded that the specific inhibitory effect of DA on neuronal activity is determined by its interaction with receptors located on the external surface of the neuronal membrane.
Stereospecificity of the effect of neuroleptics on substrate inhibition of isolated brain tyroxine hydroxylase is shown. Flupentixole cis-isomer eliminates substrate inhibition of the enzyme. The effect is concentration-dependent and is well marked within the tyrosine concentration range 10-6-10-4 M. Flupentixole trans-isomer in the same concentrations has no effect on substrate inhibition of tyrosine hydroxylase. In the presence of cis-flupentixole, the reaction rate plotted against tyrosine concentration is a hyperbole with a plateau at 160-360 microM tyrosine. In the presence of trans-isomer, as in the control sample, the relationships between the reaction rate and tyrosine concentration are depicted by a curve with a maximum (at 110-140 microM tyrosine). Like ftorphenazine, flupentixole isomer fails to eliminate the inhibitory action of alpha-methyl paratyrosine, which indicates the interaction of neuroleptics with the tyrosine-binding site of the enzyme molecules in the noncatalytic centrer. It is suggested that the interaction of the neuroleptics with the regulatory area of tyrosine hydroxylase might by important in the molecular mechanism of their action.
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Characteristics of antidromic action potentials of neurons in hypothalamic paraventricular and supraoptic nuclei were investigated during stimulation of hypothalamo-hypophyseal tract by stimuli of different amplitude and frequency. At tract stimulation with increased strength (1.5-2.5 times threshold) or frequency (above 100/s) discrete changes in antidromic action potential latency as well as variation of the spike fractionation in response to testing stimulus were observed. Leu-enkephaline administration into the third ventricle and intravenous injection of 1M NaCl solution reversibly changed the excitability of the antidromically activated neuron: leu-enkephaline mostly increased the latent period and the threshold of spike generation and decreased their capability to follow the stimulation frequency up to 10 Hz, whereas NaCl produced opposite effects. The data obtained indicate the necessity to take into account the excitability of the neurosecretory cell when using the accepted criteria of their antidromic identification.
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Administration of enkephalin into the 3rd ventricle enhanced the excitability of the paraventricular nucleus neurosecretory cells, the excitability reaching its maximum within 10 min. By the 15th min after the enkephalin administration the number of the enterochromaffin cells increases suggesting the inhibition of the secretory granules contents release into the blood. Within next 15 min the excitability of the hypothalamic neurosecretory neurons returns to its normal level. A simultaneous sharp decrease of the enterochromaffin cells occurs suggesting an endogenous activation of the secretory granules contents release.