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Sera of 80 patients with pyodermias of varius etiology were analysed for interferon-gamma (IF-gamma), antiinterferon autoantibodies (IF-a-AB), corresponding antiidiotypic antibodies (IF-AIAB) and the ratio IF-a-AB/IF-AIAB using ELISA assay. There was no correlation between serum IF-gamma and IF-a-AB. Progression of this disease was characterized by an increase of serum IF-a-AB and a decrease of IF-AIAB. Prolonged duration of this disease also caused the decrease of serum anti IF-a-AB and IF-AIAB. The ratio of IF-a-AB/IF-AIAB increased with severity and duration of this disease.

Serum levels of interferon-gamma (IF gamma), tumor necrosis factor alpha (TNF alpha) and autoantibodies (a-AT) to these cytokines were investigated in patients with Parkinson's disease (PD). The increased levels of TNF alpha (50%) and IF gamma (35%) were found in PD patients. There was close correlation between the serum level of TNF alpha and the manifestation of neurological symptoms (r = 0.434; p < 0.05), and between levels of IF gamma and the duration of this disease (r = 0.4511, p < 0.05) and patients age as well (r = 0.4358; p < 0.05). There was increased level of a-AT to TNF alpha in PD patients versus healthy controls (130.3 +/- 11.92 and 105.3 +/- 4.62, respectively, p < 0.05). The combined increase of levels of a-AT to TNF alpha and IF gamma (r = 0.91, p < 0.01) close reverse correlation between duration of PD and levels of a-AT to TNF alpha and IF gamma (r = 0.4644 and r = 0.606, respectively, p < 0.01) were also recognised. The data obtained suggest the involvement of TNF alpha and IF gamma into the pathological process during PD, which requires further investigation in this direction.

A method for determination of endo-1,4-beta-D-glucanase activity of cellulase samples based on the indirect measurement of decrease in viscosity of a carboxymethylcellulose solution in an electrochemical cell in the presence of an electron carrier was developed. A rotating disk electrode is used as the working electrode. When two reactions (enzymatic and electrochemical) proceeded in the cell simultaneously, the limiting diffusion current at a constant applied potential increases as the viscosity of the solution decreases. Conditions where the initial rate of change of diffusion current (dI/dt) is proportional to the enzyme concentration were found. A good correlation between the new method and a previously known viscometric method for determination of endoglucanase activity was observed.

By using immunoaffine chromatography and ELISA it was found that 30-35% polyclonal of anti-insulin antibodies (AB1) in sera of diabetes patients has bound with high-affinity to Nerve Growth Factor (NGF). This indicates the presence of common epitop(s) in both molecules and could be a reason for NGF deprivation during formation of the nervous system in fetuses of diabetic pregnant women. Patient sera also usually characterized by elevated level of antiidiotypic antibodies (AIAb2) which interact with membrane insulin receptors, and may induce the general metabolic disturbances in fetus and newborns from diabetic mothers, fatal sometimes. High levels of anti-insulin/NGF Ab1 may bind excess of AIAb2 and prevents the insulin receptors dysfunction (typical for newborns in satisfactory health state). On the other hand--children with elevated levels of Ab1 at age 1-3 years often revealed clinical signs of neuropathology.

Serum levels/affinities of natural autoantibodies to proteins S100, GFAP and MP65 in patients with physiological pregnancy are usually constant and may vary among individuals within relatively narrow range. In patients with early toxicosis in pregnancy dispersion of serum autoantibodies levels were often found beyond the normal range. This group includes cases with significantly elevated as well as abnormally decreased immunoreactivity parameters. Percent of newborns with different deviations from women with abnormal serum levels/affinities of autoantibodies to proteins S100, GFAP and MP65 was higher 1,5-2 fold compared with population.

The serum samples from 29 patients with Parkinson's disease were analysed for the levels of the autoantibodies (a-AB) and antiidiotype antibodies (AIAB) to the proteins of nervous system S-100, GFAP, NKP and MP-65. High levels of a-AB or AIAB to at least 3 proteins were seen in patients with severe course of the disease. No significant changes of these levels were observed in patients with light course of the disease. The plasmapheresis was carried out to some patients with severe course of the disease. After this procedure the decrease of neurological deficit from number 21 +/- 2 to 8 +/- 1 on Webster's scale and decrease of a-AB and AIAB levels to normal values (in some cases it became lower than normal values) were observed. It can be concluded that the levels of the a-AB to the nervous tissue proteins correlate with clinical condition of the patient.

20 samples of serum of patients with remote consequences of brain trauma were tested to detect autoantibodies (a-AB) against brain proteins S-100 and NKP. Essential pathology was not found out by standard solid-phase immunoassay. The original method was used to detect a-AB to the whole complex of antigen determinants. Using this method the elevation of a-AB against S-100 and NKP was shown at 16 cases. The disturbance of idiotype-antiidiotype regulation was revealed at this group of patients. It is suggested that insufficient level of corresponding antiidiotypes creates the conditions for autoimmune aggressor of a-AB against brain tissue.

The observation of 38 patients with different forms of epilepsy was carried out in terms of autoantibodies (aAB) to nervous tissue proteins: p16, p30 and S-100. The pathological increase or decrease of aAB titers to at least one of the antigens (AG) mentioned above was found in 31 cases. The qualitatively new approach was further used for the revelation of aAB to S-100. Not the very protein was adsorbed on the plates for immunoenzyme assay but antiidiotypic Abs which were the "mirror reflection" of corresponding protein molecules' determinants. The authors suggested that the method permitted to estimate the level of aAB to the whole complex of AG determinants. Thus, the percent of positive tests was approximately twice higher. The index of aAB binding by corresponding anti-idiotypes was decreased in 29 patients. It's quite possible that it formed some conditions for brain tissue damages by aAB.

The reaction of amylose with NaH and FcCH2NMe3+I- in dimethyl sulfoxide brought about a redox-labeled polymer with a low degree of modification, viz. 1 ferrocene residue per 60 glucose units. The preparation, (0.017ferrocene)amylose, displays one-electron irreversible behavior at a pyrographite electrode in terms of the Delahay formalism, the formal redox potential E degree' being equal to 0.38 V at pH 6 and 40 degrees C versus SCE. Specific to amylose enzymes endo-depolymerases, which carry out random hydrolysis, accept the labeled amylose providing a significant increase in the peak current on cyclic voltammograms. The absence of potential drifts suggests that the effect is due an increase in the diffusion coefficients of the amylose fragments in the course of enzymatic digestion of (0.017ferrocene)amylose. This proposal was confirmed by the simulation of experimental cyclic voltammograms. Several practical applications of the results of this study for electrochemical assaying the amylolytic activity and evaluation of the mechanisms of the enzymatic catalysis by amylases have been demonstrated.

The ferricenium salt FcH+BF4- behaves as a specific substrate of glucose oxidase acting instead of dioxygen with the effective parameters of the Michaelis-Menten equation kcat = 2.60 x 10(2) s-1 and KM = 2.7 x 10(-4) M at 25 degrees C, pH 6.8 and [D-glucose] = 0.001 M. The activity of glucose oxidase can easily be monitored by conventional UV-vis spectrophotometry at 617 nm following the bleaching of the ferricenium dye.