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An electron-spin resonance technique has been used to examine the influence exerted by the degree of compensation on spin effects in a set of nonmagnetic Ge:As semiconductor samples in the vicinity of the insulator–metal phase transition at temperatures 2 K ≤ T ≤ 80 K. It was found that the behavior of the paramagnetic susceptibility, specific to the Pauli paramagnetism and manifested in the spin density resonance, is drawn deep into the insulator state and is observed up to rather large degrees of compensation K ≈ 0.7 at temperature 20 K ≥ T ≥ 5–10 K. Outside this temperature range, both the quantities rapidly grow with increasing compensation and their behavior approaches the Curie law characteristic of the strong insulator state. The reason for this behavior is that the degeneracy is lifted at high temperatures and, at low temperatures, electron states are localized at the Fermi level as a result of the Coulomb blockade by compensating acceptors of the most closely lying donor states and the resulting formation of a narrow Coulomb band in the metallized impurity band. At temperature T ≥ 5–10 K, the gap is blurred by thermal excitations and has no effect on the manifestation of the Pauli paramagnetism. The behavior of the line width of the electron-spin resonance is determined by the scattering on quasi-stationary electric dipoles created by the Coulomb blockade at low temperatures and by the scattering on phonons at high temperatures. The behavior of the g-factor is qualitatively correlated with the specific features of the paramagnetic susceptibility and spin density: with decreasing temperature it weakly grows in the range of the Pauli paramagnetism and then rapidly increases in the range in which the Coulomb blockade is manifested and a transition occurs to the Curie law. By an analogy with ferromagnetic materials in which such a fast increase in the g-factor is observed, the possibility of a compensation caused ferromagnetic coupling of spins localized on donors. The microscopic model of such a coupling is discussed.

Results are presented for a study on the development of methods to remove gum, sulfur, and other impurities from diesel fuels at the site of use. The removal of dissolved impurities in diesel fuel is possible by a physicochemical method, having first enlarged these impurities using coagulants. The introduction of carbamide dissolved in water into the fuel permits a reduction in the content of gum and sulfur and an increase in the anti-wear properties of diesel fuel. The use of monoethanolamine in a mixture with isopropyl alcohol in the following step of fuel treatment increases the efficiency of the impurity removal process and further reduces the fuel sulfur and gum impurity indices.

Experiments on random-bred albino mice showed that of β2-adrenoreceptor agonist hexaprenaline sulfate significantly reduced mortality of mice from experimental sepsis (intraperitoneal administration of E. coli) in 4 and 24 h after modeling by reducing blood levels of proinflammatory cytokines TNFα, IL-1β, and IL-6. The antagonist of β2AR ICI-118,551 eliminated this effect.

Experiments on outbred albino rats showed that chronic nitrile acrylate intoxication (60 days, 0.05 LD50 per day subcutaneously) led to reduction of T-dependent humoral immune response (T-independent humoral immune response was less affected); parameters cell immunity were suppressed to a greater extent than parameters of humoral immune reactions. Equal attenuation of the functions of Th1 and Th2 lymphocytes, decrease of the blood levels of immunoregulatory, pro- and anti-inflammatory cytokines (IFN-γ, IL-2, IL-4, IL-6, IL-10, IL-13), and decrease of acetyl cholinesterase activity in thymic and splenic T lymphocytes were observed.

A low-temperature (3–100 K) electron spin resonance (ESR) study of the spin system of neutral As donors in Ge showed that on the insulator side of the insulator-metal transition the single-spin density exponentially disappears as T → 0. Such spins are bound into pairs to give an antiferromagnetic (AF) phase. Upon increasing the temperature the AF phase is destroyed, the single-spin density and, as a result, the ESR absorption signal becomes stronger. The temperature dependences of the densities of the pairs and single spins are typical for a chaotic distribution of neutral donors. In this case, there is no Neel temperature. For a low degree of compensation, the crystal lattice of Ge with the AF phase is actually a nanostructured system characterized by anisotropic internal stresses that are the strongest along one of the [110] directions. These stresses give rise to the anisotropy of the g-factor which is responsible for experimentally observed splitting of the ESR line. The compensating impurities destroy the AF phase and reduce this splitting. Local stresses are present in this case, too, but now they appear because of the Coulomb interaction of oppositely charged impurities and have no preferred orientation.

The possibility of measuring the ratio of composite ingredients using the two-energy transmission method has been studied. This technique differs from the known methods by its independence from the specific weight of the tested object. An equation of a measuring instrument with correction for the methodological error is derived. The formulas relating the error in concentration estimates to the errors in the calibration coefficients are presented.

Experiments on albino outbred rats showed that chronic poisoning with organophosphorus compounds (Russian VX, and sarin) for 30 days in a total dose of 0.3 DL50 (0.01 DL50 daily) is followed by a decrease in phagocytic and metabolic activity of neutrophils. The reduction of functional activity of monocyte phagocytic system was stipulated by the stimulation of N-cholinergic receptors of these cells. These changes were accompanied by a decrease in blood concentration of proinflammatory cytokines (TNF-α, IL-1β, and IL-6).

Experiments on outbred albino mice have shown that proserine (reversible cholinesterase inhibitor) and nicotine (nicotinic receptor agonist) in a equivalent dose of 0.2 DL(50)injected 2 h before sepsis induction significantly reduced animal mortality from experimental infection due to reduction of blood concentrations of proinflammatory cytokines TNF-α, IL-1β, and IL-6.

Experiments on outbred mice showed that acetylcholine chloride in a dose of 20 mg/kg 6 h after subcutaneous injection significantly reduces mortality of mice from sepsis induced by intraperitoneal injection of 2×10(9) E. coli bacterial bodies and the blood levels of proinflammatory cytokines TNF-α, IL-1β, and IL-6.

Sorption of 137Cs and 90Sr ionic species on soils with different agrochemical features was studied. The dependence of 137Cs sorption on peaty-bog soil on the ratio of the solid and liquid phases shows that sorption occurs by the ion-exchange mechanism. The correlation between the potassium content in soils and

Sorption of Zr(IV) from 0.1-3.0 M HNO3 aqueous solutions on KU-2 cation exchanger in the presence and in the absence of oxalate anions was studied. It was found that at certain concentrations of oxalate anions Zr(IV) sorption on the cation exchanger increases. Probable mechanisms of this phenomenon are analyzed.

Experiments on Wistar rats showed that subacute poisoning with anticholinesterase toxicants zarin and agent VX (daily subcutaneous injections in 1/7 LD50 for 6 days) led to suppression of cellular and humoral immune reactions and to a decrease in blood concentrations of cytokines (IL-2, IL-4, IFN-gamma) with a reduction of the IFN-gamma/IL-4 and IL-2/IL-4 ratios, which attests to more pronounced decrease in Th1 lymphocyte function in comparison with Th2 cells.

Experiments on outbred albino rats showed that single intraperitoneal injection of cytochrome P-450 inhibitor 2-diethylaminoethyl-2,2-diphenylpropylacetate (SKF-525A) in a dose of 50 mg/kg before acute poisoning with 1,2-dichloroethane and trichloroethane in a dose of 1.0 LD(50), metabolized in the body to compounds with higher toxicity (the phenomenon of "lethal synthesis") reduced their immunotoxicity by decreasing the formation of their biotransformation products.

Acute poisoning with tetrachloromethane in a dose of 0.75 LD(50) suppressed humoral and cell immune reactions in Wistar rats. Immunotoxicity of tetrachloromethane is realized via initiation of lipid peroxidation and inhibition of acetylcholine esterase in T lymphocytes and alpha-naphthyl AS-acetate esterase and alpha-naphthyl butyrate esterase in splenocytes.

Acute poisoning with alcohols and cholinotropic preparations carboxyphosphamide and atropine (0.8 LD(50)) was modeled on male outbred mice weighing 18-24 g. The decrease in activity of natural killer cells was most pronounced after injection of atropine, but insignificant after treatment with ethanol. The inhibitory effect of ethylene glycol, methanol, and methanol on functional activity of natural killer cells in vitro directly depended on their concentration. The effects of alcohols in equimolar concentrations of 10, 100, and 500 mM were similar. Therefore, immunotoxicity of alcohols was associated with the action of their metabolites. The ability of products formed after biotransformation of ethylene glycol, methanol, and ethanol in equimolar concentrations to cause damage to natural killer cells decreased in the following order: glyoxylic acid>formic acid>acetaldehyde>glycolaldehyde>glycolic acid. T-Activin injected subcutaneously in doses of 2.5 and 5.0 microg/kg for 3 days normalized activity of natural killer cells suppressed after acute poisoning with alcohols and cholinotropic preparations.

Experiments on Wistar rats showed that acute poisoning with chemicals in a dose of 0.75 LD(50) (dimethyl dichlorovinyl phosphate, sarin, VX substance, sulfur yperite, lewisite, tetraethyl lead, dichloroethane) inhibiting platelet acetylcholine esterase, alpha-naphthyl-AS-acetate esterase, and alpha-naphthyl-butyrate esterase suppressed T cell-mediated immune reactions.

Experiments on Wistar rats showed that the combined action of mechanical trauma and organophosphorus compound dimethyl dichlorovinyl phosphate a dose of 0.8 LD50 was accompanied by summation of their immunosuppressive effects. We observed an additive effect in relation to stimulation of the adrenal cortex. Treatment with general chemical toxicants (acrylic acid nitrile and acetonitrile, 0.8 LD50) alone or in combination with mechanical trauma produced similar increase in plasma corticosterone concentration. This effect was short-lasting and less pronounced compared to the influence of dimethyl dichlorovinyl phosphate. The immunosuppressive effect of trauma and nitriles is primarily related to the influence of poisons.

In vitro experiments on splenocytes from noninbred mice showed that ethylene glycol, methanol, and ethanol dose-dependently suppressed functional activity of T and B cells. These compounds in equimolar concentrations (10, 100, and 500 mM) produced similar effects, hence their immunotoxicity is determined by their metabolites. The suppressive effects of alcohol biotransformation products to antibody-forming activity of T and B cells decreased in the following order: glyoxylic acid - formic acid - glycolaldehyde - glycolic acid - acetaldehyde. The effects of these substances were dose-dependent. Suppression of T cells was more pronounced.

Experiments on Wistar rats showed that acute poisoning with organophosphorus compound dimethyl dichlorovinyl phosphate (0.5 LD50) was accompanied by two opposite effects: inhibition of acetylcholinesterase in T lymphocytes leading to suppression of thymus-dependent antibody formation (predominant effect) and acetylcholine-induced stimulation of antibody production. Acetylcholine activated acetylcholinesterase in intact T cells.

Experiments on Wistar rats showed that acute poisoning with organophosphorus compound dimethyldichlorovinylphosphate (0.2 and 0.8 LD50) was accompanied by suppression of the major immune reactions. Increasing the concentration of epinephrine and norepinephrine in the plasma produced less pronounced opposite effects, except for the influence on natural killer activity.

Experiments on random-bred male rats shows that acute poisoning with metaphos and acrylonitrile inhibites mainly the thymus-dependent humoral immune response, delayed type hypersensitivity reaction, and activities of natural killers and K cells. The increase in plasma corticosterone under the effect of metaphos ensures the participation of this hormone in the realization of suppression of natural killers and thymus-dependent humoral immune response (production of IgG), the contribution of the hormone to this suppression being 35.6 and 35.1%, respectively. Suppression of immune reactions by acrylonitrile is not associated with corticosterone effect.

Acute poisoning of rats with acetonitryl (0.3 and 0.8 LD50) decreased the bactericidal activity of the blood serum, serum activities of lysozyme and β-lysines, functional activity of neutrophils, counts of splenocytes producing antibodies to T-dependent and thymus-independent antigens, natural and antibody-dependent cytotoxicities, antigen-presenting function of macrophages, and delayed type hypersensitivity. The content of corticosterone in the plasma decreased under the effect of acetonitryl after 2 days. The effects of acetonitryl are dose-dependent.

Subjects with various types of personality accentuation are characterized by specific features of immunity. This proves a relationship between the function of the central nervous and immune systems. The detected features of immune response in subjects with various types of personality accentuation can be important for the formation of immunosuppression or hypersensitivity in various diseases.

Experimental acute dichloroethane intoxication (0.75 LD50) weakens the anti-infection resistance, suppresses antibody-dependent cell-mediated cytotoxicity, delayed-type hypersensitivity, and T-dependent humoral immune response and reduces the number of colony-forming units in the spleen. This suppression is probably associated with inhibition of α-naphthyl-AS-acetate esterase in immunocytes.

Acetylcholine and aceclidine reduce the mortality of mice after irradiation. This effect is evidently due to activation of M-cholinoreactive structures leading to an increase of the number of colony-forming units in the spleen, migration of T and B lymphocytes from lymphoid organs, and boosting of antibody production and of antibody-dependent cell cytotoxicity.

Experiments on mice revealed that the cholinesterase reactivator dipiroxime in a single dose of 15 mg/kg and retinol acetate in a dose stimulating thymus-dependent antibody production (3000 U per os daily for 3 days after poisoning) reverse the suppression of the main immune reactions caused by dimethyl dichlorovinylphosphate.

Cholinergic stimulation (acetylcholine, aceclidine, armin) is found to improve antiinfectious nonspecific resistance in mice. The effect depends on the dose of cholinomimetic (armin), is maximal during the first 18 hours of the infectious process, and is determined by serum antibacterial activity, lysozyme activity, and the function of neutrophils and natural killers.

Experiments on outbred and inbred male CBA mice showed that acute poisoning with ethylene glycol (0.8 LD50) increased mortality from infections, decreased the number of spleen colony-forming units, inhibited antibody formation (mainly to thymus-dependent antigens, and suppressed natural and antibody-dependent cytotoxicity and delayed-type hypersensitivity. Ethylene glycol in concentrations of 10 and 100 mM in vitro inhibited the formation of antibody-producing cells by acting on T and B lymphocytes.