[Complex rehabilitation of a patient with marked motor and cognitive impairments after a brain injury]. / Kompleksnaya reabilitatsiya patsienta posle tyazheloi zakrytoi cherepno-mozgovoi travmy s vyrazhennymi dvigatel'nymi i kognitivnymi narusheniyami.

In the presented case report, the complex approach of rehabilitation in the remote period of traumatic brain injury (TBI) allowed the achievement of the significant clinical effect. The authors analyzed the experience of reflex therapy in the treatment of TBI. The effectiveness and potential of acupuncture, objectification of the results are topical issues that require further research.

Role of nicotinic and muscarinic cholinoreceptors in the realization of the cholinergic anti-inflammatory pathway during the early phase of sepsis.

Stimulation of nicotinic and muscarinic cholinoreceptors (nAChR, mAChR) in outbred albino mice with nicotine and aceclidine, respectively, in single equilethal doses 0.5 DL(50)6 h before sepsis induction significantly reduced animal mortality due to a decrease in blood concentrations of proinflammatory cytokines IL-1ß, IL-6, and MIP-2. Stimulation of mAChR (injection of aceclidine) stimulated the neutrophilic phagocytic and metabolic activity. Realization of the cholinergic anti-inflammatory pathway (stimulation of the peripheral nicotinic cholinoreceptors (α7nAChR) and central muscarinic cholinoreceptors (mAChR) was modulated by stimulation of the muscarinic cholinoreceptors of the phagocytic monocytic system cells.

Effects of reversible inhibition of cholinesterase and nicotine on mouse mortality and blood levels of proinflammatory cytokines during the early phase of sepsis.

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-1ß, and IL-6.

[Disturbances of immune status and cytokine profile caused by chronic intoxication with organophosphorus compounds and their correction by administration of imunofan].

Experiments on noninbred rats showed that the chronic intoxication with organophosphorus compounds sarin and methylparathion (30 days; total dose, 0.9 LD50; single daily dose, 0.03 mg/kg,) significantly decreases the immune responses and reduces the concentrations of blood cytokines IFN-gamma, IL-2, IL-4, IL-6, and IL-10. The damage is more pronounced in Th1 cells than in Th2 lymphocytes. The administration of imunofan (single daily dose, 20 microg/kg) for 5 days partly recovers the immune status and the content of cytokines in the blood.

Mechanisms of immune status disorders in chronic ethanol intoxication.

Experiments of outbred albino rats showed that chronic ethanol intoxication (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1-cells, increased blood corticosterone concentration, reduced T-lymphocyte acetylcholinesterase activity, blood concentrations of IFN-γ, IL-2, IL-4, IL-10, and increased IL-6 level.

[Pharmacological correction of Th1 and Th2 lymphocyte activity and cytokine profile in ethanol intoxicated rats].

It was established in experiments on noninbred rats that their ethanol intoxication (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL-2, IL-4, IL-10, increases the concentration of IL-6, suppresses the immune responses, and reduces the interrelation IFNgamma/IL-4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes. The immunomodulator polyoxidonium administered for four days at a daily dose of 700 microg/kg fully restores the cellular and humoral immune responses and the synthesis of cytokines IFNgamma, IL-2, and IL-4 and partly restores the production of IL-10.

Changes in the cytokine profile and reduced function of lymphocyte subpopulations in subacute tetrachloromethane poisoning.

Experiments on outbred albino rats showed that subacute poisoning with tetrachloromethane in a total dose of 1.0 LD50 appreciably decreased blood concentrations of cytokines (IFN-gamma, IL-2, IL-4, IL-6, IL-10), reduced the IFN-gamma/IL-4 ratio in comparison with the control, and suppressed the immune reactions, which attests to greater damage to Th1 compared to Th2 lymphocytes.

[Reduction of the immune responses and synthesis of cytokines associated with Th1 and Th2 lymphocyte function and their correction by polyoxidonium under conditions of subacute intoxication by organophosphorus compounds].

Experiments on Wistar rats showed that subacute poisoning by organophosphorus compounds dimethyldichlorovinyl phosphate (DDVF), malation, and dimethylparation (total dose, 1.0 LD50) suppresses both cell and humoral immune responses and significantly decreases the level of blood cytokines (IFNg, IL-4) and the IFNg/IL-4 ratio in comparison to the control, which is evidence for a greater lesion of Th1 cells in comparison to Th2 cells. The immunomodulator polyoxidonium administered for four days in a daily dose of 700 microg/kg under conditions of subacute intoxication with organophosphorus compounds restores the cell and humoral immune responses and the synthesis of cytokines.

Role of cholinergic and cytokine regulation of T cell function in stimulation and inhibition of immune reactions in intoxication by organophosphorus compounds in different doses.

Experiments on outbred albino rats showed that administration of acetylcholine and aceclidine in a dose of 0.1 LD50 for 3 days and of dimethyl dichlorovinyl phosphate (organophosphorus compound) in a single dose of 0.05 LD50 stimulated the function of Th1 and Th2 lymphocytes and cytokine production by these cells. Dimethyl dichlorovinyl phosphate in a single dose of 0.5 LD50 produced an opposite effect. Acetylcholine and aceclidine stimulated activity of acetylcholinesterase in T cells, while dimethyl dichlorovinyl phosphate in a single dose of 0.5 LD50 inhibited it. During acute intoxication, the organophosphorus compound, depending on the dose, can stimulate (acetylcholine effect) and inhibit the immune reactions (acetylcholinesterase inhibition of T cells).

[The influence of calcium folinate on the immunotoxicity of methanol].

The experiments on non-inbred rats showed that calcium folinate administered upon acute poisoning (0.5LD50) with methanol partly reduced the degree of suppression of the phagocyte metabolic activity of polymorphonuclear leukocytes, the T-dependent humoral immune response, the activity of natural killers, the antibody-dependent cell-mediated cytotoxicity, and the formation of the delay-type hypersensitivity, and completely restores the function of B-cells estimated using the T-independent antibody production.

[The influence of aminostigmine on the parameters of nonspecific resistance and immune system of the organism upon acute poisoning of benzyl 3-quinuclidylate].

The results of experiments on outbred rats weighing 180 -240 g showed that the acute poisoning with benzyl 3-quinuclidylate decreases the parameters of nonspecific resistance of the organism, reduces the antibody production mainly to T-dependent antigens (sheep red blood cells), decreases the activity of natural killers and the antibody-dependent cell-mediated cytotoxicity, and suppresses the formation of delayed-type hypersensitivity. Aminostigmine partly inhibits the immunotoxicity benzyl 3-quinuclidylate.