Publications by authors named "Berchenko O"

The leading pathological mechanisms of Alzheimer's disease (AD) are amyloidosis and chronic inflammation. The study of new therapeutic drugs of the corresponding action, in particular miRNAs and curcominoids, as well as methods for their packaging, is topical. The aim of the work was to study the effect of miR-101 + curcumin in a single liposome in a cellular AD model.

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We estimated the efficacy of Brizantin preparation in suppressing nicotine dependence in rats. It was shown that nicotine-dependent rats in the situation of choice between the chamber with smoke or the chamber with food more frequently entered the chamber with tobacco smoke and stayed there longer. The rats that received Brizantin demonstrated significantly fewer visits to the chamber with smoke and spent there less time.

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We studied the effect of morphine hydrochloride, brain-specific S100 protein, and antibodies to morphine, S100 protein, and opiate mu-receptors in ultralow doses on self-stimulation of the lateral hypothalamus in morphinized rats. This reaction in morphine-withdrawn rats underwent specific changes after single administration of test preparations. Repeated treatment with preparations in the same dose equalized emotional homeostasis.

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We studied the effects of ethanol, morphine, S100 protein, and antibodies to morphine, S100 protein, and opiate -receptors in ultralow doses on self-stimulation of the lateral hypothalamus. The reaction underwent similar changes after single administration of test preparations. Tenfold treatment produced the stimulatory and stabilizing effect, which was related to ambivalent properties of preparations in ultralow doses.

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We compared the effects of neurotropic and neurospecific substances and their antibodies on conditioned activity of rats. Single treatment produced the positive effect on the latency and number of conditioned responses. Repeated treatment with test compounds in the same dose improved conditioned activity of animals.

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We studied the effects of morphine and its potentiated form on nociceptive thresholds in rats with the morphine withdrawal syndrome. Repeated combination (bipathic) treatment with morphine and its potentiated form increased nociceptive threshold and, therefore, activated the nociceptive system in the brain.

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We studied the effect of potentiated antibodies to morphine (10(-100) wt %) on self-stimulation of the lateral hypothalamus and behavioral reactions reflecting the severity of withdrawal syndrome in rats with morphine dependence. Repeated treatment with potentiated antibodies to morphine increased the rate of self-stimulation, suppressed active avoidance response, promoted freezing behavior after acoustic stimulation, and decreased tail-flick latency in rats after morphine withdrawal. Distilled water did not produce these changes.

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The effect of homeopathically potentiated antibodies to mu-receptors (10(-100) wt %) on integrative activity of rat brain was studied using the models of self-stimulation of the lateral hypothalamus and convulsions produced by electric current. Electric current was delivered through electrodes implanted into the ventromedial hypothalamus. Single treatment with potentiated antibodies to mu-receptors increased the rate of self-stimulation and decreased the threshold of convulsive seizures.

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Directed activation of a system of positive emotional reinforcement induces regulatory effect on limbic-neocortical mechanisms of the sleep-waking cycle organization in rats after chronic alcoholization carried out in periods of decreased and increased circadian rhythms of emotional activity. In animals with high level of positive emotional drive after the alcoholization self-stimulation of the lateral hypothalamus suppresses hypersynchronous paroxysmal activity in waking EEG, decreases the content of waking in the sleep-waking cycle, restores the paradoxical phase of sleep. In animals with inhibition of positive emotional drive in consequence of alcoholization self-stimulation of the lateral hypothalamus has no essential effect on the mechanisms of regulation of the sleep-waking cycle.

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Chronic alcoholization of rats prolonged their wakefulness and suppressed their slow-wave sleep due to a higher emotional activity. The data obtained suggest some adaptive changes occurring in the limbic-neocortical mechanism of the regulation of the sleep-wakefulness cycle, and positive emotional responses to chronic alcoholization.

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