A Neurophysiological Picture of the Genesis of Fatigue, Chronic Fatigue, and Overfatigue in Human Operators

The present widespread conceptual model of the neurophysiological picture of human fatigue, chronic fatigue, and overfatigue is limited to the picture of hypoexcitability and development of inhibitory processes in the CNS. The results of this study show that, when fatigue deepens and is followed by chronic fatigue and overfatigue, the inhibitory processes that developed earlier weaken. The speed of nervous processes and their lability increase in this period, exceeding the initial normal baseline values; the differential inhibition strengthens. Both main nervous processes weaken; the excitatory process begins to relatively predominate. The equalization and paradoxical phases manifest themselves in the CNS functioning. As fatigue deepens and overfatigue develops, excitability of nervous structures continues decreasing. Interhemispheric asymmetry increases.     

The synthesis of cationic glycerolipid acetals containing aliphatic and heterocyclic bases

1,3-Dioxolane series cationic lipids containing residues of aliphatic or heterocyclic nitrogenous bases were synthesized. The bases were attached to the glycerol backbone either directly (piperazine) or via a spacer group through a thioether bond.     

Increase of the heart arrhythmogenic resistance and decrease of the myocardial necrosis zone during activation of cannabinoid receptors

We have found that intravenous administration of cannabinoid receptor (CB) agonist HU-210 (0.05 mg/kg), increases cardiac resistance against arrhythmogenic effect of epinephrine, aconitine, coronary artery occlusion and reperfusion in rats. Pretreatment with CB2-receptor antagonist, SR144528 (1 mg/kg), completely abolished the antiarrhythmic effect of HU-210. However this effect of HU-210 was not attenuated by pretreatment with CB1-receptor antagonist, SR141716A (3 mg/kg). We also found that HU-210 (0.05 mg/kg) decreased the relationship between infarction size and area of ischemia. It is concluded that CB2 receptor stimulation promotes an increase in the cardiac resistance against arrhythmogenic influences and probably increases myocardial tolerance of both ischemic and reperfusion damages in rats.     

Electron microscopy of Mycobacterium leprae passed in laboratory animals

The ultrastructure of M. leprae was studied in the process of its intraplantar passage from man to mice (passages 1-8). Changes in the morphology of M. leprae, observed in the course of 3 passages, were established. From the phase of dormant forms (passage 1) the bacteria became adapted to the new host by passage 3, which was confirmed by the absence of differences in the ultrastructure of cells by passages 3-8. The possibilities of the phenotypic variability of M. leprae in the process of in vivo passage should be taken into consideration when they are used for the production of specific biopreparations, experimental modeling and the screening of antileprous preparations.     

Opioid system and cardiac resistance to ischemic and reperfusion injuries

In vivo pre-treatment with the opioid receptor antagonist D,L-naloxone completely eliminated the reperfusion-induced creatine kinase (CK) leakage from the rat isolated perfused haert. The inactive isomer L-naloxone decreased the CK release by half. The (-antagonist ICI 174,864 and k-antagonist nor-binanltorphimine exerted a weaker protective effect. The (-antagonist DAMGO, the (2-agonist DSLET, the k1-agonist spiradolin, or the sigma-agonist (+)-SKF 10047, improved myocardial cell viability after ischemia/reperfusion.     

Delta-opiate receptors and heart resistance to arrhythmogenic factors

Stimulation of peripheral delta-opioid receptors exerted no effect on arrhythmias, whereas that central delta 1- and delta 2-receptor activation decrease the heart susceptibility to arrhythmogenic action of epinephrine. Pre-treatment with the delta-opioid receptor antagonist ICI 174 prevented the antiarrhythmic effect of the central delta-receptors stimulation. The findings suggest that the heart decreased vulnerability to epinephrine-induced arrhythmias following the central delta-receptors stimulation is mediated by an enhanced vagal activity.     

The role of mu- and delta-opiate receptors in resistance of the myocardium to free radical damage]

I.v. administration of the delta-opioid (OR) receptors' agonists DSLET or DTLET prevented creatine kinase leakage from the rat isolated heart in oxidative stress damage and abolished an increase in myocardial levels of conjugated diens and malondialdehyde. The agonists also prevented a stress-induced augmentation of the superoxide dismutase (SOD) activity. All protective effects of delta-receptor stimulation was completely abolished by the delta OR antagonist ICI 174,864. The data obtained suggest that the cardioprotective effect of the delta OR stimulation in vivo is not mediated via direct cardiac delta OR activation but, probably, rather via some unknown indirect circulating humoral factor(s).     

Positively charged acyl derivatives of carbohydrates as promising transfection agents

A convenient approach to the synthesis of mono- and polycationic glycolipid amphiphiles is suggested. The compounds obtained can be used for study of the structure-activity relationship and determination of the effect of hydrophobic and cationic domains on transfection efficiency.     

Erratum to: Deferrivibrio essentukiensis gen. nov., sp. nov., a Representative of Deferrivibrionaceae fam. nov., Isolated from the Subsurface Aquifer of Caucasian Mineral Drinking Waters

Microbiology - An Erratum to this paper has been published: https://doi.org/10.1134/S0026261722700011