Medical academic journal

The review examines the recently accumulated clinical and experimental data on the mechanisms of epileptogenesis, and the most appropriate methods for recording an electroencephalogram to detect epileptiform activity. A description of epi-patterns is provided, as well as artifacts – graph elements similar to epi-patterns. All descriptions are supported by appropriate illustrations. In order to identify possible epi-activity, the need for preliminary registration of electroencephalogram with functional tests in the form of rhythmic photostimulation and hyperventilation for a person participating as a subject in studies related to physical and postural loads is emphasized.

The review summarizes current data on the properties, localization and physiological role of GABA synthesizing enzyme, glutamic acid decarboxylase, in mammalian tissues. Due to the high prevalence of the enzyme in the body’s cells and tissues, at the moment there is a large array of scattered experimental data, which needs to be processed and systematized. Presented data demonstrate the involvement of glutamate decarboxylase in different biochemical and physiological processes of the body. It has been demonstrated that the role of enzyme as the major component of the GABAergic neurotransmission in the central nervous system is the most intensively studied. However, there is only limited information regarding distribution and functional role of glutamate decarboxylase in the peripheral nervous system, and therefore requires additional research.

Research on the role of various interleukins in atherosclerosis has shown that pro-inflammatory cytokines contribute to disease progression and destabilization of atherosclerotic plaques. The review presents the latest data from the scientific literature and the study’s own findings on the effects of pro-inflammatory cytokines INF-γ and TNF-α on the formation of unstable atherosclerotic lesions. It has been shown that the deterioration of the unstable plaque cap strength and its destruction can be associated with an increase in concentration, activation and action of powerful pro-inflammatory cytokines INF-γ and TNF-α in the vascular wall.

BACKGROUND: Bacteria use various endocytic pathways during entering non-phagocytic cells. The involvement of caveolae/lipid rafts in bacterial invasion has been demonstrated for many bacterial pathogens. However, for bacteria of the genus Serratia, the involvement of membrane microdomains in the process of bacterial internalization has been poorly studied.

AIM: To evaluate the involvement of caveolae/lipid rafts in the invasion of S. grimesii and S. proteamaculans bacteria into non-phagocytic epithelial Caco-2 and M-HeLa cells using nystatin.

MATERIALS AND METHODS: M-HeLa and Caco-2 epithelial cells were incubated with 50 μM nystatin for 1 hour at 37 ºC, after which they were infected with the bacteria S. grimesii strain 30063 and S. proteamaculans strain 94, the multiplicity of infection was 100 bacteria per cell. The number of intracellular bacteria was assessed using gentamicin protection assay. The level of caveolin-1 in cells was visualized using confocal microscopy and Western blotting. The expression of Toll-like receptors genes were measured by real-time RT-PCR.

RESULTS: Treatment of epithelial cells with nystatin reduces the internalization of S. grimesii and S. proteamaculans into M-HeLa cells by 30% and does not affect penetration into Caco-2 cells. At the same time, nystatin does not affect the redistribution / the integrity impairment of lipid rafts and does not lead to the cytoskeleton reorganization of eukaryotic cells. The addition of nystatin increases the level of caveolin-1 in M-HeLa cells (caveolin-1 is not expressed in Caco-2), which leads to a change plasma membrane fluidity. Nystatin promotes the secretion of proinflammatory cytokines interleukin-6 and interleukin-8 in both cell lines. Infection of M-HeLa cells pretreated with nystatin with the studied bacteria leads to an increase in the expression of tlr2 and tlr4 genes, but does not exceed the level of their expression in control samples. Therefore, it is impossible to speak unambiguously about the participation of Toll-like receptors in the invasion of Serratia bacteria.

CONCLUSIONS: The results obtained suggest that the interaction of bacteria with eukaryotic cells induces the expression of caveolin-1, which leads to a change plasma membrane components mobility. This may be due to the fact that β1-integrin is involved in the invasion of the studied bacteria, which should be stabilized at the plasma membrane upon binding of the ligand due to the formation of a cholesterol- and sphingolipid-rich membrane microenvironment.

BACKGROUND: Connexins, particularly connexin 43, form gap junctions that mediate neuron-glial communication. To date, the expression of connexin 43 in phenotypically distinct neurolemmocytes, in particular non-myelinating (Remak cells) and repair Schwann cells, has not been studied.

AIM: To determine the presence of connexin 43 in Schwann cells of the rat sciatic nerve under normal conditions and after mechanical damage by applying a ligature.

MATERIALS AND METHODS: The study was carried out on Wistar rats (n = 10). In experimental rats, the sciatic nerve was damaged by applying a ligature (40 s). 7 days after surgery, sciatic nerve segments were isolated for subsequent immunohistochemical study using antibodies to connexin 43 and glial fibrillary acidic protein (GFAP). In the control group rats, segments of intact sciatic nerves were isolated in a similar way.

RESULTS: It has been shown that in the endoneurium of the intact rat sciatic nerve there are no cells expressing connexin 43. It was found that 7 days after injury, a large number of connexin-43-immunopositive cells of irregular shape with several processes were identified in the endoneurium of the damaged nerve. There was a lack of expression of connexin 43 in GFAP-containing Schwann cells.

CONCLUSIONS: It can be stated that nerve damage leads to active synthesis of the studied protein by endoneurium cells; however, the origin of the cells expressing connexin 43 remains to be elucidated.

Irina S. Freidlin was an outstanding Soviet and Russian immunologist, Doctor of Medical Sciences, Professor, Honored Scientist, Corresponding Member of the Russian Academy of Sciences. She was a natural for teaching and a deep scientific researcher whose interests were mainly related to the study of innate immunity.