It has recently been shown that the titer of the SARS-CoV-2 virus decreases in a cell culture when the cell suspension is irradiated with electromagnetic waves at a frequency of 95 GHz. We assumed that a frequency range in the gigahertz and sub-terahertz ranges was one of the key aspects in the “tuning” of flickering dipoles in the dispersion interaction process of the surfaces of supramolecular structures. To verify this assumption, the intrinsic thermal radio emission in the gigahertz range of the following nanoparticles was studied: virus-like particles (VLP) of SARS-CoV-2 and rotavirus A, monoclonal antibodies to various RBD epitopes of SARS-CoV-2, interferon-α, antibodies to interferon-γ, humic–fulvic acids, and silver proteinate. At 37 °C or when activated by light with λ = 412 nm, these particles all demonstrated an increased (by two orders of magnitude compared to the background) level of electromagnetic radiation in the microwave range. The thermal radio emission flux density specifically depended on the type of nanoparticles, their concentration, and the method of their activation. The thermal radio emission flux density was capable of reaching 20 μW/(m2 sr). The thermal radio emission significantly exceeded the background only for nanoparticles with a complex surface shape (nonconvex polyhedra), while the thermal radio emission from spherical nanoparticles (latex spheres, serum albumin, and micelles) did not differ from the background. The spectral range of the emission apparently exceeded the frequencies of the Ka band (above 30 GHz). It was assumed that the complex shape of the nanoparticles contributed to the formation of temporary dipoles which, at a distance of up to 100 nm and due to the formation of an ultrahigh strength field, led to the formation of plasma-like surface regions that acted as emitters in the millimeter range. Such a mechanism makes it possible to explain many phenomena of the biological activity of nanoparticles, including the antibacterial properties of surfaces.
Background. Interferons are the most important component of nonspecific (congenital) resistance of the body, the history of their discovery dates back to 1957 and the study is still ongoing. Evaluation of an individual interferon status (IS) with the estimation of the sensitivity of leukocytes to immune reactive drugs has a practical aspect. IS is a set of parameters indicating the state of nonspecific resistance.Aim. To study the problems of standardizing the IS tests with the search for possible ways of standardizing the method and calculate reference values based on a large amount of data.Materials and methods. A retrospective statistical processing was performed using the database of the IS tests performed in the clinical diagnostic department of the laboratory center of Exacte Labs LLC from September 2020 to August 2022. Enzyme immunoassay kits based on commercial reagents were used. The paper describes the methodology for studying IS with an emphasis on the least standardized procedures.Results. Reference values were calculated using three indirect methods. The analysis of the results obtained made it possible to identify age groups for which it is advisable to establish reference values. The study results showed the inconsistency of the obtained reference values as compared with the previous ones, which indicates the need for their correction.Conclusion. The considered problems of performing and standardizing the method for IS analysis are of practical importance for establishing a standard methodology and an in vitro method. The reference values have been updated to avoid errors in the interpretation of the results and to increase the clinical significance of the study.
Psoriasis is an immune-mediated disease with a complex pathogenesis. The close relationship between the development of psoriasis and the adaptive immune response is already known. However, recent data have shown that innate immune cells also play an important role in the development of psoriasis. Congenital lymphoid cells, dendritic cells, T cells, NK cells, and NKT lymphocytes are activated in psoriasis, contributing to disease pathology through IL-17-dependent and independent mechanisms. During disease progression, T cells secrete proinflammatory cytokines that induce and exacerbate the course of psoriasis. T cells have memory cell properties that respond rapidly to secondary stimulation, which contributes to disease relapse. This article presents an overview of recent findings demonstrating the role of innate immunity in psoriasis.
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