A series of biocide-containing polyethylene composites were obtained using novel guanidine-containing copolymers immobilized on an inert mineral carrier. Multispecies microbial communities were isolated from the surface of polyethylene samples either incubated or found in the environment, and their taxonomic composition was determined. Biofilms reconstructed using microorganisms obtained from different ecotopes were shown to intensively foul polyethylene surfaces. The presence of polyguanidine biocide suppressed the growth and survival of both binary and multispecies biofilms, with a cumulative effect during long-term incubation. When microorganisms were co-cultivated in binary biofilms, the phenomenon of a decrease in biocide effectiveness was demonstrated. This protective effect is potentially based on cooperative interactions inside the binary biofilm community. Scanning electron microscopy showed a pronounced difference in the architecture of reconstructed biofilms incubated in the presence of biocide in comparison to control samples, where biocide suppressed the formation of dense and well-organized three-dimensional structures. Biofilm disruption by immobilized biocides occurred primarily during the later stages of biofilm formation, probably caused by polycation interaction with their negatively charged extracellular components.

Chimeric antigen receptor (CAR)-T cell therapy, a breakthrough in hematological cancer treatment, is now being explored for autoimmune diseases like rheumatoid arthritis (RA). RA, characterized by chronic joint inflammation and autoantibody production, presents a compelling target for CAR-T cell therapy due to its potential for precise targeting of aberrant immune cells and restoration of immune tolerance. This review analyzes current strategies in CAR-T cell therapy for RA, focusing on molecular mechanisms and clinical implications. We discuss approaches such as CD19-targeted B cell depletion, simultaneous targeting of B cells and memory plasma cells, and the use of chimeric autoantibody receptors (CAARs) to target specific autoantigens. Furthermore, we explore the latest advancements in CAR-T cell engineering, including novel costimulatory domains, dual-targeting strategies, and the development of regulatory CAR-T cells (CAR-Tregs). This review provides insights into the efficacy and safety of CAR-T cell therapy for RA, highlighting its potential to revolutionize clinical applications and future directions in the field.

Backgroud. Kocuria are widespread Gram-positive bacteria. Although they are traditionally classified as non-pathogenic, recent studies have shown that they can cause problems in various fields, from livestock and aquaculture to medicine. This has led to an increased need to understand their antibiotic resistance mechanisms in order to combat them. Methods. To study the determinants of Kocuria antibiotic resistance, we used bioinformatics methods. To identify antibiotic resistance genes, we retrieved the complete genome sequences of Kocuria strains from the RefSeq database and screened them for antibiotic resistance determinants with different mechanisms of action. We also studied Kocuria strains in more detail: we sequenced whole genomes of K. carniphila 988, K. rhizophila 155, K. rosea 394 and K. rosea 397, and, in addition to bioinformatics studies, and tested five strains for their ability to grow in the presence of antibiotics. Results. For these five strains, the presence of antibiotic resistance genes in their genomes correlated well with the observed resistance to the corresponding antibiotics: all 5 studied strains have a high level of resistance to chloramphenicol, in addition, K. carniphila 988 is highly resistant to azithromycin and avilamycin. Conclusions. Therefore, it has been demonstrated that antibiotic resistance genes are present in many Kocuria genomes and these genes are functional in the strains we have studied.

Ribophagy is a crucial mechanism that maintains ribosome homeostasis in the cell by directing nonfunctional ribosomes to degradation via macroautophagy/autophagy. Impaired ribophagy may lead to ribosome quality control disorders and may consequently be associated with various diseases known as ribosomopathies. This topic has been actively studied over the past decade, but the complete mechanism of ribophagy is not fully understood. To study the mechanism of ribophagy, we performed a genome-wide CRISPR-Cas9-based screening using a fluorescent ribophagy reporter, which is a cell line with ribosomes carrying RPL29 fused with mCherry and GFP fluorescent proteins. Using the genome-wide Brunello library of guide RNAs, we identified the most promising targets for further study, including the ubiquitin ligase TRIM25, for which we have shown specific binding to the ribosome during ribophagy induction, leading to ubiquitination of the ribosome on the nascent peptide chain and degradation of the whole ribosome. Our findings also demonstrated that poly(I:C) treatment, which mimics viral infection, activates ribophagy in a TRIM25-dependent manner, suggesting the ribophagy pathway could be an antiviral defense mechanism. Taken together, we discovered a novel regulator of ribophagy, TRIM25, which provides new insights into the regulation of selective autophagy in the context of ribosomopathies.

Atherosclerosis remains a leading cause of cardiovascular morbidity and mortality worldwide, underlying major conditions such as coronary heart disease and stroke. The pathogenesis of atherosclerosis is tightly linked to chronic inflammation and dysregulated lipid metabolism, processes that are also implicated in other inflammatory diseases like rheumatoid arthritis and psoriasis. Monoclonal antibodies (mAbs) have emerged as a promising therapeutic strategy, offering targeted intervention against key molecular drivers of atherosclerosis. This review summarizes recent advances in the development and clinical application of mAbs targeting both lipid-lowering pathways—such as low-density lipoprotein (LDL) and proprotein convertase subtilisin/kexin type 9 (PCSK9)—and inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-17 (IL-17). Notably, anti-PCSK9 antibodies like alirocumab and evolocumab have demonstrated significant reductions in LDL-C levels and cardiovascular events in large-scale clinical trials. Similarly, antibodies targeting inflammatory cytokines have shown efficacy in reducing vascular inflammation and associated risks. The review also discusses the advantages and limitations of therapeutic mAbs, such as their high specificity, potential for adverse immune responses, and challenges related to tissue penetration and cost. Overall, monoclonal antibody therapy represents a significant advancement in the management of atherosclerosis, with ongoing research aimed at optimizing efficacy, safety, and accessibility. Future directions include the development of novel mAbs and combination therapies to further improve cardiovascular outcomes in patients with atherosclerotic disease.

Inhibition of mitophagy is one of the signs of chronic disease pathogenesis. Detection and measurement of mitophagy levels under in vitro and in vivo models provide a better understanding of the role of mitophagy disorder in disease development and serve as prerequisites for creating a clinically applicable system test. The development of such a system is potentially feasible, but taking into account a number of factors that will be discussed in detail in this article. Here it is considered the main models of mitophagy-based test systems and an analysis is carried out showing their advantages and disadvantages. The future potential for the development of mitophagy-based diagnostic test systems is also discussed here.