The corrosion resistance and hydroabrasive resistance of the developed epoxy composite coatings are investigated in this paper. The analysis of the penetration index change after τ = 50–150 days of immersion in a water medium and 10% sulfuric acid solution is carried out. The optimal ratio of the modifier and nanodispersed (Si₃N₄, Al₂O₃, AlN, and TiN) and fibrous (viscose, polyamide, matka silk, rong, and cashmere) fillers in the epoxy binder is determined. It was allowed to slow down the process of electrochemical reaction on the metal surface. The penetration of aggressive media in such a coating during the time t = 150 days is 0.8–2.8%. It is 1.5–2 times lower than the similar indexes of the initial epoxy matrix. The rational combination of the fibrous filler (wool, acrylic PAN, and cashmere), modifier, and nanodispersed (Si₃N₄, AlF₃, IH, and ZrH) filler in the epoxy binder is found, which allows to provide optimum indexes of wear rate. The wear rate under the action of a hydroabrasive of such a coating is I = 0.20%, which is 4 times lower than the similar indexes of the initial epoxy matrix. The wear mechanism of such coatings is caused by the physical and mechanical processes of microcutting and plastic deformation of the surface layer of the material.

—Repeated fighting experiences can lead to changes in the neurophysiology and behavior of animals and to the formation of pathological aggression. Mechanisms of adaptation to repeated aggression are thought to be controlled through the hypothalamus and HPA axis. In this work, we studied the effect of repeated (30 days) experiences of aggression on gene expression in the hypothalamus in male mice of two strains, C57BL/6J and CD1. We measured the expression levels of the HPA axis genes (Crh, Crhr1, Crhbp, Fkbp5, and Nr3c1), as well as early response gene (Fos) and dopamine receptor D1 gene (Drd1). Repeated experiences of aggression led to prolongation of Fos activation in C57BL/6J, although the expression of other studied genes remained unchanged. CD1 aggressors are characterized by a decreased expression level of Crhr1 and Crhbp genes, whose products inhibit the secretion of corticotropin-releasing hormone. Most of the studied genes showed strain variation in gene expression that is probably associated with different levels of locomotor activity and anxiety in mice of these strains. The basal expression level of the Crh gene was higher in C57BL/6J mice, while the Crhr1, Crhbp, Fkbp5, Fos, and Drd1 genes were higher in CD1 mice. Thus, repeated experiences of aggression lead to gene expression changes in the hypothalamus of male mice, which depend on the genetic background and related psychophysiological features of individuals.

The hypothalamic-pituitary-adrenal axis (HPA) plays an important role in the mechanisms of adaptation to chronic stress. A model of chronic social defeat stress (CSDS), based on the experience of defeat in daily agonistic interactions, causes the development of a depressive-like state in mice, which is often accompanied by an increase in blood corticosterone levels. In this work, we assessed what changes occur in the central (hypothalamus) and peripheral (adrenal glands) parts of the HPA axis under the influence of chronic social stress, which can affect the regulation of corticosterone synthesis and its level in the blood. The experience of chronic social stress causes an increase in the relative weight of the adrenal glands, an increase in the expression level of Crh gene in the hypothalamus and the expression of the genes for the corticosterone synthesis enzymes Star, Cyp11a1, Cyp11b1 in the adrenal glands. At the same time, in the hypothalamus the expression of Fkbp5 and Nr3c1 decreases and the expression of Crhbp increases, and in the adrenal glands the expression of the Mc2r and Hsd11b1 genes decreases, which is ultimately aimed at reducing the amount of corticosterone secreted by the adrenal glands, and thus limiting the glucocorticoid response. Thus, chronic stress leads to an imbalance of the activating and stabilizing mechanisms of HPA axis regulation and a possible inadequate response to additional stress stimuli.

This study investigated how prolonged aggression in male CD1 mice alters responses to chronic LPS (lipopolysaccharide)-induced inflammation. Experience of aggression induced pathological aggression in 36% of mice. Following LPS, aggressors resolved systemic inflammation within five days—evidenced by normalized locomotor activity, WBC (white blood cells), and lymphocyte counts—while controls remained inflamed. LPS did not alter established aggression or anxiety. Furthermore, aggressors demonstrated accelerated inflammation resolution in the brain, showing a higher proportion of resting microglia and a lower percentage of activated microglia following LPS-induced inflammation compared to control animals. Gene expression analysis revealed a more pronounced inflammatory response in the hypothalamus than in the nucleus accumbens. Aggressive mice exhibited a profile associated with inflammation resolution, indicated by increased expression of the Trem2 gene. These differential immune responses may be modulated by the dopaminergic system. Elevated Drd1 gene expression in the hypothalamus could possibly contribute to the anti-inflammatory signaling, while changes in nucleus accumbens dopaminergic activity, involving D2 receptor activation, appear linked to the development of pathological aggression. Thus, this study demonstrates that prolonged aggression induces persistent changes in behavioral, neuroimmune, and neuroendocrine systems in male CD1 mice. Aggressive animals develop a distinct neuroimmune phenotype characterized by accelerated resolution of both systemic and brain inflammation following LPS challenge.