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Dysregulation of adipose tissue functions makes a significant contribution to the pathogenesis of metabolic syndrome, one of the most common diseases in recent years. Adipose tissue is an organ that secretes at least several dozen signaling molecules, adipokines. One of the most studied and at the same time mysterious adipokines is adiponectin. The latter is due to the lack of clear ideas about the biological role of this adipokine, the presence of its several molecular forms with different activity and several types of receptors to this adipokine localized in almost all cells of the body. The purpose of this review is to summarize and analyze the available information about the molecular mechanisms of the effect of adiponectin on metabolism of carbohydrates, lipids and lipoproteins. The literature search was conducted by the keywords "adiponectin" and "metabolic syndrome" in the Pubmed and Elibrary.ru databases for the period from 1995 to 2021.According to the results of the literature analysis, it is assumed that adiponectin is involved in energy metabolism as a «satiety» hormone that promotes the utilization and storage of energy-rich substrates, fatty acids and glucose, which prevents the development or mitigates the already developed insulin resistance. This reduces the amount of plasma triglycerides and increases the level of high-density lipoproteins in the plasma. Adiponectin affects metabolic processes by activating the AdipoR1-APPL1-LKB1-AMPK, AdipoR1-APPL1-p38, AdipoR2-PPARa cascades, and possibly by activating the ceramidase and phosphoinositide pathways and insulin signaling. In addition to the AdipoR1/2 receptors, the adhesion molecule T-cadherin may be involved in the transduction of the adiponectin signal in endothelial and muscle cells. The mechanisms of signal transduction from T-cadherin, as well as from AdipoR2, remain unclear. Studies on the mechanisms of the action of individual molecular forms of adiponectin are extremely rare. The analysis shows the complex nature of adiponectin signaling, many of the mechanisms of which remain undiscovered, and it is possible that the near future will bring us significant progress in this area.

Abstract. Specific autoantibodies against acetylated, maleylated and malonic dialdehyde-(MDA)-modified lipoproteins are detectable in human plasma. Immunization of rabbits with autologous, correspondingly modified low-density lipoproteins (LDLs) did induce autoantibodies against acetylated, maleylated and MDA-modified lipoproteins. In atherosclerotic lesions from hyman aorta, the epitopes have been detected that were recognized by the antibodies to acetylated, maleylated, and MDA-modified LDLs. Such antigens were detected at all atherogenesis stages, beginning with the earliest lesions (lipid spots), and their deposition pattern was quite variable.Rabbit and human autoantibodies against acetylated, maleylated and MDA-modified lipoproteins recognized antigens in human atherosclerotic aorta. Modified proteins were localized both intra- and extracellular in tectum, superficial and deep layers of the atherosclerotic lesions. The most typical mode of depositions for all modified proteins si represented by extracellular deposits in the cap of lipid streaks and fibrous plaques, especially in transitional “shoulder” area.The intimal deposits of modified proteins shared similar features with distribution of apo-B-containing lipoproteins, like as of lipids detectable by Oil Red staining. The areas where modified proteins and apo-B-containing lipoproteins were revealed did often coincide with foci of IgG deposits. Modified proteins were not detectable in the non-affected segments of aortic intima.

Background: Restorative orbital and periorbital surgeries require implantable materials containing antimicrobial and anticancer medications. Purpose: To assess rat tissue responses to dacarbazine-containing implants made of cross-linked polyurethane of different densities. Material and Methods: Dacarbazine (DC)-containing polyurethane-urea foam (PUUF) implants were a subject of research. We studied the dynamics of DC release from these implant samples. Soft tissue cellular responses to the developed composites were assessed through the implantation of the latter in Wistar rats. Results: We found that the number of open pores impacts implant survival. There was no substantial difference in DC release between the PUUF samples with a DC weight percent of 1% and those with a DC weight percent of 0.5% at incubation days 1 to 3. At days 5, 7 and 14, an increase in DC release was higher in the former samples than in the latter samples (64% versus 55%). In animals with a subcutaneously implanted PUUF sample, there was histological evidence of (a) formation of a capsule and tight network of blood vessels surrounding an implanted sample at day 3, and (b) separation of the implanted material from the surrounding tissues by a wide cuff of lymphocytes and a thick connective tissue capsule (CTC) at day 7. Conclusion: The number of open pores impacts DC release and the speed of connective tissue ingrowth into the porous matrix. It was found that a CTC formed around all implants at early time points and at day 30, which in combination with the presence of DC in composite materials resulted in long-term cellular inflammation at the implant placement site.

In the article authors call attention to a choice of system of metrics, which permits to take a qualitative assessment of local area network functioning efficiency in condition of computer attacks.