Aims/Hypothesis: Galectin 3 appears to play a proinflammatory role in several inflammatory and autoimmune diseases. Also, there is evidence that galectin 3 plays a role in both type-1 and type-2 diabetes. During obesity, hematopoietic cell-derived galectin 3 induces insulin resistance. While the role of galectin 3 expressed in islet-invading immune cells in both type-1 and type-2 diabetes has been studied, the importance of the expression of this molecule on the target pancreatic β cells has not been defined. Methods: To clarify the role of galectin 3 expression in β cells during obesity-induced diabetogenesis, we developed transgenic mice selectively overexpressing galectin 3 in β cells and tested their susceptibility to obesity-induced type-2 diabetes. Obesity was induced with a 16-week high-fat diet regime. Pancreatic β cells were tested for susceptibility to apoptosis induced by non-esterified fatty acids and cytokines as well as parameters of oxidative stress. Results: Our results demonstrated that overexpression of galectin 3 increases β-cell apoptosis in HFD conditions and increases the percentage of proinflammatory F4/80⁺ macrophages in islets that express galectin 3 and TLR4. In isolated islets, we have shown that galectin 3 overexpression increases cytokine and palmitate-triggered β-cell apoptosis and also increases NO₂₋-induced oxidative stress of β cells. Also, in pancreatic lymph nodes, macrophages were shifted toward a proinflammatory TNF-α-producing phenotype. Conclusions/Interpretation: By complementary in vivo and in vitro approaches, we have shown that galectin 3-overexpression facilitates β-cell damage, enhances cytokine and palmitate-triggered β-cell apoptosis, and increases NO₂₋-induced oxidative stress in β cells. Further, the results suggest that increased expression of galectin 3 in the pancreatic β cells affects the metabolism of glucose and glycoregulation in mice on a high-fat diet, affecting both fasting glycemic values and glycemia after glucose loading.

Nowadays, biomedicine is a multidisciplinary science that requires a very broad approach to the study and analysis of various phenomena essential for a better understanding of human health. This study deals with the use of numerical simulations to better understand the processes of cancer viability and apoptosis in treatment with commercial chemotherapeutics. Starting from many experiments examining cell viability in real-time, determining the type of cell death and genetic factors that control these processes, a lot of numerical results were obtained. These in vitro test results were used to create a numerical model that gives us a new angle of observation of the proposed problem. Model systems of colon and breast cancer cell lines (HCT-116 and MDA-MB-231), as well as a healthy lung fibroblast cell line (MRC-5), were treated with commercial chemotherapeutics in this study. The results indicate a decrease in viability and the appearance of predominantly late apoptosis in the treatment, a strong correlation between parameters. A mathematical model was created and employed for a better understanding of investigated processes. Such an approach is capable of accurately simulating the behavior of cancer cells and reliably predicting the growth of these cells.

Adiponectin is one of the most important molecules in the body’s compensatory response to the development of insulin resistance. By trying to maintain insulin sensitivity, increase insulin secretion and prevent inflammation, adiponectin tries to maintain glucose homeostasis. Interleukin-33, which belongs to the group of alarmins, also promotes insulin secretion. Interleukin-33 might be either pro-inflammatory or anti-inflammatory depending on the disease and the model. However, interleukin-33 has shown various protective effects in CVD, obesity and diabetes. The aim of our study was to investigate the association between adiponectin and interleukin-33 in patients with metabolic syndrome. As expected, all patients with metabolic syndrome had worse parameters that represent the hallmark of metabolic syndrome compared to the control group. In the subgroup of patients with low adiponectin, we observed less pronounced characteristics of metabolic syndrome simultaneously with significantly higher values of interleukin-33 compared to the subgroup of patients with high adiponectin. Our findings suggested that adiponectin might be an early marker of metabolic syndrome that emerges before anthropomorphic, biochemical and clinical parameters. We also suggest that both interleukin-33 and adiponectin may be used to predict the inflammatory status in the early stage of metabolic syndrome.

(1) Background: Cancer stem cells (CSCs) are a subpopulation of cells in a tumor that can self-regenerate and produce different types of cells with the ability to initiate tumor growth and dissemination. Chemotherapy resistance, caused by numerous mechanisms by which tumor tissue manages to overcome the effects of drugs, remains the main problem in cancer treatment. The identification of markers on the cell surface specific to CSCs is important for understanding this phenomenon. (2) Methods: The expression of markers CD24, CD44, ALDH1, and ABCG2 was analyzed on the surface of CSCs in two cancer cell lines, MDA-MB-231 and HCT-116, after treatment with 5-fluorouracil (5-FU) using flow cytometry analysis. A machine learning model (ML)–genetic algorithm (GA) was used for the in silico simulation of drug resistance. (3) Results: As evaluated through the use of flow cytometry, the percentage of CD24-CD44+ MDA-MB-231 and CD44, ALDH1 and ABCG2 HCT-116 in a group treated with 5-FU was significantly increased compared to untreated cells. The CSC population was enriched after treatment with chemotherapy, suggesting that these cells have enhanced drug resistance mechanisms. (4) Conclusions: Each individual GA prediction model achieved high accuracy in estimating the expression rate of CSC markers on cancer cells treated with 5-FU. Artificial intelligence can be used as a powerful tool for predicting drug resistance.

Background: This cross-sectional study aimed to assess the correlation between subjective oral health status and mental health in a group of university students in Serbia. Methods: The study included 948 students, aged between 18 and 27, from the Faculty of Medical Sciences, University of Kragujevac, Serbia, and was conducted in 2020. The World Health Organization’s Oral Health Questionnaire for Adults was utilized to evaluate the respondents’ self-perceived oral health and oral hygiene practices. The existence of depressive symptoms was evaluated using the Beck Depression Inventory-II (BDI-II), and the Zung self-rating anxiety scale (SAS) was used for determining anxiety symptoms. Results: It is observed that 28.9% of respondents exhibit symptoms of depression and 42.3% showed symptoms of anxiety. Results show that students with severe depression and anxiety symptoms very often reported lower self-perceived oral health and oral health problems. Although the nature of this relationship has not been thoroughly evaluated, several studies have shown a mutually dependent connection between oral health and mental health. Conclusions: The results suggest that some aspects of oral health are associated with higher risks of developing symptoms of depression or anxiety, and vice versa.

Background: Trapa natans L. fruits and leaf extracts have a broad range of immunomodulatory, anti‐inflammatory, and antioxidant effects; however, their effects on cardiac protection have not been investigated. Objective: The study aims to test the biological activity of Trapa natans L. extract (TNE) in cisplatin (CDDP)‐induced cardiotoxicity. Methods: Wistar albino rats received a single dose of CDDP intraperitoneally and TNE ones per day for 2 weeks orally. Cardiac inflammation, necrosis, and fibrosis were determined by histological and immunohistochemical analyses. Cytokines in rat sera and cardiac tissue were detected by enzyme‐linked immunosorbent assay (ELISA) and quantitative real‐time (qRT)‐PCR. Rat macrophages cultured in the presence of TNE for 48 h were harvested for flow cytometry, while supernatants were collected for cytokine and reactive oxygen species (ROS) measurement. Results: Application of TNE significantly attenuated CDDP induced cardiotoxicity as demonstrated by biochemical and histopathological analysis. Administration of TNE once daily for 14 days decreased level of proinflammatory (TNF‐ α , IFN‐ γ , and IL‐6) and prooxidative parameters (NO ₂ , O ₂ , and H ₂ O ₂ ), while increased level of immunosuppressive IL‐10 and antioxidative glutathione (GSH), catalase (CAT) and uperoxide dismutase (SOD) in the systemic circulation. TNE treatment resulted in attenuated heart inflammation and fibrosis accompanied with the reduced infiltration of macrophages and reduced expression of proinflammatory and profibrotic genes in heart tissue of CDDP‐treated animals. In vitro lipopolysaccharide (LPS)‐stimulated macrophages cultured in the presence of TNE adopted immunosuppressive phenotype characterized by decreased production of proinflammatory cytokines and prooxidative mediators. Conclusion: Our study provides the evidence that TNE ameliorates cisplatin‐induced cardiotoxicity in rats by reducing inflammation and oxidative stress via promoting M2 macrophage polarization.